exam 2 deck Flashcards
1
Q
protozoa are a sort of strange collection of microbes that really existed as early… what?
A
they existed as early Eukarya
2
Q
does the protozoa define a specific, seperate domain or class of organisms?
A
no it doesn’t form a particular specific group within any taxonomic class, protozoa are a sort of strange collection of microbes that really existed as early eukarya
3
Q
are plants, animals or fungi a type of protazoa?
A
no
4
Q
are entamoebae and slime molds types of protazoa?
A
yes
5
Q
what are 5 groups that are protazoa?
A
ciliates, flagellates, trichomonads, microsporidia, diplomonads
6
Q
do ciliate protazoa typically cause diseases in humans?
A
no
7
Q
how are protazoa classified?
A
through their means of movement, nutrition and reproduction
8
Q
are protazoa typically intracellular
A
yes
9
Q
why are ciliates bad news for smaller organisms?
A
because ciliates can consume them whole
10
Q
are amoeba and stentor ciliates?
A
no only stentor is a ciliate
11
Q
how do are protozoan diseases transmitted to other organisms?
A
ingestion, vectors, sexual contact, transovarial, placental
12
Q
why are protozoan pathogens not well represented in foodborne illnesses?
A
because they are typically sensitive to heat, so any cooking usually kills them even if they are present in water
13
Q
are protazoan pathogens capable of surviving high temperatures?
A
no, they are typically sensitive to heat and cannot survive high temperatures
14
Q
how are vector borne transmissions distinguished?
A
vector borne transmission then is distinguished by a lack of ability to transfer the disease from one host to another; you need a mosquito or another organisms to act as a vector between hosts
15
Q
what are the 4 main malaria species?
A
16
Q
what is the general class through which maleria appears?
A
apicomplexa
17
Q
what are the unique strucutures that appear in in apicomplexa cells?
A
they have a polar ring, conoid and a microneme and rhoptry
18
Q
what is the significance of the polar ring and conoid?
A
they maintain a distinctive shape
19
Q
what is the significance of the microneme and rhoptry?
A
they aid in host cell invasion
20
Q
are apicomplexa motile?
A
no they tend to live within cells and rely on other species to transport them between hosts
21
Q
how does the polar ring and conoid aid the apicomplexas invasion of other cells?
A
it is very pointy and rigid which helps the pathogen burrow into the cell with its pointed end
22
Q
how do the microneme and rhoptry help the apicomplexa invade host cells?
A
they secrete proteins which break down host cell membranes
23
Q
what is the malaria life cycle?
A
-steps 4, 5 and 6are called the cyclical stage
-The ring stage is where you have one parasite in the centre of a red blood cell. and that undergoes a, a procedure in three, three broad steps whereby it multiplies. at that third step, the merozoites are produce in dozens inside a red blood cell And that eventually ruptures. And all of those parasites that are released will then go on to infect other red blood cells.
24
Q
how come blood products aren’t tested for parasites before transfusion happens?
A
if you’ve got dormant parasites in the liver for two years that are in such low numbers, you can hardly detect them in the blood. They can still potentially be transferred to other hosts through a blood transfusion,
25
what do sporozoites undergo in the liver?
they undergo schozogony which results in the merozoites which infect the red blood cells
26
why is the circumsporozoite protein important?
because most the successful vaccines target that
27
why is heparin sulfate glycosaminoglycan (GAG) important?
because that is the host liver cell antigen which the parasite will bind too. there's an interaction between the circumsporozoite protein and that binds to the GAG on the host cells.
28
how are the symptoms during the schizogony stage?
mild, malaria hepatitis is rare and the variation in liver involvment is rare because the parasites coat themselves in host liver cell membranes because it gives them a greater chance at survival
29
malaria pathogenicity
the exonemes help the parasites rupture out of red blood cells. And the dense granules on the far right hand side express antigens that appear on the red blood cell surface. So if a red blood cell is infected, it will have it will have malaria antigens on its surface.
30
why is it not useful to vaccinate against the antigens appearing on infected red blood cell surfaces?
he potential combination of antigens that could be on an infected red blood cell fall into the thousands, because there's loads of different combinations of different antigen classes. So, the dense granule produced antigens tend not to be able to be vaccinated against.
31
why are micronemes important for the apicomplexa?
the micronemes allow the apicomplexa to glide across the surface of the redblood cell and orient themselves ti exusre the apical complex is facing into the cells
32
why are rhoptres important?
they secrete enzymes, proteolitic enzymes which break down the red blood cell surface and form a vacuole which the parasite can enter
33
what are the fever patterns of P. vivax and P. ovale
you have a tertian fever; one day of fever for every 2 days of no fever/symptoms
34
# what are the fever patterns of P. vivax and P. ovale
what are the fever patterns of P. malariae
you have a fever once every 4 days; quartan fever
35
what are the fever patterns of P. falciparum
for every 2 days of fever you have 1 day without fever; tertian fever, the body is more sensitive to falciparum as fever is triggered at lower levels of toxin production
36
cyclical malarial fever
37
why do you get headaches and fever symptoms with malaria?
the immune system is very sensitive to hemozoin, which is the by product of malarial cells breaking down haemoglobin, hemozoin is released when the red blood cells rupture
38
how to malaria quinine treatments work?
thye work by preventing the parasites from breaking down their own toxic byproducts; the protozoa poison themselves with their own hemozoins and toxic oxygen species
39
what conditions are protective against malaria?
40
how is fever triggered by malaria?
the hamozoins trigger an immune response, the immune response affects the hypothalamus and then that results in elevated core body temperature
41
what is the pyrogenic threshold?
the amount of parasites needed per microlitre of blood to trigger an immune response
42
# what is the pyrogenic threshold?
what is the typical pyrogenic threshold?
between 200-1500 parasites per microlitre (ul) of blood
43
what is the pyrogenic threshold of P. falciparum?
about 150 parasites per microlitre (ul) of blood
44
what is toxoplasmosis
it is an apicomplexan disease caused by toxoplasma gondii
45
is apicomplexan an obligate intracellular parasite
yes
46
which hosts should be more concerned with toxoplasmosis
at risk hosts
47
what are the routes of spread of T. gondii?
48
is toxoplasma gondii reliant on humans?
no, it cycles through wild animals and typically gets to humans through undercooked meat products, blood or organ transplants, pregnancy or the fecal matter from pets
49
what does tachyzoites refer to?
tachyzoites means a fast replicating form of parasite
50
what does bradyzoites mean?
bradyzoites refers to a slow, dormant form of parasite that is barely even metabolising so this form is not concerning for humans unless you have a weakened immune system
51
in neonates, when is a toxoplasma infection most concerning?
during the 1st and 2nd trimesters
52
what are the possible outcomes of neonatal toxoplasmosis?
ocular abnormalities, brain damage or foetal death
53
why is a 3rd trimester toxoplasma infection not as concerning?
the symptoms are milder however potential damage is possible and damage to brain and eye tissue that leads to developmental problems, blindness and deafness is still possible
54
are humans terminal hosts of toxoplasma?
yes, this means they are accidental hosts
55
what are merozoites?
a merozoite is an apicomplexa protozoa that is in an infective form
56
why can toxoplasma be so dangerous for neonates?
because protozoa are very large cells compared to say bacteria thus a small number of cells can cause significant damage to developing tissue so not many cells are required to cause lesions
57
what are the symptoms caused by T. gondii infections?
flu-like illness that is caused by an immune response not the parasite itself
58
what is a dormant T. gondii infection
it is a stand off between parasites and the host where neither wins.
bradyzoites exist as cysts in neuron and muscle tissue, the infection is reactivated if the host becomes immunocompromised
59
what people are at risk to toxoplasmosis?
if the person has taken steroids, immunosuppressant drugs, suffers from HIV/Aids
60
how can toxoplasmosis affect immunocomprimised people?
it can cause pneumonia, carebral calcification, nephritis, skin rashes
61
how can complex cases of toxoplasmosis be treated?
they can be treated with a combination of pyrimethamine, sulfadiazine and folinic acid
62
why is it difficult to treat protozoan disease compared to bacterial diseases?
the protozoan cells are closer to our own cells so there are fewer targets
63
what is african trypanomiasis?
sleeping sickness
64
what is african trypanomiasis caused by?
trypanosoma brucei, central and west african distribution
65
what are the two types of trypanosoma brucei
trypanosoma brucei gambiense
trypanosoma brucei rhodesiense
66
what is american trypanosomiasis?
chagas disease, endemic in south america especialy in Brazil
67
what is chagas disease caused by?
trypanosoma cruzi
68
african trypanosomiasis life cycle
69
what is a vector for human african trypanosomiasis
Tsetse flys
70
# Tsetse flys
what are Tsetse fly habitats
forests/shrub land
rivers and watering holes
animal reservoirs
concetrations close to human settlements
they are very difficult to eradicate but traps have helps reduce their numbers
71
how has human african trypanosomiasis spread been controlled?
using traps has been very effective as apposed to vaccines or drugs as the vectors that spread them are controlled
72
when do symptoms for human african trypanosomiasis usually show up?
they can take months to years from initial infection to show up
73
why is it difficult to treat sleeping sickness?
because early stage disease mirrors many other diseases but the most effective drugs needs to be given early
74
human african trypanosomiasis symptoms
75
how can african trypanosomiasis cause coma?
if the parasite crosses the choroid plexus to the brain and CSF
76
how can african trypanosomiasis be diagnosed
through the cerebral spinal fluid
77
what can happen if african trypanosomiasis is left untreated?
it can cause weight loss and neurological impairment
78
what is the biggest factor in protozoan induced damage
low level chronic activation of the immune system; If we can't clear these pathogens from our body within a few weeks or even months, you get a chronic infection. The immune system is always trying to fight back, and that causes inflammation, scarring and other kinds of damage
79
how can trypanosomes be treated?
drugs that target the glycosome, which does not occur in human cells
80
what drug can treat trypanosomes?
suramin is a drug that binds to enzymes in the cytoplasm. suramin bound enzymes are dysfunctional as their ATP synthesis is reduced so cell cannot maintain energy levels
81
how is american trypanosomiasis spread?
through blood transfusions because vector to human contact has become less common, urban areas are more impacted
82
from what vector is chagas disease spread?
Triatomine bugs which infect the host in low quality housing usually,
83
chagas disease symptoms
2 stages
Acute stage occurs shortly after infection with swelling at the site of the infection
chronic stage, occurs to 30% of people after an asymptomatic period of several years
84
85
how does the Triatomine bug infect people
it defacates on the eye, or defaction of the vector is rubbed into the eye by the host inadvertdly, which rubs the pathogen into the eye mucosa reuslting in Romaña's sign
86
what occurs in the chronic stage of chagas disease?
27% of people get cardiac symptoms; heart is the most likely organ to be affected
3-6% develope megaviscera or peripheral nerve damage
the parasite resides in the tissue cells of the host
chronic stage causes these parasites to build up and build up in these muscle tissues there will be some level of immune activation against Chagas disease pathogens. This can happen over years. You've got low level immune activity attacking your heart tissues and it never eliminates the parasites, it doesn't completely wipe them out and Neither does the pathogen completely wipe the host out. So for years and years, you've got this chronic infection and the immune system in trying to get rid of these parasites I s constantly irritating the tissues. It's constantly causing lesions and inflammation in the heart tissues themselves And long term that's going to cause scarring. So over several years it's like collateral damage. Your own immune system trying to wipe out these parasites damages your own heart tissues. the heart is going to be less efficient and effective And eventually that could be fatal because the heart simply doesn't have the tone or strength to continue to pump blood around the body
87
what is the name of the chagas disease parasite
trypanosoma cruzi
88
what happens to the chagas disease parasite once it enters the cytoplasm of a muscle cell?
it becomes an amastigote which has a residual flagellum as it is no longer necessary
89
why is the kinetoplast in sleeping sickness and chagas disease parasites important?
it can be a target for drug treatments as human cells do not have it
90
why can cerebral spinal fluid be useful in detecting chagas disease
because about 70% of people have parasites in CSF
91
is leishmaniasis an intracellular parasite?
yes it is an obligate intracellular parasite
92
how is leishmaniasis spread
transmitted by female sandflies
93
what sort of disease does leishmaniasis occur as?
cutaneous, mucocutaneous and visceral disease
94
life cycle of leishmaniasis
95
what are the clinical presentations of cutaneous leishmaniasis?
lesions may not be as painful as they look which can help in diagnosing them
96
what happens shortly after a bite from an infected sandfly?
one or more skin sores can arise
97
what happens if a bite from an infected sandfly remains untreated
the sores can last from weeks to years and develope raised edges with a central crater
98
when can mucocutaneous leishmaniasis happen?
it can happen months-years after the cutaneous lesion has healed
99
how can mucocutaneous leishmaniasis be differentiated?
scanty presence of parasites and naso-pharangeal tissues are affected
100
what is the main cause of the tissue damage seen in mucocutaneous leishmaniasis?
constant low level activation of the immune system causing inflammation and tissue destruction as it tries to eradicate vesicles containing parasites. it is a chronic long term infection
101
how can mucocutaneous leishmaniasis be treated?
you can surgically remove infected tissue and give drugs
102
where does visceral leishmaniasis infections occur
they happen internally where it mainly affects the liver and spleen- It's chronic long term infection causing immune system targetted collateral damage to organs and structures.
103
how can leishmaniasis be treated?
they have a kinetoplast which can be targetted by drugs
104
how can visceral leishmaniasis infections be fatal?
they can cause damage to liver and spleen via the massive swelling of these organs which can eventually result in them no longer functioning if not treated
105
which form of leishmaniasis is most often seen as the most serious?
visceral leishmaniasis because it will always be fatal if left untreated
106
where is the kinetoplast?
note the flagella is also no longer there
107
What are the major routes of transmission for protozoan infections?
Ingestion, vector-borne, sexual contact, transovarial, and placental transmission.
108
Name the four classifications of protozoa based on their structure and movement.
Ciliates, flagellates, amoebae, and Apicomplexa.
109
What is schizogony, and why is it significant in protozoan lifecycles?
Schizogony is asexual reproduction leading to multiple daughter cells, significant in Plasmodium spp. for rapid proliferation.
110
Why are vector-borne protozoan diseases challenging to control?
They require managing not only the pathogen but also the vector populations, such as mosquitoes or ticks.
111
Which protozoan species can transmit through ingestion and cause waterborne diseases?
Giardia lamblia and Cryptosporidium spp.
112
What structural adaptations allow Apicomplexa protozoa to invade host cells?
Specialized structures like apical complexes, micronemes, and rhoptries.
113
How do vector-borne protozoa differ in their transmission from waterborne protozoa?
Vector-borne protozoa require an intermediate host for transmission, whereas waterborne protozoa are typically ingested as cysts.
114
What is the main survival strategy of protozoa in the environment?
Formation of cysts that can withstand harsh environmental conditions.
115
What distinguishes Apicomplexa from other protozoan groups?
Apicomplexa are obligate intracellular parasites with a polar ring structure and no external means of movement.
116
Name two protozoan diseases caused by amoebae.
Amoebic dysentery and primary amoebic meningoencephalitis (PAM).
117
Name the four main species of Plasmodium that cause malaria.
P. falciparum, P. vivax, P. malariae, and P. ovale.
118
What is the exoerythrocytic stage in the malaria lifecycle?
It is the stage where sporozoites infect liver cells and undergo schizogony to produce merozoites.
119
How does Plasmodium evade the host immune system?
By hiding in liver cells and red blood cells, and coating themselves in host cell membranes.
120
What are the protective factors against malaria in certain populations?
Sickle cell trait, thalassemia, lack of the Duffy antigen, and glucose-6-phosphate dehydrogenase deficiency.
121
What triggers cyclical fever in malaria?
The synchronous rupture of red blood cells releasing merozoites and toxins like hemozoin.
122
What is the role of the circumsporozoite protein in malaria?
It aids in the initial attachment of sporozoites to liver cells and is a target for vaccines.
123
Which Plasmodium species can cause dormant liver stages?
P. vivax and P. ovale.
124
What is the pyrogenic threshold, and how does it differ in P. falciparum?
It is the parasite density needed to trigger fever; P. falciparum has a lower threshold (~150 parasites/µL blood).
125
How does quinine work against malaria parasites?
By preventing the parasites from detoxifying hemozoin, effectively poisoning them.
126
Why is P. falciparum considered more severe than other malaria species?
It triggers fever at lower parasite densities and causes continuous fever with fewer symptom-free days.
127
What are the main infective forms of Toxoplasma gondii?
Tachyzoites (rapidly replicating) and bradyzoites (dormant cysts).
128
How is Toxoplasma gondii transmitted to humans?
Through contaminated food, water, cat feces, or transplacentally during pregnancy.
129
Why are humans considered terminal hosts for Toxoplasma gondii?
Humans are not part of its natural lifecycle, which primarily cycles between cats and prey animals.
130
What are the severe outcomes of congenital toxoplasmosis?
Brain damage, ocular abnormalities, and fetal death, particularly during the first trimester.
131
What is the significance of bradyzoite cysts in Toxoplasma infections?
They remain dormant in host tissues and can reactivate if the host becomes immunocompromised.
132
How does toxoplasmosis affect immunocompromised individuals?
It can cause invasive infections like pneumonia, cerebral calcification, and nephritis.
133
What is the role of tachyzoites in acute infections?
They are the rapidly replicating stage responsible for active tissue invasion and damage.
134
How is toxoplasmosis diagnosed in pregnancy?
Through serological testing and amniocentesis for fetal infection.
135
What treatments are available for severe toxoplasmosis?
Pyrimethamine combined with sulfadiazine and folinic acid.
136
Why are pregnant individuals advised to avoid handling cat litter?
To prevent exposure to Toxoplasma oocysts shed in cat feces.
137
What are the two types of human African trypanosomiasis?
T. brucei gambiense (chronic) and T. brucei rhodesiense (acute).
138
What vector transmits African sleeping sickness?
The tsetse fly (Glossina spp.).
139
What is Romana's sign in Chagas disease?
Swelling around the eyes caused by Trypanosoma cruzi infection via triatomine bug feces.
140
How does Trypanosoma cruzi evade the host immune system?
By forming intracellular amastigotes within host cells.
141
What chronic complications can arise from Chagas disease?
Cardiac damage, megaviscera, and peripheral nerve damage.
142
How is sleeping sickness treated in its early stages?
With drugs like suramin targeting the glycosome for ATP synthesis disruption.
143
What are the reservoirs for Trypanosoma species?
Domestic animals, wildlife, and humans.
144
What are the symptoms of late-stage sleeping sickness?
Coma, neurological impairment, and weight loss.
145
What measures are effective for controlling tsetse fly populations?
Insecticide-treated traps and managing habitats like watering holes.
146
Why has blood transfusion become a significant route for Chagas disease transmission?
Due to difficulty in screening for low levels of parasites in donors.
147
What are the three clinical forms of leishmaniasis?
Cutaneous, mucocutaneous, and visceral leishmaniasis.
148
Which vector transmits Leishmania spp.?
Female sandflies (Phlebotomine spp.).
149
What are the symptoms of cutaneous leishmaniasis?
Skin sores with raised edges and central craters.
150
Why is visceral leishmaniasis the most severe form?
It affects internal organs like the spleen and liver and is often fatal if untreated.
151
What is the role of amastigotes in Leishmania infections?
They are the intracellular stage that replicates within host macrophages.
152
How can leishmaniasis be prevented?
Using insecticide-treated nets and avoiding exposure to sandfly habitats.
153
What is the main diagnostic marker of visceral leishmaniasis?
Enlargement of the spleen and liver.
154
How does mucocutaneous leishmaniasis differ from cutaneous forms?
It affects mucosal tissues, often leading to deformities in the nasal and oral regions.
155
Why are sandflies challenging to control with standard nets?
They are small enough to pass through most standard net mesh.
156
What is the role of the kinetoplast in Leishmania?
It aids in energy metabolism and is a target for drug development.
157
What are the main features that differentiate protozoa from other microorganisms?
Protozoa are single-celled eukaryotes with a nucleus and organelles, unlike bacteria, which are prokaryotic.
158
What are the primary routes of protozoan disease transmission?
Ingestion, vector-borne, sexual contact, transovarial, and placental.
159
Why do most protozoa not survive high temperatures?
They lack the ability to withstand heat, making cooking an effective method to kill them.
160
How do protozoan cysts contribute to their survival?
Cysts are a dormant, protective form that allows protozoa to survive harsh environmental conditions.
161
What is the function of the apical complex in Apicomplexa protozoa?
It aids in host cell invasion by secreting enzymes that digest cell membranes.
162
How do flagella and cilia aid protozoa in their lifecycle?
They provide movement, aiding in feeding, evasion, or host cell targeting.
163
Why are vector-borne protozoan diseases particularly difficult to control?
They require the control of both the pathogen and the vector population.
164
What distinguishes Apicomplexa from other protozoa in terms of movement?
They lack external movement structures like cilia or flagella and rely on host invasion for transport.
165
How does phylogenetics classify protozoa?
Protozoa are not a distinct taxonomic group but are spread across multiple eukaryotic lineages.
166
What environmental factors favor the survival and spread of protozoa?
Warm climates, water bodies, and poor sanitation.
167
Name an example of a sexually transmitted protozoan infection.
Trichomonas vaginalis.
168
How do ingestion-based protozoan diseases spread in human populations?
Through contaminated food or water and fecal-oral transmission.
169
What are the differences between trophozoite and cyst forms of protozoa?
Trophozoites are the active, feeding form, while cysts are dormant and resistant to environmental stress.
170
How does plasmodial streaming in amoebae aid their movement?
It allows amoebae to flow over surfaces by extending their cytoplasm.
171
What role do ciliates play in protozoan pathogenesis?
Most ciliates do not cause diseases in humans, but exceptions like Balantidium coli can cause gastrointestinal issues.
172
What are the four primary species of Plasmodium that cause malaria?
P. falciparum, P. vivax, P. malariae, and P. ovale.
173
How is malaria transmitted to humans?
Through the bite of infected female Anopheles mosquitoes.
174
What is the exoerythrocytic stage of the malaria lifecycle?
The stage where sporozoites infect liver cells and undergo schizogony to produce merozoites.
175
What role does the circumsporozoite protein play in malaria pathogenesis?
It enables sporozoites to attach to liver cells and initiate infection.
176
Why are P. vivax and P. ovale infections prone to relapse?
They form dormant hypnozoites in the liver.
177
What is the pyrogenic threshold for P. falciparum, and why is it significant?
~150 parasites/µL blood, significantly lower than other species, making it more likely to trigger symptoms.
178
How does Plasmodium evade the immune system?
By hiding in liver and red blood cells and using host cell membranes for camouflage.
179
What distinguishes P. falciparum from other Plasmodium species in terms of severity?
It causes more severe symptoms due to higher toxin production and lower pyrogenic thresholds.
180
What is the cyclical fever pattern of P. vivax and P. ovale infections?
Tertian fever: one day of fever followed by two fever-free days.
181
How do quinine and related drugs work against malaria parasites?
By inhibiting the parasite's ability to detoxify hemozoin, leading to self-poisoning.
182
What are the symptoms associated with the erythrocytic stage of malaria?
Cyclical fever, chills, headache, and anemia.
183
What is the role of hemozoin in malaria pathogenesis?
It acts as a pyrogen, triggering fever by stimulating the immune system.
184
Why is the liver stage of malaria asymptomatic?
Parasites remain hidden within liver cells, avoiding detection by the immune system.
185
What genetic factors provide resistance to malaria?
Sickle cell trait, lack of the Duffy antigen, and glucose-6-phosphate dehydrogenase deficiency.
186
How does malaria influence public health in endemic regions?
It imposes a high disease burden, impacting economic productivity and healthcare resources.
187
What are the primary sources of Toxoplasma gondii infection?
Undercooked meat, contaminated water, and cat feces.
188
Why are humans considered accidental hosts for Toxoplasma gondii?
Humans are not part of its natural lifecycle, which cycles between cats and rodents.
189
What are tachyzoites and bradyzoites?
Tachyzoites are fast-replicating forms, while bradyzoites are dormant cysts in tissues.
190
What are the risks of congenital toxoplasmosis during pregnancy?
Brain damage, ocular abnormalities, and fetal death, especially in the first trimester.
191
How does toxoplasmosis present in immunocompromised individuals?
It causes severe infections such as cerebral calcification, pneumonia, and nephritis.
192
How does the immune system maintain a 'stand-off' with Toxoplasma gondii in healthy individuals?
By preventing bradyzoites from reactivating while allowing their dormancy in tissues.
193
How can toxoplasmosis be diagnosed during pregnancy?
Through amniocentesis or serological testing for antibodies.
194
What is the role of cat litter in Toxoplasma transmission?
Cats shed oocysts in their feces, which can infect humans handling litter.
195
Why is Toxoplasma gondii a concern in blood transfusions?
Dormant bradyzoites in the donor's blood can reactivate in immunocompromised recipients.
196
What treatments are available for severe toxoplasmosis?
Pyrimethamine, sulfadiazine, and folinic acid.
197
What factors can reactivate dormant Toxoplasma infections?
Immunosuppression from conditions like HIV/AIDS or steroid use.
198
What is the primary target of Toxoplasma gondii in human hosts?
Muscle and nerve tissues.
199
How does Toxoplasma gondii evade the immune system during acute infections?
By rapidly replicating as tachyzoites and hiding within host cells.
200
What are the symptoms of mild toxoplasmosis in healthy individuals?
Flu-like symptoms, including fatigue and muscle aches.
201
Why is raw or undercooked meat a significant risk factor for Toxoplasma infection?
Bradyzoite cysts in infected animal tissue can survive if not adequately cooked.
202
What are the two diseases caused by Trypanosoma species?
Sleeping sickness (African trypanosomiasis) and Chagas disease (American trypanosomiasis).
203
What vector transmits African trypanosomiasis?
The tsetse fly (Glossina spp.).
204
What is Romana’s sign in Chagas disease?
Swelling around the eyes caused by Trypanosoma cruzi infection.
205
How does Trypanosoma brucei evade the immune system?
By continuously varying its surface glycoproteins.
206
What chronic complications arise from Chagas disease?
Cardiac damage, megaviscera, and peripheral nerve damage.
207
How can Trypanosoma infections be diagnosed?
Through blood smears, cerebrospinal fluid analysis, or serology.
208
What is the primary vector for Chagas disease?
Triatomine bugs, also known as 'kissing bugs.'
209
What environmental factors increase the risk of Chagas disease?
Poor-quality housing and proximity to insect reservoirs.
210
How does suramin work against Trypanosoma infections?
By disrupting ATP synthesis in the parasite's glycosome.
211
What are the symptoms of early-stage African sleeping sickness?
Fever, swollen lymph nodes, headaches, and rash.
212
What is the key distinguishing feature of T. brucei gambiense infections?
They cause chronic disease with symptoms appearing months or years after infection.
213
How does Chagas disease transmission differ in urban areas?
It is increasingly spread via blood transfusions rather than vector bites.
214
What structures in Trypanosoma are unique drug targets?
The kinetoplast and glycosome.
215
Why are vector-control measures critical in reducing Trypanosoma transmission?
They target the tsetse fly and triatomine bug populations, interrupting the lifecycle.
216
How can sleeping sickness progress if left untreated?
Parasites invade the central nervous system, causing coma and death.
217
what does Cryptosporidium parvum cause?
Cryptosporidiosis
218
what does Cyclospora cayetanesis cause?
Cyclosporiasis
219
what does Giardia lamblia cause?
Giardiasis
220
what does Balantidium coli cause?
Balantidiasis (dysentery)
221
what does Acanthamoeba spp. cause?
Keratitis
222
how can protozoa survive in water
they change to a cyst form
223
what happens to the protozoa cysts if you ingest them?
in the gut the cyst will transform into their trophozoite forms
224
what is the life cycle of cryptosporidium?
225
what is the life cycle of entamoeba coli?
226
what is the prevelance of Giardia in rich countries?
2-7%
227
what is the prevelance of giardia in poor countries?
20-30%
228
what is the main symptom of giardia?
it causes diarrhoea for several weeks, abdominal cramps, gas production, lots of fat is in the faecal material
229
what is the mechanism of action for giardia?
toxins called giardins affect cntractile proteins in the gut this induces apoptosis and activation of lymphocytes; resulting in malabsorption and increased transit
230
how do giardia physically affect the gut?
they line the gut and damage the villi and because the cells are comparable in size to ours a large number or giardia cells can cover large areas of the body making the infection spread across a wider range
231
what can treat Giargia?
metronidazole
232
what is metronidazoles mechanism of action
the drug targets anaerobic metabolic pathways which human cells do not have
233
what are key charachteristics of luminal protozoan parasites? such as Giardia and other flagellate organisms
234
do flagellates have mitochondria?
no
235
how are protazoa infections diagnosed and why?
using microscopy techniques because protazoa do not form colonies on agar
236
what test is used to diagnose protozoa?
the ova, cyst and parasites method
237
cryptosporidium cell cycle
large resoevoirs in cattle herd and water run off from farm land, this pathogen can affect anybody but is more serious in immunocomprimised people
238
does crytosporidium have vectors?
no
239
what are high risk resevoirs for cryptosporidium?
large resoevoirs in cattle herd and water run off from farm land
240
what is the treatment and recovery like for immunocompetent people suffereing from cryptosporidiosis?
fluid and electrolyte replacment
some protective immunity comes naturally as it happens to young people who end up developing protections after exposure to the illness
illness is self limiting as it lasts 1-2 weeks
241
what is the treatment and recovery like for immunosuppressed people suffereing from cryptosporidiosis?
severe diarrhoea causing dehydration and weight loss
not self-limiting, there is no targeted treatment, no actual drugs that can actually kill the pathogen
vigorous rehydration and anti-diarrhoeal drugs needed
extraintenstinal infection can be fatal
242
how is cryptosporidiosis relevent to poverty
A major cause of childhood(<1 y.o.) diarrhoea
Associated with malnutrition
243
what happens to cryptosporidium when it is outside the host?
it forms cysts
244
are there any drugs available to treat the cryptosporidium pathogen?
there is no targeted treatment, no actual drugs that can actually kill the pathogen
245
is cryptosporidium an apicomplexa?
yes
246
what is the pathogenicity of cryptosporidium?
there is no scientiific consensus on the pathogenicity mechanism
247
is cryptosporidium intracellular?
it is partly intracellular
248
what are the possible affects crypotosporidum potentially has on host cells?
*Impaired Na+ and H2O
absorption?
*Increased Cl- secretion?- this would result in water being drawn out of cells via osmotic effect
*Induction of host cell
apoptosis?
249
how does cryptosporidium protect itself from the immune system
it coats itself with the host cells membrane to evaid detection
250
what stains can be used to easily detect cryptosporidia cysts via light microscopy?
Ziehl neelsen stain- the cryptosporidia are pink
Aurimine stain shows bright
green Cryptosporidia using
UV microscopy
Immunofluorescent stains
offer greater accuracy- but need a UV floresce microscope
251
what species cause acanthamoeba Keratitis?
Caused by A. polyphaga and A. castellanii
252
what is Keratitis?
Inflammation of cornea
253
who is most at risk of Acanthamoeba Keratitis
* Almost exclusive to contact lens wearers.
* Risk factors: swimming in pools, lakes or sea water while wearing contact lenses; storing lenses in home made solutions; poor lens hygiene.
254
what are the symptoms of Acanthamoeba Keratitis?
* Severe pain
* Redness
* Scant (if any) discharge, very unlikely to cause discharge- basically is doesnt cause discharge unlike other eye infections
* scarring and unceration of the cornea as the Acanthamoeba imbedds itself in
Proximity of eyes and brain means The protozoa also causes granulomatous encephalitis
255
is Acanthamoeba Keratitis
common?
yes it is extremely common in the environment, can be found in evironmental and tap water too
256
why can the eye being an immune privaledged site pose problems?
you tend to get limited inflammation in the ey, you do get some inflammation, but the limitated capacity meant the parasites can build up in number because the immune response in the eye is quite weak initially
257
what are the treatments for Acanthamoeba Keratitis ?
Treatment: multiple antimicrobials
including topical antiseptics;
hospitalization is often necessary
If severe corneal scarring occurs,
corneal transplantation may be
required
Severe loss of vision or of the eye may
occur, even if the condition is diagnosed
early and managed appropriately
* Therapy and treatment can last for
more than a year.
258
Acanthamoeba Keratitis – laboratory diagnosis
* Agar plate seeded with bacteria (such as E.coli) and inoculated with swab from
infected eye
* Active forms of the amoeba will scoot around the plate as they
phagocytose the bacteria – the trail can be seen under a microscope
* Molecular methods such as PCR, may also be used
259
what is the virus lipid membrane (envelope) made of?
The viral envelope is made from fatty lipids molecules taken form the host cells.
260
What are the main routes of protozoan transmission?
Ingestion, vector-borne, sexual contact, transovarial, and placental.
261
Name the four classifications of protozoa based on movement.
Ciliates, flagellates, amoebae, and Apicomplexa.
262
How do protozoan cysts contribute to survival?
They are dormant forms that resist environmental stress, aiding in transmission.
263
What is schizogony, and why is it significant?
It is asexual reproduction, producing multiple daughter cells, critical in Plasmodium spp. for rapid infection.
264
Which protozoa are waterborne and cause diarrheal diseases?
Cryptosporidium parvum, Cyclospora cayetanensis, Giardia lamblia, and Balantidium coli.
265
How do protozoa differ from bacteria in cellular structure?
Protozoa are eukaryotic with organelles, while bacteria are prokaryotic without organelles.
266
What are trophozoites in protozoan lifecycles?
The active, feeding, and reproducing stage.
267
What distinguishes Apicomplexa from other protozoan groups?
They have a unique apical complex for host cell invasion.
268
How does the size of protozoa compare to bacteria?
Protozoa are larger, often comparable to human cells.
269
Why is microscopy the gold standard for diagnosing protozoan infections?
Protozoa cannot form colonies on agar plates, so direct visualization is necessary.
270
How do protozoa cause host cell damage?
Through physical destruction, toxin release, or immune response activation.
271
What is the primary difference between vector-borne and waterborne protozoa?
Vector-borne protozoa require an intermediate host, while waterborne protozoa are typically ingested.
272
Name a sexually transmitted protozoan.
Trichomonas vaginalis.
273
How do amoebae like Acanthamoeba spp. move?
By extending pseudopodia.
274
What are the primary environmental conditions for protozoa survival?
Moisture, nutrients, and moderate temperatures.
275
How does Cryptosporidium parvum resist water treatment?
It forms oocysts that resist chlorine and filtration.
276
Why are protozoan diseases more prevalent in developing countries?
Poor sanitation, unsafe water, and lack of healthcare infrastructure.
277
What distinguishes trophozoites from cysts?
Trophozoites are metabolically active, while cysts are dormant and resistant.
278
Why is Giardia lamblia reclassification important?
Its various names (G. intestinalis, G. duodenalis) reflect its taxonomy and prevalence in literature.
279
What are the key characteristics of protozoa that impact their pathogenicity?
Ability to invade host cells, evade immune responses, and transition between life stages.
280
Name five protozoa that cause waterborne diseases.
Cryptosporidium parvum, Cyclospora cayetanensis, Giardia lamblia, Balantidium coli, Acanthamoeba spp.
281
What is the primary disease caused by Cryptosporidium parvum?
Cryptosporidiosis.
282
How is Giardia lamblia transmitted?
Through ingestion of cysts in contaminated water or food.
283
What distinguishes Acanthamoeba spp. from other waterborne protozoa?
It causes keratitis, an eye infection, instead of gastrointestinal disease.
284
How does Cryptosporidium parvum cause diarrhea?
By impairing Na+ and water absorption and inducing host cell apoptosis.
285
What diagnostic stain is used for Cryptosporidium detection?
Ziehl-Neelsen or immunofluorescent staining.
286
What are the symptoms of giardiasis?
Chronic diarrhea, malabsorption, abdominal cramps, and fatigue.
287
How do Giardia trophozoites damage the gut?
By attaching to the intestinal lining, causing villous atrophy and malabsorption.
288
What role does Acanthamoeba spp. play in encephalitis?
It can spread to the brain from the eye, causing granulomatous encephalitis.
289
What is the primary treatment for giardiasis?
Metronidazole.
290
How does Acanthamoeba keratitis primarily occur?
From contaminated contact lenses or poor lens hygiene.
291
What are the symptoms of Cryptosporidium infection in immunocompromised patients?
Severe diarrhea, dehydration, and weight loss.
292
How is Balantidiasis transmitted?
By ingestion of cysts in contaminated water or food.
293
What are oocysts in Cryptosporidium?
Dormant forms that resist harsh environments and aid in transmission.
294
How can waterborne protozoa be controlled?
By improving water treatment, sanitation, and public health education.
295
Why is Cryptosporidium difficult to eliminate in water supplies?
It resists conventional chlorination and small filtration systems.
296
How does Cyclospora cayetanensis differ from Cryptosporidium?
It causes prolonged diarrhea and is primarily linked to contaminated produce.
297
What are the symptoms of Acanthamoeba keratitis?
Severe eye pain, redness, and potential vision loss.
298
Why is Acanthamoeba keratitis difficult to treat?
Antimicrobials poorly penetrate the cornea, requiring prolonged and intensive therapy.
299
What are granulomatous amoebic encephalitis risk factors?
Immunosuppression and environmental exposure to Acanthamoeba-contaminated water.
300
What are the two major forms of human African trypanosomiasis?
T. brucei gambiense (chronic) and T. brucei rhodesiense (acute).
301
What is the vector for malaria?
Female Anopheles mosquitoes.
302
Name the protozoa that causes Chagas disease.
Trypanosoma cruzi.
303
What is Romana’s sign in Chagas disease?
Swelling near the eye due to Triatomine bug feces.
304
How does Leishmania spp. evade the immune system?
By surviving within host macrophages.
305
What are the clinical forms of leishmaniasis?
Cutaneous, mucocutaneous, and visceral.
306
How is American trypanosomiasis transmitted?
By Triatomine bug bites or contaminated food.
307
What are the symptoms of visceral leishmaniasis?
Fever, weight loss, anemia, and hepatosplenomegaly.
308
How does Plasmodium spp. cause cyclical fever?
Through synchronized rupture of red blood cells releasing merozoites.
309
What is the role of sandflies in transmitting Leishmania?
They serve as vectors, transmitting the parasite during feeding.
310
What are the stages in Trypanosoma brucei infection?
Chancre formation, hemolymphatic stage, and meningoencephalitic stage.
311
How is malaria treated?
Using antimalarial drugs like chloroquine and artemisinin.
312
What is the vector for babesiosis?
Ticks, primarily Ixodes species.
313
What are the symptoms of cutaneous leishmaniasis?
Skin sores with raised edges and central craters.
314
How does trypanosomiasis lead to neurological symptoms?
Parasite invasion of the central nervous system.
315
What are the symptoms of acute Chagas disease?
Fever, swelling at the infection site, and lymphadenopathy.
316
Why is vector control critical in managing protozoan diseases?
It interrupts the lifecycle of the pathogen and reduces transmission.
317
How does the kinetoplast in Trypanosoma aid its survival?
It facilitates energy metabolism and is a drug target.
318
What drugs are used to treat sleeping sickness?
Suramin for early stages and eflornithine for later stages.
319
What are the major complications of chronic Chagas disease?
Cardiac damage and megaviscera.
320
What are the primary diseases caused by Giardia lamblia?
Giardiasis, characterized by chronic diarrhea, malabsorption, and abdominal discomfort.
321
How does Giardia lamblia cause malabsorption in the intestines?
By attaching to the intestinal lining, damaging villi, and interfering with nutrient absorption.
322
What is the prevalence of Giardia infections in developed vs. developing countries?
Developed countries: 2–7%; Developing countries: 20–30%.
323
What are the long-term effects of chronic giardiasis?
Persistent diarrhea, fatigue, abdominal pain, and symptoms resembling irritable bowel syndrome (IBS).
324
What is the role of cysts in the lifecycle of Giardia lamblia?
Cysts are the dormant, environmentally resistant form that aids in transmission and survival outside the host.
325
How is cryptosporidiosis transmitted?
Through ingestion of oocysts in contaminated water or food, or direct contact with infected individuals or animals.
326
What are the symptoms of cryptosporidiosis in immunocompetent individuals?
Self-limiting diarrhea lasting 1–2 weeks, abdominal cramps, and nausea.
327
Why is cryptosporidiosis more severe in immunocompromised patients?
They cannot clear the infection effectively, leading to prolonged diarrhea, dehydration, and potentially systemic infection.
328
What is the diagnostic method for Cryptosporidium?
Microscopy with Ziehl-Neelsen stain or immunofluorescent staining to detect oocysts in stool samples.
329
What factors increase the risk of cryptosporidiosis outbreaks?
Heavy rainfall causing runoff of contaminated animal feces into water supplies.
330
How does Cryptosporidium impair intestinal function?
By inducing host cell apoptosis and disrupting ion transport, leading to diarrhea.
331
What treatment options are available for cryptosporidiosis?
Supportive care with fluid and electrolyte replacement; no effective targeted antimicrobial therapy exists.
332
How does Balantidium coli differ from other waterborne protozoa?
It is a ciliate and primarily causes balantidiasis, which includes symptoms of severe dysentery.
333
What are the risk factors for acquiring Acanthamoeba keratitis?
Contact lens use, exposure to contaminated water, and poor lens hygiene.
334
What are the symptoms of Acanthamoeba keratitis?
Severe eye pain, redness, blurred vision, and potential vision loss.
335
Why is Acanthamoeba keratitis rare but serious?
It often requires intensive treatment and can lead to permanent vision damage or eye loss.
336
How does Acanthamoeba cause keratitis?
By attaching to the cornea, releasing cytotoxic enzymes, and penetrating deeper eye tissues.
337
How is Acanthamoeba keratitis diagnosed?
Using agar plates seeded with bacteria to detect amoebic trails, or PCR for molecular identification.
338
What is Cyclospora cayetanensis, and how is it transmitted?
A protozoan that causes cyclosporiasis, transmitted through contaminated fresh produce and water.
339
What are the symptoms of cyclosporiasis?
Watery diarrhea, bloating, fatigue, and loss of appetite, often lasting several weeks.
340
How is Cyclospora cayetanensis diagnosed?
Through stool examination using UV fluorescence or modified acid-fast staining.
341
What are the common reservoirs for Cryptosporidium in the environment?
Lakes, rivers, and water runoff contaminated with animal feces, particularly from cattle.
342
How do waterborne protozoa survive in unfavorable environmental conditions?
By forming cysts or oocysts that are resistant to desiccation, chlorine, and other treatments.
343
What is the primary method for preventing waterborne protozoan infections?
Ensuring safe drinking water through filtration and proper sanitation.
344
Why is Cryptosporidium difficult to remove from drinking water supplies?
Its oocysts are small and resistant to standard filtration and chlorine-based treatments.
345
How does Cyclospora differ from Cryptosporidium in its clinical presentation?
Cyclospora causes longer-lasting diarrhea and is often associated with outbreaks linked to contaminated produce.
346
What are the symptoms of Balantidiasis?
Diarrhea, abdominal pain, nausea, and sometimes dysentery with blood and mucus in the stool.
347
Why is Acanthamoeba not typically considered a gastrointestinal pathogen?
It primarily infects the eyes or brain rather than the gut.
348
How can Acanthamoeba keratitis be prevented?
By using sterile solutions for contact lenses, avoiding tap water for rinsing, and practicing proper lens hygiene.
349
What is the significance of villous atrophy in Giardia infections?
It reduces the absorptive surface of the intestines, leading to malabsorption and diarrhea.
350
what dot he surface proteins on the virus lipid membrane do?
These help the virus recognise and bind to cells in the host organism
351
what is the purpose of the Genetic material (DNA or RNA)
The virus genetic material contains the instructions for making new copies of the virus
352
why is the protein coat for a virus needed?
The capsid contains the virus genetic material
353
draw a diagram of a virus
354
what is something all viruses have?
a viral genome (DNA or RNA) and a viral capsid (protein coat)
355
why is an envelope important for a virus?
Envelope = lipid bilayer with glycoproteins, can help virus bind to cells
356
is a virus more stable with or without an envelope?
viruses without an envelope are more stable and more resistant to pH, temperature changes and the air.
357
do enveloped viruses get into your cells easier?
yes because of the lipid bilayer with the surface proteins.
358
what is the helical capsid formation?
there is a directional assembly around the genome
359
what is the icosahedric capside formation?
there is assembly/packaging around the genome
360
what is a scaffolded icosahedric capsid?
Capsid assembly: formation of the capsid shell.
Packaging: viral genome placement inside a capsid or an envelope
361
what is acapsid
a very strong Closed 3-dimensional structure
No holes - to remain Stable
Built of repeating protein structures
362
how are capsids formed?
by the self assembly of viral protein subunits into different capsomers which then undergo self assembly to form a spherical viral capsid
363
what is the viral envelope?
a lipid bilayer
364
what is the viral envelope involved with?
virus attachment to cells- Envelope proteins recognised by cellular receptors
Can fuse with the hose cell membrane
365
how can a virus exit a cells machinery?
Virus can exit cells using the cell machinery-
Can avoid cell damage (potentially avoiding the immune response!)- the virus envelope is most important for exiting the cells, the virus is able to co-opt the host cell membrane and use it to hide from the host immune system- it does not need to produce its own cell membrane
366
why do non-enveloped viruses usually cause more damage?
When exiting cells they disrupt the integrity of the membrane and can cause cell lysis.
367
how are non enveloped viruses more stable?
Non-enveloped viruses are more resistant to pH, heat, dryness, alcohol, soap!
368
how do enveloped viruses enter the cell differently?
369
define a capside
a protein coat that encloses and protects the genetic material/genome.
370
define a capsomer
clusters of proteins that compose
The capsid
371
define a protein envelope
a lipid bilayer that surrounds the capsid
of some viruses.
372
define a peplomer
Proteins on the envelope of the virus
(like Glycoprotein)
373
what is a virion?
A Complete virus particle or infectious particle is called a VIRION
374
why is Knowing the structure of viruses important?
Can help in creating treatments
Can help in developing vaccines
Knowing what kills the viruses (soap, alcohol, bleach)
375
how are viruses grouped?
based on phenotypic characteristics
-Morphology
Nucleic acid type (DNA/RNA)
Replication cycle in the cells
Host
Disease caused
376
what does a viridae refer too?
a specific family of viruses
377
what do all viruses need to produce?
mRNA
378
what is the Baltimore classification system used?
classify viruses based on their manner of messenger RNA (mRNA) synthesis.
379
why is it difficult to classify viruses?
We don’t know all properties of viruses or all known viruses
We do not know if viruses have a one common ancestor
Viruses can mutate and change
Polythetic classification (as opposed to monothetic!)
No single property but a portfolio of properties: target cells, biochemistry, structure and mainly now genome sequences
Related viruses share many of these, but often not all.
380
what is a susceptible cell?
A susceptible cell has a functional receptor for a given virus - the cell may or may not be able to support viral replication
381
what is a resistant cell?
A resistant cell has no receptor - it may or may not be competent to support viral replication
382
what is a permissive cell?
A permissive cell has the capacity to replicate virus - it may or may not be susceptible
383
what is a susceptible AND permissive cell
A susceptible AND permissive cell is the only cell that can take up a virus particle and replicate it
384
how does pH allow genetic material to be released from virus cells?
within the cells endosomes can be formed, when the virus is in the endosome the pH changes, this causes the capsid to release the genetic information stored in the virus and allows the virus to replicate.
385
what are the stages of the viral infectious cycle?
Very simply the viral life cycle is:
1. Attachment to cells
2. Enter & uncoating
3. mRNA
3. Translation using host ribosomes
4. Assembly
5. Egress (exit)
386
what is viral pathogenesis?
Viral Pathogenesis: the process by which a virus causes a disease
387
what is viral virulence?
Virulence can be quantitated:
- Virus titer
- Mean time to death
- Mean time to appearance of signs
- Measurement of fever, weight loss
Many signs/symptoms of disease are caused by immune response!
388
what is the difference between signs and symptoms?
Symptoms = What only you can feel
Signs = what others detect
389
what can viral virulence be influenced by?
Influenced by dose, route of infection, species, age, sex, and susceptibility of host
Not correct to compare virulence of different viruses
390
what does virulence depend on?
391
how do viruses affect us?
392
how can viruses be useful?
Oncolytic viruses
Alternatives to antibiotics
Gene therapy
Biological control-an alternative to pesticides?
393
what do we need to study viruses?
we must have living appropriate cells to study viruses
394
how can we grow viruses for studying?
using cell cultures with HeLa cells
and HEp-2 cells or we can
embtyonated eggs can be used to develope vaccines
in vivo (live animals)
395
what is the cytopathic affect?
Cytopathic effect (CPE) is the term used to describe the structural changes that occur in a host cell after it has been infected by a virus
396
how can the cytopathic effect be important in cell culture
- in cell culture, testing for cytopathic effect can help to quantify the effect a virus has on susceptible and permissible cells by showing how thye can cause cell damage and death
- a cytopathic effect shows damage and changes to cells
397
Why are virus diagnostics needed?
1. Appropriate management of patients.
2. Routine public health measures
3. Surveillance
398
why is Appropriate management of patients improtant?
Avoids further unnecessary testing
Avoids unnecessary drug use (antibiotics!)
Informs patient treatment and prognosis
Are treatment strategies working (viral load testing)
399
why are virus diagnostics needed for Routine public health measures necessary?
Screening of donated blood (HIV, HepB, HepC)
Notifiable infections (Measles, Rubella, Mpox, etc.)
Activate contact tracing
Limit spread or outbreak
Put mechanisms in place to contain and eradicate
400
# Surveillance
why are virus diagnostics needed for Surveillance?
To monitor the significance and prevalence of viruses in a community.
Monitoring and tracking of outbreaks (e.g. COVID-19)
Evidence of reemerging or emerging viruses –
Individuals travelling from other countries (e.g. polio in London).
Viruses spreading within animal communities (e.g. H5N1).
Viruses with zoonotic potential
401
What is the definition of a virus?
A virus is an obligate intracellular parasite comprising genetic material (DNA or RNA), often surrounded by a protein coat (capsid) and sometimes a lipid membrane (envelope).
402
What are the two types of viral genetic material?
DNA and RNA.
403
What is the function of the viral capsid?
To protect the viral genome and assist in delivering it to host cells.
404
What is the difference between enveloped and non-enveloped viruses?
Enveloped viruses have a lipid bilayer with glycoproteins, making them less resistant to environmental conditions; non-enveloped viruses are more resistant and often cause more cellular damage.
405
How do surface proteins on viruses aid infection?
They help the virus recognize and bind to host cell receptors for entry.
406
What are the three forms of viral capsids?
Helical, icosahedral, and scaffolded icosahedral.
407
How are viruses classified under the Baltimore classification system?
Based on their nucleic acid type, sense (positive or negative), and method of replication.
408
What are the main stages of the viral life cycle?
Attachment, entry and uncoating, mRNA production, protein synthesis, assembly, and egress.
409
What is a virion?
A complete infectious virus particle.
410
What is the significance of viral genome integration into host DNA?
It can contribute to long-term infections, oncogenesis, or beneficial adaptations, such as the formation of the human placenta.
411
What is viral tropism?
The specificity of a virus for a particular host cell type, determined by receptor compatibility.
412
How does the host immune system contribute to disease symptoms?
Many symptoms, such as fever and inflammation, result from the immune system's response to infection.
413
What methods are used to study viral capsid structures?
Techniques like cryo-electron microscopy (cryo-EM).
414
What factors influence viral virulence?
Dose, route of infection, host species, age, sex, and immune status.
415
Why are non-enveloped viruses more resistant to environmental factors?
They lack a fragile lipid envelope and rely on a robust capsid for protection.
416
What are examples of diseases caused by RNA viruses?
Influenza, HIV, and SARS-CoV-2.
417
How do viruses like HIV evade immune detection?
By using host cell membranes as an envelope and integrating their genome into host DNA.
418
What are examples of viruses named after locations?
Zika virus (Zika Forest, Uganda) and West Nile virus (West Nile region).
419
What is the role of peplomers in viruses?
Surface glycoproteins involved in receptor recognition and entry.
420
How do antiviral treatments target viruses?
By disrupting capsid integrity, replication enzymes, or entry mechanisms.
421
What is viral pathogenesis?
The process by which a virus causes disease in a host.
422
What are the two main contributors to viral disease symptoms?
Effects of viral replication and the host immune response.
423
What is the difference between acute and long-term viral infections?
Acute infections cause rapid onset of symptoms and resolution, while long-term infections persist and may involve latency.
424
Name a virus that causes oncogenesis.
Human papillomavirus (HPV), which is associated with cervical cancer.
425
How does HIV affect the immune system?
It infects CD4+ T cells, weakening the immune response and leading to AIDS.
426
What is the primary symptom of respiratory syncytial virus (RSV) infection in children?
Severe lower respiratory tract infections.
427
How does the influenza virus evade the immune system?
Through antigenic drift and shift, leading to changes in surface proteins (H and N).
428
What is the significance of the 1918 influenza pandemic?
It caused widespread mortality, killing an estimated 20 million people worldwide.
429
What are zoonotic viruses?
Viruses that are transmitted from animals to humans, such as SARS-CoV-2.
430
What role do bacteriophages play in the environment?
They infect bacteria, contributing to microbial balance and nutrient cycling.
431
How is viral virulence quantified?
By measuring virus titer, mean time to death, symptom severity, and weight loss in experimental models.
432
What is the economic impact of viruses on agriculture?
Viruses like tomato spotted wilt virus cause significant crop losses, estimated at billions of dollars annually.
433
Name an example of a beneficial virus.
Oncolytic viruses, which can selectively kill cancer cells.
434
How does viral resistance to treatment occur?
Through mutations in viral genes targeted by antiviral drugs.
435
What is the impact of Ebola virus outbreaks on local economies?
Decreased trade, tourism, agricultural production, and economic growth.
436
What are the symptoms of measles?
High fever, cough, runny nose, conjunctivitis, and a characteristic rash.
437
How do phage therapies work?
By using bacteriophages to specifically target and kill antibiotic-resistant bacteria.
438
What is the relationship between viruses and the human microbiome?
The human virome includes viruses that coexist with bacteria and contribute to immune modulation.
439
How does viral integration affect human evolution?
Endogenous viral elements in DNA have influenced traits like placental development.
440
How are viruses used in gene therapy?
As vectors to deliver therapeutic genes to correct genetic disorders.
441
What are the components of a typical virus?
Genetic material, capsid, and sometimes an envelope with surface proteins.
442
How are viruses classified phenotypically?
By morphology, genome type, replication method, host range, and disease caused.
443
What is the Baltimore classification system?
A system that groups viruses into seven categories based on mRNA synthesis methods.
444
What are double-stranded RNA viruses, and why are they rare?
Viruses with both strands of RNA; this structure is uncommon in nature.
445
How does the viral envelope facilitate infection?
It allows fusion with host cell membranes for genome entry.
446
What is the main function of the capsid?
To protect the viral genome from environmental damage.
447
How do helical capsids differ from icosahedral capsids?
Helical capsids coil around the genome, while icosahedral capsids form geometric shells.
448
What is the significance of viral symmetry?
It ensures capsid stability and efficient genome packaging.
449
Why are non-enveloped viruses more environmentally stable?
They lack a fragile lipid bilayer, making them resistant to desiccation and heat.
450
How does viral mutation impact classification?
Mutations can change surface proteins and replication mechanisms, altering classification.
451
What is the importance of surface proteins in vaccines?
They are targets for immune system recognition and response.
452
How does viral size compare to bacteria?
Viruses are much smaller, often requiring electron microscopy for visualization.
453
What is the function of viral mRNA during infection?
It serves as a template for protein synthesis using host cell machinery.
454
How are viruses named?
Based on disease caused, host infected, location of discovery, or discoverers.
455
What are examples of viruses that cause gastrointestinal diseases?
Norovirus and rotavirus.
456
How does norovirus resist disinfection?
Its non-enveloped structure makes it resistant to alcohol-based sanitizers.
457
What are the implications of polythetic classification for virology?
It groups viruses by shared but not universal properties, reflecting their diversity.
458
Why are bacteriophages considered potential alternatives to antibiotics?
They specifically target bacteria without harming human cells.
459
How do viruses use host cell membranes for immune evasion?
By incorporating host lipids into their envelope, they camouflage themselves.
460
Why is understanding viral structure important for public health?
It informs disinfection methods, vaccine design, and antiviral drug development.
461
why is Surveillance-reported by diagnostic labs?
UK Health Safety Agency (UKHSA) (former PHE).
Reporting weekly of Notifiable diseases and Non-notifiable diseases' insidence rates.
We could use these data to predict future peaks for increased incidence rates of infections and prepare healthcare settings for expected addmissions
462
what is Sentinel surveillance of Influenza-like illness (ILI)?
In addition to reported hospital testing
In Europe, ~5% of GPs are involved with sentinel surveillance
People attending the clinic with ILI have swabs sent to clinical virology labs
Monitors rates of circulating influenza and other respiratory viruses
Can see unusual patterns, monitoring of circulating sub-types
463
what kind of patients does Sentinel surveillance include?
it includes patients who have gone to their doctors but are not sick enough to go hospital
464
what is clinical virology dependent on and why?
it is dependant on good sampling
-This is very important because in many cases we are going to do diagnostics using PCR. -This is very important because in many cases we are going to do diagnostics using PCR and the nucleic acids can be degraded very quickly. So we really need to collect the sample and preserve it with nuclease inhibitors or freeze it.
465
what will the sample collected in clinical virology be dependent on?
The type of sample will largely be determined on the signs/symptoms of disease
This can indicate what organ systems are involved
466
what is a direct method to help detect an infectious virus?
Isolation of virus
Cultivation in cell culture followed by identification
467
what are 2 indirect methods used in clinical virology?
(indirect methods cannot detect infectious virus)
2 methods are:
Detection of virus components
Serology
468
what entails Detection of virus components
looking for virions, viral antigens, viral nucleic acids
469
what is serology?
Detection of antibodies in the patient’s serum
470
what is an OBLIGATE INTRACELLULAR PARASITE?
they can only be grown inside a host cell
471
what is the "host range"?
gFor new viruses very often trial and error to find out what the virus can infect-the ‘host range'
to figure this out we can use cell lines, embryonated eggs or live animals (in vivo)
472
why can cell lines be useful in studying viruses?
hen you culture a virus into a cell line, you can, for instance, do microscopy and look for cytopathic effect. You can see the comparison between a culture that has and has not been infected. And you can look at the cells, the morphology, the shape and decide whether something about the cells is changing
473
what kind of assay can be used to study the cytopathic effect?
plaque assay
- it is a Key technique in virology.
Time-consuming and not suitable for all viruses.
Mostly research technique, but still used in diagnostics (enrichment).
474
what are plaque forming units?
Viruses will spread by probability to the surrounding cells better than any other cells further away. So in the end, if the virus causes a cytopathic effect it will cause a hole in the monolayer that can be detected by staining or by the naked eye, and we don't know how many viral particles are in there. What we know is that that is the plaque forming unit.
475
does plaque assay use living cells?
yes
476
what kind of seuqencing can you use when the target virus is unknown?
metagenomic sequencing
477
what kind of sequencing can be used when you know or suspect the virus?
amplicon sequencing that amplifies a region of the viral genome
478
how can virus sequencing be used to detect and stop new viruses spreading?
new sequences can be sequenced using metagenomic sequencing and aligned to known virus sequences
If it is an unknown virus, similarities in related viruses can be identified
From the sequencing, you could predict whether the virus might resist particular treatment of particular or be susceptible to a particular treatment. you could test for mutations via sequencing and changes to the genome of known viruses
479
what is direct detection?
Detection of virions, viral nucleic acids or viral antigens
480
what is a virion?
Virion: A complete virus particle
481
what is viral nucleic acid?
Viral nucleic acid: the genetic material of a virus, either RNA or DNA
482
what is a virus antigen?
Antigen: molecular structures on the surface of viruses that can be recognized by the immune system
483
how does a florescence microscope make use of antibodies?
antibodies are very specific, So they become a great tool for diagnostics because they can identify a particular molecule or component in a very specific wayWe can take advantage of antibodies, make them against a particular antigen, and then we can label them.We can label them with enzymes or fluorophores something that allows us to visualise the presence of that antibody.
When we want to use this in terms of microscopy, what we do is we incubate the antibodies with the sample normally on a glass surface, and then we can either couple a second antibody or directly detect the floraphores for the was attached to it. And then you get images that come through for us and that gives us much more sensitivity and also provides the specificity of knowing we are detecting a particular antigen.
484
what are negri bodies?
negri bodies can be detected to determine whether someone has rabies
485
what are the pros and cons of using an electron microscope?
Much better resolution than a light microscope.
A scanning transmission electron microscope has 50 pm resolution
Most light microscopes are limited to about 200 nm
Can view the structure of virions
During the 1970s new groups of hard to culture viruses discovered in faeces (rotaviruses, calciviruses, astroviruses, HepA)
One method: negative staining. Virus dilution on carbon coated grid. Virions adhere to the surface. Electron dense fluid added and surrounds virions.
Thin tissue sections can also be imaged.
Low sensitivity (need 106 virions/mL, ok for faeces but difficult for respiratory samples).
Impractical for large scale testing.
486
pros and cons of PCR for testing viral nucleic acids
Polymerase Chain Reaction
Quick and (fairly) easy
Can be easily scaled up for high-throughput testing
Initially expensive, but cheaper in high volume
Very sensitive and highly specific
Can be quantitative (qPCR)
487
A positive PCR may not indicate active infection
Why do you think this might be?
So detecting the viral nucleic acid doesn't mean you're detecting an infection. It can mean youre detecting part of the virus. But in many cases, after a viruses infects you the genome of the virus can hang around for a really long time.
488
explain the process of rt-PCR
489
explain the process of qPCR
490
explain the process of RT-qPCR
You can measure light in the machine as the reaction happens to determine how much viral material is present in the sample
491
what does a low amount CT value for rt-qPCR mean
there is alot of viral material
492
what does a high-ct value mean?
there is very little viral material present becuase you need to do more cycles to reacht the light threshold to determine a positive result.
493
what is a cycle threshold?
The number of cycles of PCR needed until the sample is detectable.
The lower the number, the less cycles, the more viral nucleic acids present.
494
what is serology?
Serology is the scientific study of serum and other body fluids. In practice, the term usually refers to the diagnostic identification of antibodies or antigens in serum
495
what are serology methods?
Methods include:
ELISA
Agglutination
Precipitation
Complement fixation
496
what is an ELISA test?
Enzyme-linked immunosorbent assay (ELISA) or Enzyme Immunoassay (EIA)
Still used, but replaced by PCR in many instances.
An antibody to the target is absorbed on the solid surface. The unknown sample is added. If antigen (like viral protein) is present it will bind to the antibody. An enzyme labelled antibody is then added. A substrate is added. The enzyme, if present, will cause the substrate to change colour.
High sensitivity
Lots of different assay formats, easily adaptable
497
how does an ELISA test work?
can be direct or indirect form of ELISA
the sandwich ELISA is the most common form and works like this-
you have a plate that is coated with one particular antibody.
you would then add Your sample, presumably containing the virus or parts of the virus.
This would be recognised by this antibody, then you can wash off the rest of the sample and then you can add what we call the detection antibody,
which is another antibody that will detect the same virus or the same part of the virus.
498
what is a lateral flow test?
a form of Immunochromatography available for HIV, dengue, influenza, COVID-19, RSV (not all in common usage)
499
how do lateral flow tests work?
Antigens move through a support (filter paper, nitrocellulose film)
Labelled antibody reacts with sample containing antigen.
Second antibody produces a colour change
Can incorporate a positive and negative control
Less sensitive
Useful for rapid testing, point-of care testing
500
how does a Haemagglutination assay work?
also makes use of antibodies
Sialic acid receptors on RBCs bind to the HA protein on the surface of influenza and keep the RBCs in suspension.
No flu-RBCs settle
501
what is the difference between and accurate and precuse test?
Accurate: A test that provides a result close to the real value
Precise: A test is repeatable and the result reproducible
502
what is the difference between sensitivity and specificity?
Sensitivity: The probability of a positive test from a truly positive sample (true positive rate)
Specificity: The probability of a negative test from a truly negative sample (true negative rate)
503
why is it dififcult to diagnose viral infections?
many have similar "flu-like" symptoms because it is the bodies immune system that causes the same key symptoms not the virus itself
504
What is the primary goal of clinical virology?
To diagnose viral infections, monitor viral diseases, and guide appropriate patient treatment and public health responses.
505
Why is it challenging to diagnose viral infections based on symptoms alone?
Many viral infections share similar symptoms, such as fever, chills, and fatigue, caused by the immune response rather than the virus itself.
506
What is the significance of viral load monitoring in patient management?
It helps assess the effectiveness of treatment and detect potential resistance to antiviral therapies.
507
Name three reasons why virus diagnostics are essential.
Patient management, routine public health measures, and surveillance.
508
What is sentinel surveillance in virology?
A system where specific GPs or clinics collect and test swabs from individuals with influenza-like illness to monitor viral patterns.
509
How do public health agencies track the spread of viruses like SARS-CoV-2?
Through wastewater monitoring, hospital data collection, and sentinel surveillance systems.
510
What role does the UKHSA play in clinical virology?
It reports weekly on notifiable diseases and monitors circulating viruses like influenza and RSV.
511
Why is viral genome sequencing important in diagnostics?
It identifies novel viruses, tracks mutations, and determines susceptibility to treatments.
512
What is the importance of accurate sampling in viral diagnostics?
It ensures the quality of nucleic acids or antigens for reliable testing.
513
What are the two broad categories of virology diagnostic methods?
Direct methods (detect infectious virus) and indirect methods (detect viral components or antibodies).
514
What is a plaque assay, and when is it used?
A technique to quantify infectious virus by counting plaques formed in a cell monolayer; mainly used in research and antiviral testing.
515
How does PCR aid in detecting viral nucleic acids?
It amplifies specific viral DNA or RNA sequences, making detection highly sensitive and specific.
516
What is quantitative PCR (qPCR), and how does it differ from standard PCR?
qPCR measures the amount of DNA in real-time during amplification, providing both detection and quantification.
517
What does a low cycle threshold (Ct) value in qPCR indicate?
A high viral load in the sample.
518
What is multiplex PCR, and why is it advantageous?
A PCR method that detects multiple viruses simultaneously by using different fluorophores for each target.
519
What is the principle of ELISA in viral diagnostics?
It uses antibodies to detect viral antigens or antibodies in a sample through enzyme-substrate reactions producing color changes.
520
What is the purpose of a lateral flow test?
To provide rapid point-of-care detection of viral antigens, such as in COVID-19 testing.
521
How does haemagglutination assist in virus detection?
By observing the ability of viruses to agglutinate red blood cells, used for viruses like influenza.
522
What are Negri bodies, and what do they signify?
Intracellular inclusions diagnostic for rabies, detectable through fluorescence microscopy.
523
Why is electron microscopy valuable in virology?
It provides high-resolution images of virions, helping identify viruses that are difficult to culture.
524
How does metagenomic sequencing aid in identifying unknown viruses?
By sequencing all genetic material in a sample to compare against known viral genomes.
525
What is serology, and how is it applied in virology?
The study of serum to detect antibodies or antigens, used to confirm past or current infections.
526
What are the strengths of PCR in viral diagnostics?
High sensitivity, specificity, and scalability.
527
Why are fluorescent microscopes used in diagnostics?
They detect labeled antibodies bound to viral antigens, providing specificity and sensitivity.
528
What are the limitations of using light microscopy for viral detection?
Poor resolution for small viruses and inability to detect specific viral features.
529
What factors influence the choice of diagnostic technique?
Suspected virus, sample type, clinical urgency, and resource availability.
530
What are the common viral causes of aseptic meningitis?
Enteroviruses (Coxsackie, echovirus) and mumps.
531
What are the uncommon viral causes of aseptic meningitis?
Polio, LCMV, HSV-2, and adenovirus.
532
What specimens are collected for diagnosing aseptic meningitis?
NP-throat, CSF, urine, stool, and serum for LCMV.
533
What are the common viral causes of encephalitis?
Arboviruses and HSV-1/-2.
534
What are the uncommon viral causes of encephalitis?
Mumps, measles, influenza, rubella, VZV, rabies, EBV, and enteroviruses.
535
What specimens are collected for diagnosing encephalitis?
NP-throat, stool, CSF, brain biopsy (if herpes is suspected), and serum.
536
What are the common viral causes of URI, bronchitis, or 'flu'?
Rhinovirus, parainfluenza, influenza, adenovirus, enteroviruses, and RSV.
537
What are the uncommon viral causes of URI, bronchitis, or 'flu'?
Measles, coronaviruses (NL, HK), and bocavirus.
538
What specimens are collected for URI, bronchitis, or 'flu'?
NP-throat and nasal aspirate.
539
What is the common viral cause of croup?
Parainfluenza.
540
What are the uncommon viral causes of croup?
RSV, adenovirus, and influenza.
541
What specimens are collected for diagnosing croup?
NP-throat and nasal aspirate.
542
What are the common viral causes of pneumonia?
RSV, adenovirus, influenza, and metapneumovirus.
543
What are the uncommon viral causes of pneumonia?
Parainfluenza, CMV, rhinovirus, measles, rubella, and enterovirus.
544
What specimens are collected for diagnosing pneumonia?
NP-throat, stool, tracheal aspirate, nasal aspirate, urine, and serum.
545
What are the common viral causes of bronchiolitis?
RSV and influenza.
546
What is an uncommon viral cause of bronchiolitis?
Parainfluenza, adenovirus, and rhinovirus.
547
What specimens are collected for diagnosing bronchiolitis?
NP-throat and nasal aspirate.
548
What are the common viral causes of vesicular rashes?
VZV, HSV-1, and HSV-2.
549
What are the uncommon viral causes of vesicular rashes?
Vaccinia and enteroviruses.
550
What specimens are collected for vesicular rashes?
Vesicular fluid, NP-throat, stool (for enterovirus), and serum.
551
What are the common viral causes of non-vesicular rashes?
Measles, rubella, and enterovirus.
552
What are the uncommon viral causes of non-vesicular rashes?
EBV and hepatitis B virus.
553
What specimens are collected for non-vesicular rashes?
NP-throat, stool (for enterovirus), and serum.
554
What are the common viral causes of congenital infections?
CMV, HSV-2, and rubella.
555
What are the uncommon viral causes of congenital infections?
Parvovirus B19.
556
What specimens are collected for congenital infections?
NP-throat, stool, pleural fluid, pericardial fluid, and serum.
557
What are the common viral causes of eye lesions?
HSV-1, HSV-2, and adenoviruses.
558
What is an uncommon viral cause of eye lesions?
Measles.
559
What specimens are collected for diagnosing eye lesions?
Eye swabs, NP-throat, and nasal washing.
560
What are the common viral causes of gastroenteritis?
Rotavirus, norovirus, and adenovirus.
561
What are the uncommon viral causes of gastroenteritis?
Enterovirus (newborns) and influenza.
562
What specimens are collected for diagnosing gastroenteritis?
Stool, NP-throat, and urine.
563
What are the common viral causes of hepatitis?
Hepatitis A, B, C, D, EBV, CMV, and VZV.
564
What are the uncommon viral causes of hepatitis?
Enterovirus, adenovirus, and HSV-1/-2.
565
What specimens are collected for diagnosing hepatitis?
Serum, NP-throat, stool, and urine.
566
What are the common viral causes of parotitis?
Mumps and parainfluenza.
567
What are the uncommon viral causes of parotitis?
Adenovirus, LCMV, EBV, and enterovirus.
568
What specimens are collected for diagnosing parotitis?
NP-throat, urine, nasal aspirate, and serum.
569
What are the advantages of virus isolation as a diagnostic method?
Produces further material for studying the agent, usually highly sensitive, and is 'open-minded' (applicable to unknown agents).
570
What are the disadvantages of virus isolation?
It is slow, time-consuming, expensive, requires selection of appropriate cell type, and is useless for non-viable viruses or non-cultivable agents.
571
What are the advantages of electron microscopy in virology diagnostics?
Rapid, detects viruses that cannot be grown in culture, detects non-viable viruses, and is 'open-minded.'
572
What are the disadvantages of electron microscopy?
It is relatively insensitive, cumbersome for large sample numbers, and limited to detecting a few infections.
573
What are the advantages of serological identification methods like EIA?
Rapid, sensitive, provides serotype information, and readily available as diagnostic kits.
574
What are the disadvantages of serological identification?
Not applicable to all viruses, interpretation can be difficult, and it is less sensitive than PCR.
575
What are the advantages of PCR for detecting viral genomes?
Rapid, very sensitive, applicable to all viruses including non-cultivable ones, can be multiplexed, allows good quantitation of viral load, and additional reagents/primers can be easily made.
576
What are the disadvantages of PCR?
High sensitivity may detect irrelevant co-infections, risk of DNA contamination, requires good quality control, and is targeted to specific agents.
577
What are the advantages of using antibody seroconversion in diagnostics?
Useful for excluding or confirming past infections when direct detection samples are unavailable.
578
What are the disadvantages of antibody seroconversion?
It is slow, retrospective (requires paired sera), and not suitable for rapid diagnosis.
579
What are the advantages of IgM serology in viral diagnostics?
Rapid and useful for diagnosing recent infections.
580
What are the disadvantages of IgM serology?
Interpretation can be difficult, targeted to specific agents, and false positives may occur.
581
What is the primary aim of this viral diagnostics practical?
To interpret and perform various diagnostic assays for viruses, including PCR, haemagglutination, haemagglutination inhibition assays, and plaque assays, to diagnose infections and determine viral characteristics.
582
Why is it important to use multiple assays for diagnosing viral infections?
Each diagnostic assay has advantages and limitations, so combining assays provides a comprehensive diagnosis and helps guide effective treatment plans.
583
What safety precautions must be followed during the practical?
Wear appropriate PPE (lab coat, gloves, safety spectacles), avoid handling mobile phones, keep benches clean, and properly dispose of waste according to lab protocols.
584
What is the purpose of using PCR in this experiment?
To identify the presence of common respiratory viruses in patient samples by amplifying specific viral genomic sequences.
585
Why can a single PCR reaction distinguish between seven respiratory viruses?
Specific primers are designed to amplify unique sequences from each virus, allowing differentiation based on band patterns in agarose gel electrophoresis.
586
What are the justifications for using PCR as a diagnostic tool?
It is highly sensitive, specific, and rapid, making it effective for detecting viral genomes even at low concentrations.
587
What does the absence of a band in PCR results indicate?
It indicates that no viral genomic material was detected in the sample, either due to the absence of the virus or an inadequate sample.
588
What is the purpose of the haemagglutination assay in this experiment?
To quantify the total number of viral particles in patient samples by measuring their ability to agglutinate red blood cells (RBCs).
589
How is the haemagglutination titre calculated?
It is determined as the highest dilution (lowest concentration) that still causes haemagglutination.
590
What is the significance of haemagglutination in viral diagnostics?
It provides a relative measure of the viral particle count in a sample, though it does not indicate infectivity.
591
Why are sheep erythrocytes used in the HA assay?
They are highly sensitive to haemagglutination by many viruses, including influenza.
592
Why does the assay not provide information about infectivity?
It measures total viral particles, including both infectious and non-infectious forms.
593
What is the purpose of the haemagglutination inhibition assay in this practical?
To identify the specific subtype of influenza virus infecting each patient by testing the ability of antibodies to inhibit haemagglutination.
594
How does the HI assay work?
Antibodies specific to a virus bind its antigens, preventing the virus from agglutinating red blood cells. If haemagglutination is inhibited, the virus-antibody match is confirmed.
595
Why are positive controls (H1N1 and H3N2) used in the HI assay?
To validate the assay and ensure that the antibodies are functioning correctly.
596
What justifies the use of the HI assay in diagnosing influenza subtypes?
It is rapid, specific, and effective for differentiating between influenza A subtypes, critical for targeted treatment and surveillance.
597
What does a red pellet formation in the HI assay indicate?
That haemagglutination was inhibited, suggesting a specific virus-antibody match.
598
What is the purpose of the plaque assay in this experiment?
To measure the level of infectious virus in patient samples and assess susceptibility to the antiviral drug oseltamivir (Tamiflu).
599
How is the infectious virus titre calculated in a plaque assay?
By counting the number of plaques formed, adjusting for the sample volume, and correcting for the dilution factor.
600
What is the significance of comparing plaque assay results with HA assay results?
It allows differentiation between total viral particles and infectious viral particles, highlighting the proportion of the virus that is infectious.
601
How can oseltamivir susceptibility be tested in the plaque assay?
By observing changes in plaque count or appearance when the virus is cultured in the presence of oseltamivir.
602
Why is the plaque assay important for guiding treatment plans?
It determines viral infectivity and drug susceptibility, essential for selecting effective antiviral therapies.
603
What are the two influenza A subtypes circulating in humans?
H1N1 and H3N2.
604
Why are H5N1 and H7N9 subtypes concerning for public health?
They cause severe respiratory infections with high mortality rates and are transmitted inefficiently between humans, but mutations could increase their transmissibility.
605
What are the two classes of antiviral drugs used for influenza treatment?
Neuraminidase inhibitors (e.g., oseltamivir) and adamantanes (e.g., amantadine).
606
What are the symptoms of severe lower respiratory tract infections caused by influenza?
Persistent coughing, difficulty breathing, fever, and fatigue.
607
How does oseltamivir reduce the spread of influenza virus?
By inhibiting the neuraminidase enzyme, it prevents the release of new virions from infected cells.
608
Why is it important to vaccinate against influenza annually?
The vaccine protects against circulating strains, which change frequently due to antigenic drift.
609
Why are multiple diagnostic assays needed for viral identification?
Each assay provides unique information, such as total viral particles, infectivity, or subtype, which are collectively necessary for accurate diagnosis.
610
What is the importance of dilution series in assays like HA and plaque assays?
They ensure accurate quantification of viral particles or infectious units by finding the optimal concentration for measurement.
611
Why is patient case history critical in viral diagnostics?
It provides context for the infection, such as potential exposure sources and risk factors, aiding in targeted diagnostic testing.
612
What does the presence of cytopathic effects (CPE) in TCID50 assays indicate?
That the virus is infectious and capable of inducing visible changes in cultured cells.
613
Why is sterile technique critical in viral diagnostics experiments?
To prevent contamination of samples, ensure reliable results, and maintain laboratory safety.
614
What is the significance of using controls in diagnostic assays?
Controls validate assay performance, detect potential errors, and ensure reliability of the results.
615
Why must viral samples be handled in a biosafety cabinet?
To minimize exposure to infectious agents and protect the operator from aerosolized particles.
616
What is the role of centrifugation in sample preparation?
To separate viral particles or cellular debris from the supernatant, ensuring clean samples for assays.
617
Why are primers crucial in the PCR reaction?
They define the target sequence to be amplified and ensure specificity for the viral genome.
618
How is gel electrophoresis used in PCR analysis?
It separates DNA fragments by size, allowing visualization of amplified products to confirm the presence of viral genomes.
619
Why is multiplex PCR advantageous in diagnostic testing?
It allows simultaneous detection of multiple viruses, saving time and resources.
620
What could cause a false negative result in a PCR test?
Poor sample quality, insufficient viral load, or primer mismatches with viral sequences.
621
What does a lattice formation in the HA assay indicate?
That viral particles are present and have agglutinated the red blood cells.
622
What does a 'button' appearance in the HA assay signify?
Absence of haemagglutination, indicating no viral particles at that dilution.
623
Why are serial dilutions performed in the HA assay?
To determine the endpoint titre, which is the highest dilution at which haemagglutination occurs.
624
How is HI used to identify specific influenza subtypes?
By observing whether subtype-specific antibodies inhibit haemagglutination, indicating a match between the virus and antibody.
625
What could cause a false positive in the HI assay?
Non-specific binding of antibodies or cross-reactivity with other viruses.
626
What is the importance of using red blood cells in HI assays?
They provide a visual and quantifiable readout of haemagglutination or inhibition.
627
What does each plaque represent in a plaque assay?
A single infectious viral particle that has lysed host cells in the monolayer.
628
Why are agar overlays used in plaque assays?
To restrict viral spread and allow localized plaque formation for quantification.
629
How can plaque assays determine antiviral efficacy?
By comparing plaque counts between treated and untreated samples, revealing the drug’s effect on viral infectivity.
630
Why are neuraminidase inhibitors like oseltamivir essential in influenza treatment?
They prevent viral release from infected cells, limiting spread within the host.
631
How does antigenic drift affect influenza diagnosis?
It alters viral surface proteins, potentially reducing assay sensitivity if based on outdated antigens.
632
What is the significance of differentiating H1N1 from H3N2 subtypes?
It informs vaccine development and treatment strategies specific to circulating strains.
633
What is the purpose of running a no-template control in PCR?
To check for contamination and ensure the specificity of amplification.
634
Why is quantitative data from assays like PCR and plaque assays crucial?
It enables precise measurement of viral load or infectivity, informing disease severity and treatment response.
635
How does combining HA and HI assays enhance diagnostic accuracy?
HA determines viral particle presence, while HI confirms subtype specificity through antibody interaction.
636
Why is rapid diagnostics critical during viral outbreaks?
It allows timely treatment, prevents further spread, and informs public health interventions.
637
How does diagnostic testing support antiviral development?
By identifying susceptible viral strains and monitoring resistance emergence.
638
What is the role of diagnostic techniques in epidemiological surveillance?
To track virus circulation, mutation, and emergence of new strains.
639
does a virus grow?
no
640
What are the seven stages of the virus replication cycle?
Attachment, Penetration, Uncoating, Replication, Assembly, Maturation, and Release.
641
What mnemonic can help remember the stages of virus replication?
"A PURple Apple Might Redden," with the first letters representing each stage.
642
Why is the attachment stage critical for viral infection?
Attachment involves the virus binding to specific cell surface receptors, which determines its tropism and ability to infect target cells.
643
What is viral tropism?
The specificity of a virus for particular host cells or tissues, dictated by the presence of suitable cell surface receptors.
644
Describe the importance of penetration in the virus life cycle.
Penetration allows the virus to enter the host cell and avoid extracellular factors like mucus flow that could remove it.
645
What is uncoating, and why is it essential?
Uncoating involves the release of the viral genome from the capsid into the host cell to enable replication and transcription.
646
How do enveloped and non-enveloped viruses differ in their methods of penetration?
Enveloped viruses often use membrane fusion, while non-enveloped viruses commonly use endocytosis or pore formation.
647
What dictates the replication strategy of a virus?
The type of nucleic acid genome the virus contains (e.g., dsDNA, ssRNA).
648
What are the Baltimore classification system's seven classes of viruses?
* Class I: dsDNA
* Class II: ssDNA
* Class III: dsRNA
* Class IV: +ssRNA
* Class V: -ssRNA
* Class VI: RNA that reverse transcribes
* Class VII: DNA that reverse transcribes
649
Why must RNA viruses encode their own RNA-dependent RNA polymerase (RdRp)?
Host cells lack the enzymes needed to transcribe mRNA from an RNA genome.
650
What is unique about retroviruses compared to other RNA viruses?
Retroviruses reverse transcribe their RNA genome into DNA, which integrates into the host genome for transcription.
651
What experimental evidence demonstrated the importance of viral attachment proteins?
Mutations in CCR5 (a coreceptor for HIV) prevent HIV attachment, making individuals resistant to infection.
652
How was receptor-mediated endocytosis identified as a viral entry mechanism?
Drugs inhibiting clathrin-mediated endocytosis blocked viral entry, proving its role in infection.
653
Why are transgenic mouse models significant in virology?
They allow the study of viruses, like poliovirus, in systems expressing human-specific receptors.
654
How does viral assembly vary between helical and icosahedral viruses?
Helical viruses wrap their genome with capsid proteins as it's synthesized, while icosahedral viruses often assemble capsids first and then insert the genome.
655
What experiment demonstrated the infectious nature of +ssRNA genomes?
Injecting poliovirus RNA into cells led to new virion formation, showing that its genome acts directly as mRNA.
656
How do antiviral drugs target the attachment stage of the virus life cycle?
They inhibit interactions between viral attachment proteins and host receptors.
657
Why are RdRps a major target for antiviral therapies?
They are essential for RNA virus replication and are unique to viruses, minimizing host toxicity.
658
What is the significance of high mutation rates in RNA viruses?
It allows rapid evolution and adaptation but also creates challenges for vaccine development.
659
How does the viral release mechanism influence disease spread?
Viruses released by budding can avoid immediate immune detection, while lytic release causes host cell destruction and inflammation.
660
Name a virus for each class in the Baltimore classification system.
* Class I: Herpes simplex virus (HSV)
* Class II: Parvovirus B19
* Class III: Rotavirus
* Class IV: Poliovirus
* Class V: Influenza virus
* Class VI: HIV
* Class VII: Hepatitis B virus (HBV)
661
What are the main structural differences between enveloped and non-enveloped viruses?
Enveloped viruses have a lipid bilayer with embedded proteins, while non-enveloped viruses consist of a protein capsid only.
662
How do segmented viral genomes contribute to genetic diversity?
They allow reassortment when multiple strains infect the same cell, potentially creating novel viruses.
663
What is the role of scaffolding proteins in complex virus assembly?
They aid in the assembly of large icosahedral viruses, such as herpesviruses, ensuring proper capsid formation.
664
Why is the study of viral uncoating significant for antiviral development?
Interrupting uncoating can block the release of viral genomes, halting replication.
665
What evolutionary advantage do viruses gain from using host enzymes for replication?
It reduces the viral genome size and reliance on viral-encoded enzymes.
666
How does the immune system detect intracellular viruses during replication?
It recognizes viral RNA or DNA via pattern recognition receptors like TLRs and activates interferon responses.
667
Why do RNA viruses lack proofreading during replication, and what is the consequence?
Their RdRps lack proofreading capabilities, leading to higher mutation rates and greater genetic variability.
668
What are the two primary mechanisms viruses use to enter host cells?
Membrane fusion and receptor-mediated endocytosis.
669
What determines a virus's tropism for specific cells?
The presence of compatible receptors on the host cell surface and intracellular factors that support replication.
670
How do viruses like influenza penetrate host cells?
They bind to sialic acid residues on the host cell surface and enter through receptor-mediated endocytosis.
671
What is the significance of clathrin in viral entry?
Clathrin is involved in forming vesicles during receptor-mediated endocytosis, aiding the internalization of certain viruses.
672
How does pH change in endosomes affect viral entry?
Low pH triggers conformational changes in viral proteins, facilitating uncoating and genome release.
673
What is the central dogma for viruses with a DNA genome?
DNA → mRNA → Protein, using host or viral polymerases.
674
How do negative-sense RNA (-ssRNA) viruses replicate their genomes?
They must first transcribe their genome into positive-sense RNA using viral RNA-dependent RNA polymerase (RdRp).
675
What distinguishes the replication of double-stranded RNA (dsRNA) viruses?
They require RdRp to transcribe mRNA directly from the dsRNA genome within viral replication complexes.
676
Why is reverse transcription important in retroviruses?
It converts RNA into DNA, allowing integration into the host genome and persistent infection.
677
How do viruses regulate the timing of early and late gene expression?
Early genes are transcribed to produce regulatory proteins, while late genes encode structural proteins for assembly.
678
What ensures the accuracy of genome packaging during assembly?
Specific signals or sequences on the viral genome, such as packaging signals, are recognized by capsid proteins.
679
How do segmented RNA viruses like influenza ensure proper genome assembly?
Each segment has unique packaging signals that guide their inclusion into the viral particle.
680
Why are assembly intermediates common in large viruses?
They stabilize partially assembled capsids and ensure correct folding and interactions during assembly.
681
What role do scaffolding proteins play in the assembly of complex icosahedral viruses?
They guide capsid assembly but are later removed to allow genome insertion.
682
How is viral budding different from lytic release?
Budding occurs without lysing the host cell, allowing enveloped viruses to acquire their lipid envelope.
683
What is the primary method of release for non-enveloped viruses?
Lysis of the host cell.
684
How does neuraminidase aid influenza virus egress?
By cleaving sialic acid residues, preventing virion aggregation and allowing release.
685
What is the advantage of cell-to-cell spread for viruses like herpesviruses?
It enables evasion of host immune responses by avoiding extracellular exposure.
686
What role do viral late proteins play in egress?
They facilitate capsid maturation, membrane acquisition, and the release of virions.
687
How does syncytium formation aid viral transmission?
It allows direct spread between adjacent cells by forming multinucleated giant cells.
688
How was the concept of viral tropism experimentally confirmed?
By showing that certain viruses, like HIV, only infect cells expressing specific receptors like CD4 and CCR5.
689
What evidence demonstrated the necessity of endosomal acidification for viral entry?
Drugs inhibiting endosomal acidification, such as bafilomycin, blocked infection by influenza and other pH-sensitive viruses.
690
How were reverse transcriptase inhibitors validated experimentally?
By demonstrating their ability to block retroviral replication in vitro without affecting host DNA polymerases.
691
What is the importance of plaque assays in virology research?
They quantify infectious virus particles and help determine virus titers.
692
How does site-directed mutagenesis contribute to virology?
By enabling researchers to study the effects of specific mutations on viral proteins and their functions.
693
How do viruses like HSV evade the host immune response?
By encoding proteins that inhibit antigen presentation, interferon responses, or apoptosis.
694
What role do pattern recognition receptors (PRRs) play in detecting viruses?
They recognize viral nucleic acids or proteins and activate innate immune responses.
695
How do viruses exploit host factors for replication?
By using host enzymes, ribosomes, and metabolic pathways to synthesize viral components.
696
What is the significance of interferons in antiviral defense?
They induce the expression of antiviral proteins, such as RNases and protein kinases, that inhibit viral replication.
697
How do viruses like influenza and SARS-CoV-2 suppress interferon signaling?
By encoding proteins that block interferon production or downstream signaling pathways.
698
Why is understanding viral replication essential for vaccine development?
It identifies critical stages and proteins that can be targeted to prevent infection.
699
What theoretical model explains the high mutation rates of RNA viruses?
The "error threshold hypothesis," where mutation rates are balanced to maintain viability and adaptability.
700
How can CRISPR-Cas systems be used to study viral replication?
By selectively editing viral genomes or host factors to understand their roles in infection.
701
What are quasispecies, and why are they significant in virology?
Quasispecies are genetically diverse populations of viruses within a host, contributing to rapid adaptation and drug resistance.
702
Why are host factors critical for developing broad-spectrum antivirals?
Targeting conserved host pathways reduces the risk of resistance compared to targeting variable viral proteins.
703
How does understanding viral life cycles aid in outbreak response?
By identifying transmission stages and interventions to block spread (e.g., vaccines or antivirals).
704
Why is surveillance of zoonotic viruses essential?
It helps detect emerging threats early, such as influenza or coronaviruses, and prevent pandemics.
705
How can virology research inform therapeutic development?
By revealing host-virus interactions and viral vulnerabilities that can be targeted with drugs or biologics.
706
What are the implications of RNA virus recombination for vaccine design?
Recombination can create novel strains, requiring updated vaccines to maintain efficacy.
707
Why is understanding viral assembly crucial for antiviral strategies?
Disrupting assembly can prevent the formation of infectious particles, effectively stopping replication.
708
What determines a virus's host range?
The compatibility of viral attachment proteins with specific host cell surface receptors.
709
How do enveloped viruses differ in entry mechanisms compared to non-enveloped viruses?
Enveloped viruses enter via membrane fusion or endocytosis, while non-enveloped viruses enter through pore formation or endocytosis.
710
What experimental evidence supports clathrin-mediated endocytosis as an entry mechanism?
Inhibition of clathrin-coated vesicle formation blocked viral entry into host cells.
711
What is the significance of caveolae-mediated endocytosis in virology?
It represents an alternate entry route used by some viruses, such as simian virus 40 (SV40).
712
How do viruses overcome cellular barriers during penetration?
They exploit natural cellular processes like receptor-mediated endocytosis or create pores for genome entry.
713
What is the difference between Class I and Class II viruses in the Baltimore classification?
Class I viruses have dsDNA genomes, while Class II viruses have ssDNA genomes that require conversion to dsDNA for replication.
714
How do negative-sense RNA viruses replicate their genome?
They use a viral RNA-dependent RNA polymerase to synthesize complementary positive-sense RNA, which serves as mRNA and a replication template.
715
Why do retroviruses require reverse transcriptase?
To convert their RNA genome into DNA, which integrates into the host genome for replication.
716
What are defective interfering (DI) particles?
virus mutants that are created when a virus's genome is damaged during replication
717
How do segmented viral genomes, like those of influenza, contribute to reassortment?
Segments from different strains can mix during co-infection, creating novel hybrid viruses.
718
How does viral genome packaging ensure specificity?
Viral capsids have specific sequences or structures that recognize and encapsulate the correct genome.
719
What are interfering (DI) particles?
Mutant viral genomes that compete with wild-type viruses during replication but cannot independently replicate.
720
What are the roles of scaffolding proteins in large viral capsids?
They aid in assembling complex capsid structures and are later removed for genome insertion.
721
How is the maturation step crucial for infectivity?
Proteolytic cleavage of viral proteins during maturation activates structural changes necessary for infectivity.
722
What experiment demonstrated the importance of protease-mediated maturation?
Inhibition of HIV protease blocked maturation, rendering virions non-infectious.
723
How do enveloped viruses exit the host cell?
By budding through the host membrane, acquiring a lipid envelope with embedded viral proteins.
724
What is the mechanism of non-enveloped virus release?
Lysis of the host cell, which releases mature virions but often causes cell death.
725
Why is budding a stealthy release mechanism?
It minimizes immune system activation by avoiding abrupt cell death.
726
How does neuraminidase facilitate influenza virus release?
It cleaves sialic acid residues, preventing the virus from sticking to the cell surface.
727
How do viruses suppress the host immune response?
By downregulating MHC molecules, blocking interferon signaling, or directly degrading immune proteins.
728
What are viral immune evasion proteins?
Proteins like HIV Nef or herpes ICP47 that block immune recognition and response pathways.
729
Why do viruses induce apoptosis in host cells?
To aid in viral release or limit immune detection by destroying infected cells before immune activation.
730
How does the host’s innate immune system detect viral infections?
Through pattern recognition receptors (PRRs) like TLRs, which recognize viral RNA/DNA or other pathogen-associated molecular patterns (PAMPs).
731
What is the significance of cytokine storms in viral infections?
An excessive immune response that can cause severe tissue damage and worsen disease outcomes.
732
What is the quasispecies theory in virology?
RNA viruses exist as a population of closely related variants due to high mutation rates, enabling rapid adaptation.
733
How does antigenic drift differ from antigenic shift?
Antigenic drift involves small mutations over time, while antigenic shift involves major genomic reassortments, often leading to pandemics.
734
Why is the RNA world hypothesis relevant to virology?
It suggests that RNA viruses may represent relics of ancient RNA-based life forms, providing insights into early evolution.
735
do viruses grow and divide?
no, they assemble
736
what is the innoculation phase of a viral infection?
Inoculation phase: During this phase, the virus undergoes the first step of the viral life cycle: attachment (to host cells).
737
what happens during the eclipse phase?
Eclipse: Viruses are now being manufactured within the host cells.
This phase include the penetration step where virus enter the cells and the uncoating of the genetic material.
Finally, we see the manufacture of the viral components (viral proteins, and new genetic materials)- replication occurs
738
what happens during the viral maturation phase?
Maturation: After synthesis of capsids, enzymes and other materials, new virus particles (virions) are formed during the assembly step.
Total virus count increases before release occurs.
739
name the key steps in the viral life cycle
740
what methods can viruses take to enter cells
uncoating at the plasma membrane and uncoating within endosomes
741
how do viruses travel in and out of the cell?
Endocytosis
Cytoskeletal transport, microtubules
Nuclear import/export
Transcription machinery
Translation machinery
Secretory pathway
742
what is necessary for a virus to enter into a cell
Glycoproteins on the surface of the virus will recognize attachment and entry receptors to initiate the penetration of the viral particle in the cells. And those receptors also make the specificity of the cells to be permissive to the entry of the virus.
viruses enter specific cells due to the receptor specificity
743
are viruses and receptors specific
Different viruses can bind to same receptors (e.g: Adenovirus and Coxsackievirus B3)
Same virus can bind to multiple receptors (e.g: Retroviruses can bind to 16 receptors) and cause damage to multiple different tissues
744
do some viruses need multiple receptors to enter a cell?
yes, HIV for example needs two receptors to enter a cell, one receptor will be a core receptor that provides stability for the virus on the surface of the cell
745
what are the two modes of virus entry?
746
what is the main dofference between a virus fusing with the cell membrane vs a virus forming an endosome to enter a cell?
when a virus fuses with the cell membrane it expresses all the glycoproteins on the surface of the cell, this can indicate to the immune system that the cell is infected
747
how does uncoating of the viral particle from its vesicle happen?
748
where does uncoating of the viral particle from its vesicle happen?
it can happen in the cytoplasm or the nucleus
749
why is it difficult to penetrate the cytoplasm?
The cytoplasm is crowded!
and Movement of large protein complexes will not occur by diffusion
750
how can a virus travel to the nucleus
it can hijack the microtubule network and bind to kinase motor proteins
751
why is the central dogma not applicable to RNA viruses?
RNA viruses are an exception to this dogma because their molecular biology does not involve DNA
752
what is translational shutoff?
One well studied viral strategies is the translational shutoff:
1. Virus stop cellular translation
2. Use the translation complex for its own translation
753
WHAT can a DNA virus do to cause translational shutoff?
-they can block polymerase 2
-suppression of maturation of mRNA
-blocking nuclear pores from exporting the host cells mRNA to its cytoplasm
754
WHAT can a RNA virus do to cause translational shutoff?
block host cell mRNA machinery in the cytoplasm
block host cell mRNA from accessing the ribosome
755
what are the 2 types of viral proteins?
non-structural proteins
strucutral proteins
756
what is the purpose of non-structural proteins?
Genome
replication, Antagonise host responses
these proteins are produced early on in the cycle
| wha
757
what is the purpose of structural proteins?
enable Virus assembly
these proteins are formed later in the cycle
758
what is a key similarity between all viral genomes?
Viral genomes must make mRNA
that can be read by host ribosomes
759
where does dsDNA replication occur?
in the cell nucleus.
uses RNA polymerase 2 to develope mRNA that travels to the cytoplasm and forms proteins needed to create its virus, such as herpes simplex virus
760
how does ssDNA replication occur?
DNA can be positive or negative, DNA dependant RNA polymerase synthesises viral mRNA which can be exported to the cytoplasm to create a viral protein.
here we also have a supplementary step to produce a virus where the viral double stranded DNA will be seperated again into a negative and positve strand which can then be encapsulated into a virus once again
761
how does ssRNA (+) replication occur?
the virus remains in the cytoplasm
it is instantly ready to create proteins because it is the same polarity as messenger RNA; the genome once released into the cells is ready to produce viral proteins using cellular machinary without any other steps
762
what viruses use ssDNA?
TT virus (ubiquitous human virus) and B19 parvovirus (fifth disease)
763
how do ssRNA (+) viruses create their own genomes?
they use the proteins they produce to create more viral RNA by creating their own RNA dependant RNA polymerase encoded by the virus
764
what are some ssRNA (+) viruses
mosquito borne flaviviruses such as Zika virus
765
how do ssRNA (-) viruses create their own genome
mainly cytoplasmic but can occur in the nuclease (influenza virus) potentially because the virus is trying to hide
the negative RNA is used to produce a positive strand that can then uses host ribosomes in the cytoplasm to produce proteins
the positive strande formed also uses RNA dependant RNA polymerase encoded by the virus to replicate and create more negative ssRNA to be encapsulated into the virus
766
where does dsRNA replicate and form proteins?
replication occurs in the cytoplasm only
767
how does dsRNA form proteins?
the double stranded RNA splits and forms proteins using host cell machinery in the cytoplasm
768
how does dsRNA replicate?
the single stranded protein formed by dsRNA replicates using RNA dependent RNA polymerase and is then encapsulated into the virus
769
give an example of a virus with dsRNA
rotavirus
770
where does retro-virus replication occur
in the nucleus
771
how does retrovirus form proteins?
once the VIrus enters the host cell it will import its genetic material, positive RNA, to the nucleus where it is converted to negative dsDNA using reverse transcriptase and RNA dependant DNA polymerase; the dsDNA will then create proteins and more viral particles using host machinery
772
where does dsDNA gapped virus replication occur?
in the nucleus
773
how does dsDNA gapped virus form proteins?
the genetic material will enter the nucleus where polymerase 2 (from the host) will form cccDNA, the cccDNA can be used to create mRNA for proteins transcription and also form +RNA which can be reverse transcribed, via reverse transcription, to create more viral dsDNA
774
is mRNA always positive?
yes
775
# 1.
name a type of retro-virus
HIV
776
WHAT are hepatitis B and hepadnavirdae and example of?
dsDNA gapped viruses
777
what are viral factories?
Viral factories, also known as viroplasm, are subcellular microenvironments where viruses replicate
778
where do viruses get their envelopes from?
Envelopes of viruses are derived from membrane, could be internal membrane or plasma membrane.
779
what are secretory pathways important for enveloped viruses?
Often enveloped viruses use secretory pathways to assemble, mature, and egress the cell.
once encapsulation occurs the virus can use the ER to create its own envelope and mature from the ER to the golgi where it uses the low pH of the exosomes it enters to mature the envelope proteins and egress the cell; not all virions mature correctly; not all end up being capable of being infectious
780
can a haemagluttination assay inform us of how many infectious viral particles there are
no, it is an indirect test and simply informs us of the presence of a virus
781
why is cellular exocytosis pathway popular for many viruses?
Cellular exocytosis pathway is very popular mainly because it is not disturbing the cell and once you are in the vesicles you are protected from immunde detection
782
what are the steps for when a virus is budding off an infected cell
783
where does maturation occur when a virus is undergoing the budding off process
outside the cell
784
what are the two forms of naked virus egress?
non-lytic viral egress
lytic viral egress
785
what happens during non-lytic vial egress?
the virus can use double membrane-vesicles formed via autophagy, the viral particles remain in the vesicles where they mature until the vesicles fuse to the membrane and the viruses are released
the multiple viral particles can also remain in exosomes which are encosed in multivesicular bodies that release the particles into the extracellular space without removing their exosomes; this makes it easier for them to evade the immune system the viral particles can also infect the next cell together
786
what happens during lytic viral egress?
Cell lysis: apoptosis, necroptosis
Viral proteins induce rupture of the cell membrane (e.g viroporin, poliovirus)
Loss of membrane integrity with inhibition of protein synthesis
787
what methods can a virus take to transmit itself to other cells
788
what is an entry inhibitor?
789
what are nukes and non-nukes?
790
what are integrase inhibitors?
791
what are protease inhibitors?
792
What are the primary steps of the virus life cycle?
Attachment, Entry, Uncoating, Genome Replication, Protein Translation, Assembly, Release, and Transmission.
793
Why do viruses require a host cell for replication?
Viruses depend on the host cell machinery for transcription, translation, and genome replication as they lack metabolic enzymes and ribosomes.
794
How does the growth curve of viruses differ from cellular organisms like bacteria?
Viruses do not grow or divide. Instead, they assemble from components produced inside the host cell.
795
What mechanisms do viruses use to enter host cells?
Direct membrane fusion or receptor-mediated endocytosis.
796
What determines the specificity of viral entry into host cells?
The interaction between viral glycoproteins and specific host cell receptors.
797
How do viruses like HIV utilize multiple receptors for entry?
HIV requires CD4 as a primary receptor and CCR5 or CXCR4 as coreceptors for stable attachment and entry.
798
Why is the cytoplasm described as a challenging environment for viral movement?
It is crowded with proteins and organelles, necessitating the use of active transport along microtubules via motor proteins like kinesin.
799
How do viruses ensure the translation of their proteins in the host cell?
Viruses often shut down host protein synthesis and repurpose the translation machinery for viral mRNA.
800
What are the two major categories of viral proteins produced during infection?
Early non-structural proteins (e.g., polymerases) for replication and late structural proteins (e.g., capsids, envelopes) for virion assembly.
801
How do RNA viruses bypass the central dogma of molecular biology?
RNA viruses use their RNA genomes directly for translation or as templates for replication without needing a DNA intermediate.
802
What is the universal requirement for all viruses during genome replication?
The production of mRNA that can be read by host ribosomes.
803
What are the seven classes of viral genomes in the Baltimore classification system?
Class I: dsDNA
Class II: ssDNA
Class III: dsRNA
Class IV: +ssRNA
Class V: -ssRNA
Class VI: +ssRNA with DNA intermediate
Class VII: Gapped dsDNA.
804
How do retroviruses like HIV replicate their genomes?
They reverse transcribe their RNA genome into DNA, which integrates into the host genome for transcription and replication.
805
Why do RNA viruses encode their own RNA-dependent RNA polymerase?
Host cells lack the enzymes necessary to replicate RNA genomes or transcribe mRNA from RNA templates.
806
Where does viral assembly typically occur within the host cell?
Assembly occurs in specific locations such as the nucleus for DNA viruses or the cytoplasm for RNA viruses.
807
What are viral factories, and why are they important?
Viral factories are localized sites within the host cell where viral components concentrate to enhance replication and assembly efficiency.
808
How do segmented genomes like influenza ensure proper genome packaging?
Each segment contains unique packaging signals that ensure all required segments are included in the virion.
809
What are the two main mechanisms of viral release?
Budding (non-lytic) for enveloped viruses and cell lysis (lytic) for non-enveloped viruses.
810
How does budding benefit enveloped viruses?
It allows them to acquire a lipid envelope from the host membrane, aiding in immune evasion.
811
What is the advantage of direct cell-to-cell transmission for viruses like HIV?
It avoids extracellular immune detection, facilitating persistent infection.
812
How was the role of receptor-mediated endocytosis in viral entry demonstrated experimentally?
Drugs that inhibit endocytosis prevented viruses like influenza from entering host cells.
813
Why is the study of viral uncoating crucial for drug development?
Interrupting uncoating can block genome release, halting the infection process.
814
How do segmented genomes like influenza contribute to viral evolution?
Reassortment between segments of different strains can generate new, potentially pandemic-causing viruses.
815
What are some diseases caused by positive-sense RNA viruses?
Zika virus (microcephaly) and dengue fever.
816
Why is the influenza virus an exception among RNA viruses regarding replication?
It replicates its RNA genome in the nucleus instead of the cytoplasm, unlike most RNA viruses.
817
What makes the HIV infection strategy highly efficient?
Integration of its genome into the host DNA allows persistent infection and transmission.
818
How does understanding viral entry inform vaccine design?
Targeting viral glycoproteins or host receptors can prevent virus-host cell interactions.
819
Why are RdRp enzymes a major focus for antiviral therapies?
They are unique to RNA viruses and essential for replication, making them ideal targets.
820
What is the significance of viral protein diversity for diagnostic and therapeutic development?
It provides specific targets for assays and treatments, depending on the virus's lifecycle and pathogenesis.
821
What distinguishes viruses from other microorganisms?
Viruses are obligate intracellular parasites that require host cell machinery to replicate, lacking independent metabolic systems and ribosomes.
822
What is the primary difference between the replication of DNA and RNA viruses?
DNA viruses often replicate in the nucleus using host DNA polymerase, while RNA viruses replicate in the cytoplasm using viral RNA-dependent RNA polymerase (RdRp).
823
What are the environmental conditions required for virus stability outside a host?
Non-enveloped viruses are generally stable in harsh conditions, while enveloped viruses are more fragile and require moist environments.
824
What is viral tropism, and why is it important?
Viral tropism refers to the specificity of a virus for certain host cells or tissues, determined by receptor compatibility and intracellular factors.
825
How do viruses like SARS-CoV-2 achieve high infectivity?
By binding to ubiquitous receptors like ACE2, which are present in multiple tissues.
826
Why is glycoprotein variation important in viral attachment?
Glycoproteins like hemagglutinin (influenza) determine host range and mediate receptor binding, making them targets for immune recognition and vaccines.
827
How does low pH in endosomes assist viral uncoating?
It triggers conformational changes in viral proteins, enabling genome release into the cytoplasm or nucleus.
828
What experimental evidence supports the role of clathrin-mediated endocytosis in viral entry?
Inhibitors of clathrin-coated vesicle formation block infection by viruses like influenza and dengue.
829
What is the advantage of direct fusion over endocytosis for viral entry?
Direct fusion delivers the genome into the cytoplasm without relying on intracellular transport mechanisms.
830
How do viruses override host translational machinery?
By producing proteases that cleave host factors or by modifying ribosomes to preferentially translate viral mRNA.
831
What are internal ribosome entry sites (IRES), and why are they important for RNA viruses?
IRES elements allow translation initiation in a cap-independent manner, ensuring viral protein synthesis even when host translation is suppressed.
832
Why is polyprotein synthesis an efficient strategy for viruses like poliovirus?
A single large polyprotein is produced and cleaved into functional proteins, reducing the need for multiple initiation events.
833
How do DNA viruses ensure fidelity during replication?
DNA viruses often utilize host DNA polymerases, which have proofreading activity, to minimize replication errors.
834
Why do RNA viruses exhibit higher mutation rates than DNA viruses?
RNA-dependent RNA polymerase (RdRp) lacks proofreading activity, leading to frequent errors during replication.
835
What is the 'error threshold hypothesis' in RNA virus evolution?
It suggests that high mutation rates enhance adaptability but must be balanced to avoid loss of viability due to excessive errors.
836
What is reassortment, and which viruses use it?
Reassortment is the exchange of genome segments between viruses during co-infection, commonly seen in segmented viruses like influenza.
837
What role do scaffolding proteins play in virus assembly?
They guide capsid formation and ensure correct assembly but are removed before genome packaging.
838
How do viruses ensure genome encapsidation specificity?
Viral genomes contain packaging signals recognized by capsid proteins, ensuring only viral genomes are packaged.
839
Why is maturation essential for viral infectivity?
Maturation processes, like protease-mediated cleavage of structural proteins, ensure the virus is structurally competent to infect new cells.
840
How does apoptosis facilitate viral spread?
Apoptotic cell death releases viral particles without triggering inflammation, enabling silent spread.
841
Why do non-enveloped viruses typically use lytic release?
They lack membranes and depend on host cell destruction to release virions into the environment.
842
How do viruses like herpes evade immune detection during spread?
By using cell-to-cell transmission mechanisms, bypassing extracellular spaces where antibodies can neutralize them.
843
What are the primary mechanisms by which viruses spread to other cells?
Direct cell-to-cell contact, extracellular release, and vector-mediated transmission.
844
How does direct cell-to-cell transmission protect viruses from immune detection?
It avoids the extracellular space where antibodies and immune cells could neutralize the virus.
845
What is syncytium formation, and how does it aid viral transmission?
Syncytium formation occurs when viral proteins induce the fusion of neighboring host cells, creating multinucleated cells that facilitate direct viral spread without exiting the host.
846
How do viruses like HIV exploit filopodia for cell-to-cell spread?
They travel along actin-based filopodia to reach neighboring cells, enhancing direct transmission efficiency.
847
What role does budding play in the spread of enveloped viruses?
Budding allows viruses to acquire a lipid envelope from the host cell membrane while releasing new virions without lysing the host cell.
848
How do viruses use the lytic cycle to spread?
Viruses like bacteriophages replicate within the host cell until it bursts, releasing new virions into the surrounding environment.
849
What is transcytosis, and how does it facilitate viral transmission?
Transcytosis involves viruses being transported across epithelial barriers within vesicles, enabling entry into underlying tissues.
850
How do vector-borne viruses spread between hosts?
Through the bite of an infected vector (e.g., mosquito, tick), which transmits the virus directly into the bloodstream or tissues of a new host.
851
What is vertical transmission in viruses, and provide an example?
Vertical transmission occurs from mother to offspring, such as HIV or Zika virus passing through the placenta or during childbirth.
852
How do viruses like influenza utilize aerosols for transmission?
They are expelled in respiratory droplets during coughing or sneezing and inhaled by new hosts, leading to respiratory tract infections.
853
How do fecal-oral transmission pathways work for viruses like rotavirus?
Viruses are shed in feces, contaminate water or food, and infect new hosts when ingested.
854
What role do extracellular vesicles play in viral transmission?
Some viruses exploit exosomes or microvesicles for packaging and transport, shielding them from immune detection during cell-to-cell transfer.
855
How does apoptosis promote viral transmission?
During apoptosis, cellular components, including virions, are released in apoptotic bodies that can infect neighboring cells.
856
What is the 'viral synapse,' and how does it enhance efficiency in viral spread?
A viral synapse is a specialized junction between an infected cell and a target cell that facilitates direct virus transfer, as seen in HIV transmission.
857
How do segmented RNA viruses like influenza use reassortment for transmission?
During co-infection of a single host cell, genome segments from different viral strains mix, producing novel variants capable of infecting new cells or hosts.
858
How do plant viruses achieve cell-to-cell transmission?
They move through plasmodesmata, which are intercellular channels connecting plant cells.
859
What are virological advantages of airborne transmission?
It enables rapid spread over long distances and does not require direct contact between infected and susceptible individuals.
860
How does viral shedding contribute to transmission?
Viruses are released into bodily fluids (saliva, urine, feces) or secretions (mucus, semen), facilitating transfer to other hosts or environments.
861
How do viruses manipulate immune cells for transmission?
Viruses like HIV infect immune cells like macrophages and dendritic cells, which migrate to other tissues or hosts, spreading the infection.
862
How do zoonotic viruses achieve transmission between species?
By adapting to infect both animal reservoirs and humans, often facilitated by genetic mutations that enhance receptor binding in the new host.
863
who is most at risk from RSV?
Very young, very old and immunocompromised
most at risk
RSV is the most common cause of respiratory infection in infants
and young children
864
how many people die from RSV?
* Up to 199,000 deaths/year
* Virtually all infected by age 2
* RSV first discovered in 1956
865
are RSV virions pleomorphic?
yes
866
what family does RSV belong too?
Mononeavirales-pneumoviridae-orthopneumovirus
867
RSV pathogenesis?
RSV causes syncytia
More serious disease: atelectasis, respiratory failure
Infection results in inflammation, infiltration of inflammatory cells (neutrophils, monocytes), increased mucous production, sloughed cells.
A link to the development of asthma
868
how is RSV diagnosed?
Diagnosis is usually by PCR as part of a respiratory panel.
Rapid antigen tests are available
869
how is RSV treated?
patient management & isolation,
* No vaccine, no treatment
* palivizumab, a humanised monoclonal antibody requiring monthly administration.
£££ reserved for high risk children
870
symptoms of RSV IN CHILDREN
871
how was the new vaccine for RSV different from the old more dangerous one that harmed babies by enhancing the disease?
the new vaccine targets the pre-fusion F glycoprotein
872
what family does rhinovirus belong too?
Picornavirales-picornaviridae-enterovirus-Rhinovirus
873
what the identified strains of rhinovirus?
3 groups/species of Rhinovirus: A, B & C
Approx 160 serotypes identified
874
what receptor does Rhinovirus A and B use?
Rhinovirus A & B predominantly use ICAM1 as a receptor
875
what receptor does rhinovirus C use?
RV-C uses CDHR3 receptor
876
how is rhinovirus transmitted?
Transmitted through
aerosols/microdroplets and fomites
877
what temperature does rhinovirus like
Rhinoviruses like it a bit colder! They
prefer 32oC
878
is there a rhinovirus vaccine?
no
879
when do symptoms for Rhinovirus show up?
Symptoms apparent ~2 days post infection, healthy individuals are mostly asymptomatic
880
how rhinovirus cause infection
881
what is the main treatment for rhinovirus?
Innate Immunity, Immune response to RV infection results in proinflammatory cytokines and increased airway
responsiveness, not alot of research is done on treatments because the virus is not a big healthcare burden
882
when was RSV discovered?
1956
883
when was rhinovirus discovered?
Virus isolated from samples taken from healthcare
workers with a cold in 1953
Primary cause of the ‘common cold’
884
what is the health burden of rhinovirus?
Responsible for over 50% of Upper Respiratory TI
885
RSV seasonality?
december-may
886
rhinovirus seasonality?
all year round
887
detail the RSV genome
888
what are upper respiratory tract viral infections
889
what are lower respiratory tract infections
890
what can coronavirus infect?
Coronavirus infect pigs, cows, bats, horses,
camels, cats, dogs, rodents, birds…. Potential for zoonotic spillover
891
how many coronavirus can infect humans?
7 coronavirus (so far!) can infect humans:
Including 4 ‘common cold’ endemic strains:
229E, OC43, NL63, HKU1
Coronaviruses are responsible for 10-15% of
common colds
892
what are the 3 severe covid strains
3 more severe strains: SARS (2002), MERS
(2012), SARS-CoV-2 (2019)
893
what family do coronavirus belong too?
Nidovirales-Coronaviridae-Coronavirus
894
what are the largest know viruses?
coronaviruses- 4 Structural proteins, 16 Non-Structural proteins
895
how many genes does RSV have
10 genes that encode 11 proteins
896
covid pathogenesis
So here we have an infection of an epithelial, cell in the respiratory tract. so the virus undergoes its classic cycle, however, after the first 1 or 2 cell infections, some cytotoxic damage occurs where the cells start to sense infection and secrete some cytotoxins And those chemical, particles are gonna be sent to the neighbour cells or tissue to prepare them for the coming infection. And this gonna also attract you can see here immune cells like macrophages, neutrophil or dendritic cells.
897
what is the cytokin storm and the problems it can cause
sometimes there is an overreaction from the cell as cytokines are produced too much, this is the cytokine storm And when you have this, you attract too many immune cells, and you're gonna induce a lot of cell deaths, And this is gonna trigger the pathogenesis we see with many respiratory viruses, including SARS-CoV-2; So it will be like respiratory distress symptoms which can cause death; the cytokine storm can spread to other organs
898
treatment for covid
vaccine, developed by sequencing the the Virus RNA, the virus is sequencing helps predict future prevelent strains
899
what is the seasonality of covid
all year round
900
what is the seasonality of influenza?
influenza happens during the cold months from december to march
901
what happens when a new dominant influenza strain emerges?
the old strains rarely co-circulate in the same place
902
what are the 2 main surface proteins on influenza?
hemagglutinin and neuraminidase as they give the specificity for the virus to enter and infect cells
903
what are examples of poly proteins?
RSV and coronavirus
904
# 1.
how is infleunza segmented?
influenze genetic material is seperated into 7 or 8 segments as it is not a polyprotein. Each segment of the genome is bound to nucleoproteins in a ribonucleoprotein complex (RNP)
905
what shape is influenza?
it is pleomorphic
906
does influenza B and C infect agricultural animals?
no only influenza A spreads between the humans and animals B and C only infect humans
907
how is infuenza named?
908
what are the symptoms of influenza?
909
how is influeenza spread?
droplets and fomites
910
influenza viral life cycle
1. the first step will be the binding to your cells. The HA proteins bind to sialic acid receptors on the host cell
- 2 - then internalisation of the viral particle requires endocytosis and acidification of the endosome releases the capside and RNA genome into the cytosol
3. during uncoating RNPs are released into host cytosol. RNPs transported to the nucleus where mRNA is transcribed, RNPs are transported to the nucleus by microtubules
4. Viral mRNA exported out of the nucleus and translated by
host ribosomes. Viral polymerase subunits and NP proteins move to the
nucleus to form RNPs
5. Assembly & budding: HA, NA and M2 proteins trafficked to the cell
membrane. RNPs in the nucleus move to the cytosol then the cell membrane. Virions bud from the cell membrane
911
antigenic shift vs antigenic drift
Drift: Accumulation of mutations in antigens
(particularly HA, also NA))
* Occurs most frequently in Influenza A, then B
Shift: Different strains infecting the same host
cells can undergo ’reassortment’
* Occurs among influenza viruses of the same
genus. Most common in IAV (particularly avian
influenza)
912
why does influenza have such a high pandemic risk?
because they undergo antigenic shift, different viral strains can infect the same cell which can cause their genome to mix and create a new strain; influenza can also undergo antigenic drift which allows random mutations which can improve their ability to spread; these mutations can be spread through antigenic shift
913
# 1.
can non-segmented viruses undergo reassortment and antigenic shift
no
914
what happened influenza B yamagata during covid?
it disappeared
915
What are the most common respiratory viruses discussed in the documents?
Respiratory Syncytial Virus (RSV), Rhinovirus, Coronaviruses, and Influenza.
916
How are respiratory viruses primarily transmitted?
Via aerosols, respiratory droplets, and fomites. Direct contact can also spread the virus.
917
What is the importance of seasonality in respiratory virus infections?
Respiratory viruses like RSV and influenza peak in colder months due to factors like low humidity and increased indoor crowding.
918
Why is viral diversity important in respiratory viruses?
It enables adaptation to new hosts, evasion of immunity, and zoonotic spillover.
919
What is the classification of RSV?
Enveloped, negative-sense, single-stranded RNA virus.
920
What are the two subtypes of RSV, and what distinguishes them?
Subtypes A and B, distinguished by variations in their F (fusion) and G (glycoprotein) proteins.
921
Why is RSV particularly dangerous for infants and young children?
Their immature immune systems cannot effectively combat the virus, leading to severe respiratory distress and complications.
922
What are the symptoms of severe RSV infection?
Wheezing, rapid breathing, loss of appetite, fever, and respiratory failure in severe cases.
923
How does RSV evade the immune system?
By inhibiting apoptosis and IFN signaling through proteins like SH and NS2, delaying cell death to maximize replication.
924
What are the treatment options for RSV?
Supportive care (oxygen therapy, fluids), and in high-risk children, prophylactic monoclonal antibodies like palivizumab.
925
What is the classification of rhinovirus?
Non-enveloped, positive-sense, single-stranded RNA virus.
926
What are the main symptoms of rhinovirus infection?
Runny nose, sneezing, coughing, sore throat, headache, and fatigue.
927
Why is reinfection with rhinovirus common?
Due to the presence of over 160 serotypes and limited cross-immunity.
928
How does rhinovirus induce asthma exacerbations?
By increasing airway responsiveness through pro-inflammatory cytokine production and disrupting cellular junctions.
929
What are the primary transmission routes for rhinovirus?
Aerosols, fomites, and direct contact.
930
How are coronaviruses classified?
Enveloped, positive-sense, single-stranded RNA viruses. They belong to the Nidovirales order and Coronaviridae family.
931
What are the three severe coronavirus strains that caused epidemics or pandemics?
SARS-CoV (2002), MERS-CoV (2012), and SARS-CoV-2 (2019).
932
What structural proteins are present in coronaviruses?
Spike (S), Envelope (E), Membrane (M), and Nucleocapsid (N) proteins.
933
What is zoonotic spillover, and how is it related to coronaviruses?
It is the transmission of viruses from animals to humans, facilitated by high mutation rates and adaptability. Examples include SARS-CoV from bats and MERS-CoV from camels.
934
How does SARS-CoV-2 utilize host cell receptors for entry?
It binds to ACE2 receptors and requires TMPRSS2 or similar coreceptors for entry.
935
What are common symptoms of COVID-19, and how do they differ from other coronaviruses?
Fever, fatigue, respiratory distress, and gastrointestinal symptoms like diarrhea. SARS-CoV and MERS-CoV have similar respiratory symptoms but vary in systemic effects.
936
How is influenza classified?
Enveloped, negative-sense, segmented RNA viruses. They belong to the Orthomyxoviridae family.
937
What are the key surface proteins of influenza, and why are they significant?
Hemagglutinin (HA) for cell binding and Neuraminidase (NA) for viral release. Their variation determines viral subtypes (e.g., H1N1).
938
What is the difference between antigenic drift and antigenic shift?
Drift refers to small mutations in HA/NA, while shift involves reassortment of genome segments between different strains, leading to pandemics.
939
How does influenza replicate despite being an RNA virus?
Unlike most RNA viruses, influenza replicates in the nucleus, utilizing host transcription machinery.
940
Why is annual vaccination required for influenza?
Due to antigenic drift, circulating strains change frequently, necessitating updates to vaccine formulations.
941
What is a cytokine storm, and how does it affect respiratory virus infections?
It is an excessive immune response characterized by overproduction of cytokines, leading to tissue damage and systemic inflammation.
942
How do respiratory viruses like RSV and SARS-CoV-2 induce immune responses?
By activating pattern recognition receptors (e.g., TLRs, RLRs), triggering interferon production and inflammatory pathways.
943
What role does apoptosis play in viral infections?
It is a host defense mechanism to limit viral spread, but some viruses inhibit apoptosis to sustain replication.
944
What experimental breakthroughs enabled rapid SARS-CoV-2 vaccine development?
Genome sequencing and mRNA vaccine technology, which encoded the spike protein for immune training.
945
Why was the first RSV vaccine trial unsuccessful?
It used an inactivated virus that caused vaccine-enhanced respiratory disease in infants.
946
How does sequencing benefit the study of respiratory viruses?
It tracks mutations, informs vaccine updates, and monitors emerging strains globally.
947
What are the main characteristics of respiratory viruses?
They target the respiratory tract, are highly transmissible, and include RNA and DNA viruses like RSV, rhinovirus, coronaviruses, and influenza.
948
Why are respiratory viruses a global health concern?
They cause significant morbidity and mortality, especially in vulnerable populations like infants, the elderly, and immunocompromised individuals.
949
What are common diagnostic methods for respiratory viruses?
RT-PCR, antigen tests, serology, and viral culture.
950
How does RSV differ from rhinovirus in its structure?
RSV is an enveloped, negative-sense RNA virus, while rhinovirus is non-enveloped and positive-sense.
951
Describe the epidemiology of RSV.
RSV is the leading cause of lower respiratory tract infections in infants worldwide, with seasonal peaks in colder months.
952
How does the RSV F protein contribute to infection?
The F protein facilitates membrane fusion, enabling viral entry and syncytium formation.
953
What challenges are associated with RSV vaccine development?
Vaccine-enhanced disease risk, genetic diversity of RSV strains, and the immaturity of infant immune responses.
954
What recent advancements have been made in RSV treatment?
Novel monoclonal antibodies targeting the F protein and ongoing trials of live-attenuated vaccines.
955
What cellular receptor does rhinovirus use for entry?
The intercellular adhesion molecule-1 (ICAM-1).
956
How does rhinovirus evade the immune system?
By rapidly mutating its capsid proteins, reducing antibody recognition.
957
Why is rhinovirus associated with asthma exacerbations?
It induces pro-inflammatory cytokines like IL-6 and IL-8, worsening airway inflammation.
958
What environmental factors increase rhinovirus transmission?
Cold temperatures and low humidity, which promote viral stability and indoor crowding.
959
What are the zoonotic reservoirs for SARS-CoV, MERS-CoV, and SARS-CoV-2?
SARS-CoV: bats; MERS-CoV: camels; SARS-CoV-2: suspected bats or pangolins.
960
What is the significance of the spike (S) protein in coronaviruses?
It mediates receptor binding and membrane fusion, making it a primary target for vaccines and antivirals.
961
How do coronaviruses maintain genetic diversity?
Through high mutation rates and recombination between strains during co-infections.
962
What are the long-term complications of COVID-19?
Persistent symptoms like fatigue, cognitive dysfunction, and respiratory issues, collectively termed 'long COVID'.
963
What are the differences between SARS-CoV-2 and earlier coronaviruses?
SARS-CoV-2 has higher transmissibility, a longer presymptomatic phase, and widespread global impact.
964
What are the four types of influenza viruses, and which cause human disease?
Types A, B, C, and D. Types A and B cause significant human disease, with type A responsible for pandemics.
965
How does antigenic drift affect influenza virus evolution?
Small mutations in HA and NA proteins allow the virus to evade pre-existing immunity.
966
Why is influenza capable of causing pandemics?
Antigenic shift, through reassortment of genome segments between animal and human strains, generates novel subtypes.
967
How does the influenza vaccine work?
It induces antibodies against HA and NA proteins, reducing infection severity and spread.
968
What role do antivirals like oseltamivir play in influenza treatment?
They inhibit neuraminidase, preventing viral release from infected cells.
969
How does a cytokine storm exacerbate respiratory virus infections?
Excessive immune activation damages host tissues, leading to severe inflammation and multi-organ failure.
970
What immune evasion strategies are used by RSV and influenza?
RSV: blocks interferon responses via NS proteins; Influenza: antigenic variation and inhibiting IFN signaling.
971
How do respiratory viruses disrupt epithelial barriers?
By infecting and lysing epithelial cells, exposing underlying tissues to secondary infections.
972
How has RT-PCR improved respiratory virus detection?
It provides rapid, sensitive, and specific identification of viral RNA.
973
Why is sequencing critical for respiratory virus surveillance?
It identifies mutations, tracks new variants, and informs vaccine updates.
974
What experimental models are used to study respiratory viruses?
Animal models (e.g., mice, ferrets) and organoid cultures of human respiratory epithelium.
975
How was the rapid development of SARS-CoV-2 vaccines achieved?
By leveraging mRNA technology and pre-existing knowledge of coronavirus spike protein structures.
976
What is the role of monoclonal antibodies in RSV prevention?
They neutralize the F protein, preventing viral entry and spread.
977
Why are universal influenza vaccines being developed?
To provide broad protection against diverse strains by targeting conserved regions of HA and NA.
978
What are key challenges in antiviral drug development for respiratory viruses?
High mutation rates, genetic diversity, and the need for early administration to be effective.
979
What receptors do influenza HA proteins bind to during viral attachment?
HA proteins bind to sialic acid receptors, except for HA17 and HA18.
980
What mechanism is used for viral internalisation?
Receptor-mediated endocytosis.
981
How does low endosomal pH facilitate viral internalisation?
It triggers the fusion of the viral envelope with the endosomal membrane.
982
What happens during the uncoating stage of the influenza viral life cycle?
Ribonucleoproteins (RNPs) are released into the host cytosol.
983
Where are RNPs transported after being released into the cytosol during the influenza viral life cycle?
They are transported to the nucleus, where mRNA transcription occurs.
984
Where is viral mRNA transcribed, and where is it translated during the influenza viral life cycle?
Viral mRNA is transcribed in the nucleus and exported for translation by host ribosomes in the cytoplasm.
985
Which proteins return to the nucleus to form RNPs during the influenza viral life cycle?
Viral polymerase subunits and nucleoprotein (NP) proteins.
986
What key viral proteins are trafficked to the cell membrane for assembly during the influenza viral life cycle?
HA, NA, and M2 proteins.
987
Where do RNPs move during viral assembly in the influenza viral life cycle?
From the nucleus to the cytosol and then to the cell membrane.
988
How are virions released from the host cell in the influenza viral life cycle?
Virions bud from the cell membrane.
989
What is the role of neuraminidase (NA) in the release of influenza virions?
NA cleaves the viral particle off the cell membrane, allowing virion release.
990
define viral gastroenteritis
Viral gastroenteritis = inflammation of the lining of the stomach, small and large intestine.
991
what are gastroenteritis viruses?
For gastroenteritis viruses, the gut has to be BOTH the portal of entry and the target tissue.
Replicate in the gut and remain in the gut.
Induce symptoms in the gut, usually diarrhoea and/or vomiting
All gastroenteritis viruses transmit via the oral-faecal route,
… but not all the viruses that transmit via the oral-faecal route are gastroenteritis viruses
992
when do gastroenteritis viruses become serious?
Most people recover without problems, but complications derive from dehydration.
Highly contagious and extremely common.
993
how are gastroenteritis viruses spread?
GE viruses spread via the oral-faecal route.
Usually enter via food and water => food poisoning
Excreted in faeces
Poor hygiene, sanitation, clean water availability
994
why can gastroenteritis cause severe outbreaks?
Highly transmissible => fast replication and highly resistant.
995
how is gastroenteritis treated?
These are not normally serious as long as fresh drinking water is available (developing countries!)
Fluid intake needs to be higher than that lost through vomiting and diarrhoea
996
what is the problem with diagnosing gastroenteritis viruses?
* Most GE viruses remain poorly characterised.
* Most GE viruses do not grow well in laboratory settings.
* Very small amounts (10-100 vp) are sufficient to cause infection, so highly transmissible.
* GE viruses are rarely detectable in food (only exception are the Bivalbia shellfish).
Routine food screening is not feasible and most food contaminations are identified retrospectively from patients’ clinical samples.
997
what is the only way to detect GE viruses?
using bivalbia fish because they are filter feeders; if they filter feed using infected water they retain the viruses too
998
why are shellfish like Bivalbia resevours for GE viruses
because they are filter feeders that retain viruses when filter feeding using infected water
999
what diagnostic methods are available for GE viruses?
1000
can any current methods estimate the amount of GE infections caused by viruses?
no, current methods result in underestimation
1001
do any current GE diagnostic methods inform us of their infectivity
no
1002
what is the best treatment for GE viruses?
HACCP guidelines for handling and safe management of food.
1003
what family are rotaviruses a part of?
Reoviridiae family
1004
what is the structure of rotaviruses?
Non-enveloped, dsRNA viruses protected by 3 protein capsid layers.
1005
are rotaviruses hit and run viruses?
yes
1006
how is the rota virus genome divided?
18kB dsRNA genome divided into 11 segments (codes for 12 proteins: 1 in each segment and 2 in segment 11).
1007
how are rotavirus genomes protected?
they are protected by 3 capsid layers
1008
why is VP4 important for the rotavirus?
VP4 is the one that mediates attachment to the cells So a virus that does not have VP4 is not infectious.
1009
what is a major problem with the VP4 protein?
The problem with VP4 is produced as an inactive protein; for VP4 to be attached to cells The end of the protein has to be chopped so it can interact with the host cell receptor and induce fusion.
1010
how is VP4 activated for Rotaviruses?
The virus produces the protein as an inactive form, and this is how it is originally in the capsid. to be infectious has to be cleaved. A protease has to process this protein. the protease is peptidase. the proteases of the stomach cleave the VP4 protein and activate the virus
1011
what is virus tropism?
Viral tropism is the ability of a virus to infect specific cells, tissues, or species. tropism is determined by the host not the virus.
1012
label how all the VP proteins exist on the 3 capsid layers of a rotavirus
1013
what is unique about when rotaviruses enter a host cell?
rotaviruses keep their internal capsids in the cytosol of the cell. These capsids have holes, as you can see here in this cartoon for VP2. And these holes allow the messenger RNA to be released into the cytosol because those messenger RNA need to be transformed into protein by cellular ribosomes.
1014
why do rotaviruses keep their internal capsids in the cytosol of the cell? (the Avoiding Immune Detection reason)
## Footnote
why do rotaviruses keep the internal capsids in the cytosol of the cell
-Avoiding Immune Detection:
The host's innate immune system can recognize viral dsRNA as a pathogen-associated molecular pattern (PAMP).
By keeping the dsRNA genome enclosed in the inner capsid, rotaviruses shield it from these immune sensors, reducing the likelihood of immune activation.
1015
why do rotaviruses keep their internal capsids in the cytosol of the cell? (the Controlled Transcription reason)
-Controlled Transcription:
The inner capsid of rotavirus contains viral RNA-dependent RNA polymerase (RdRp) complexes. These allow the virus to transcribe messenger RNA (mRNA) from the dsRNA genome while keeping the dsRNA safely enclosed.
This mechanism ensures efficient production of viral mRNA without exposing the genome to immune surveillance.
Maximises transcription and replication efficiency of virus genome.
1016
what is the pathology of rotavirus?
* 1. Virus infects the tips if the microvilli in the intestine
* 1. Massive change in the host ability to reabsorb water. lots of water is lost, as it cannot be reabsorbed
* 1. Most effective treatment is re-hydration (avoid de-hydration
1017
what is the most effective treatment for GE viruses?
* Most effective treatment is re-hydration (avoid de-hydration
1018
what are the reasons for high rotavirus transmission
1019
what are the main targets for rotavirus?
children
1020
what is the seasonality of rotavirus?
all year round; annual RV epidemics occur
1021
what is the treatment for rotavirus?
fluid therapy for children
rehydration for adults
1022
how many people die from rotavirus?
1M deaths pa (mainly in developing countries).
1023
what is the rotavirus economic cost?
Major cause of hospitalisations for acute gastroenteritis in developed countries.
$1B pa in the US alone
~75K hospitalisation pa in under 5yo in the EU
1024
what is the problem with rota virus immunity?
Poor immunity that does not protect against future infections (hit’n’run).
Maternal passive immunity can protect for few months, but children become then susceptible.
1025
rotavirus vaccination
Live attenuated vaccines approved for use in the US and UK: routine vaccination with 3 doses at ages of 2, 4 and 6 months.
1026
what are the single most major cause of non-bacterial GE
noroviruses causes around 45 percent of GE cases in the UK
1027
what is the seasonality of norovirus and why?
winter months, probably because people live and gather more closely
1028
what is the direction of a positive sense ssRNA?
The positive sense would be the one that goes five prime to three prime.
positive sense RNA is the one that can be directly recognised to make protein
1029
why do Norovirus have the VPg protein on the 5' end of their RNA?
the VPg protein is recognised by host ribosomes and initiates translation to form proteins
1030
how does norovirus ensure more strucutural proteins are made than non-structural proteins?
by using subgenomic RNA which priortises the structural RNA
1031
what is a key charachteristic of norovirus symptoms?
projectile vomiting
1032
what is the cost of norovirus?
80 millian a year
1033
do we have any treatments for norovirus?
No effective treatment available; prevention remains best treatment (eg isolation of affected individuals, disinfection…)
1034
what is the best treatment for norovirus?
prevention remains best treatment (eg isolation of affected individuals, disinfection…)
1035
do adenovirus serotypes 40 and 41 grow in cell cultures?
no
1036
What is the approximate size of a rotavirus particle?
70 nm icosahedral viruses.
1037
What are the morphological features of rotavirus?
Rotavirus has 'spokes' radiating from a central 'hub,' resembling a wheel (rota in Latin).
1038
Describe the genome of rotavirus.
Linear, double-stranded RNA (dsRNA) with 18 kb, divided into 11 segments.
1039
What is the approximate size of an adenovirus particle?
80-110 nm.
1040
What are the morphological features of adenovirus?
Adenovirus has an icosahedral structure and may have long fibers extending from the apices.
1041
Describe the genome of adenovirus.
Linear, double-stranded DNA (dsDNA) with 36 kb, containing inverted terminal repeats and a protein primer at each 5’ terminus.
1042
What is the approximate size of a calicivirus particle?
35 nm.
1043
What are the morphological features of calicivirus?
It has 32 cup-like indentations on its surface (calix means 'cup' in Latin).
1044
Describe the genome of calicivirus.
Linear, single-stranded positive-sense RNA (+ssRNA), 7.5 kb. It has a VPg protein at the 5’ terminus and a poly(A) tail at the 3’ terminus.
1045
What is the approximate size of an astrovirus particle?
30 nm.
1046
What are the morphological features of astrovirus?
Arrangements of capsomeres give the appearance of a 5- or 6-pointed star on the surface (astron means 'star' in Greek).
1047
Describe the genome of astrovirus.
Linear, single-stranded positive-sense RNA (+ssRNA), 7 kb, with a poly(A) tail at the 3’ terminus.
1048
What is the infectious dose of norovirus?
Less than 10 viral particles.
1049
What are the consequences of norovirus having a low infectious dose?
* Permits droplet or person-to-person spread.
* Facilitates secondary spread.
* Increases the likelihood of foodborne outbreaks, particularly through food handlers.
1050
How long can asymptomatic shedding of norovirus occur?
Up to 2 weeks.
1051
What are the consequences of prolonged asymptomatic shedding?
* Increases the risk of secondary spread.
* Poses challenges for food safety, as asymptomatic food handlers may unknowingly spread the virus.
1052
How stable is norovirus in the environment?
It can survive:
* Chlorine concentrations up to 10 ppm.
* Freezing.
* Heating to 60°C.
1053
What are the consequences of norovirus’s environmental stability?
* Difficult to eliminate from contaminated water sources.
* Virus can remain viable in ice and steamed oysters, contributing to foodborne outbreaks.
1054
What is the level of strain diversity in norovirus?
Norovirus exhibits multiple genetic and antigenic types.
1055
What are the consequences of norovirus’s substantial strain diversity?
* Requires advanced diagnostics to identify specific strains.
* Repeat infections are common due to varying antigenic types.
* Can lead to underestimation of prevalence in epidemiological studies.
1056
Can infection with norovirus lead to long-term immunity?
No, reinfection is possible.
1057
What are the consequences of norovirus’s lack of lasting immunity?
* Childhood infection does not guarantee protection in adulthood.
* Developing a vaccine with lifelong protection is challenging.
1058
To which family do noroviruses (NoV) belong?
Noroviruses belong to the Caliciviridae family.
1059
What are the four genera within the Caliciviridae family?
Vesivirus, Lagovirus, Sapovirus, and Norovirus.
1060
Which two Caliciviridae genera infect humans?
Sapovirus and Norovirus.
1061
What condition do human-infecting noroviruses cause?
Winter vomiting disease.
1062
What type of genome do noroviruses have?
Non-enveloped, 7.5 kB, single-stranded positive-sense RNA (+ssRNA).
1063
To which Baltimore classification group do noroviruses belong?
Group IV.
1064
Why are noroviruses called 'hit-and-run' viruses?
They complete their replication cycle in approximately 12 hours, allowing rapid infection and transmission.
1065
How many open reading frames (ORFs) does the norovirus genome have?
Three ORFs.
1066
What proteins are encoded by ORF1?
Non-structural proteins involved in replication, such as RNA-dependent RNA polymerase (RdRp), VPg, and protease.
1067
What proteins are encoded by ORF2 and ORF3?
ORF2 encodes VP1 (major capsid protein), and ORF3 encodes VP2 (minor capsid protein).
1068
What is the priming strategy used by noroviruses for genome replication?
The viral RNA genome uses a 5' VPg (13–15 kDa) protein to prime RNA synthesis.
1069
What is the function of VP1 in norovirus?
VP1 is the major capsid protein that self-assembles to form the viral capsid.
1070
Why is VP1 important for norovirus structure?
It determines the size, shape, and antigenic properties of the viral capsid.
1071
How does VP1 contribute to immune evasion?
Variations in VP1 allow the virus to evade host immune responses by altering antigenic sites.
1072
What is the role of VP2 in norovirus?
VP2 is the minor capsid protein that stabilizes the capsid structure and interacts with VP1 during assembly.
1073
How does VP2 enhance viral replication?
VP2 assists in packaging the viral genome and enhances the stability of the virus particle.
1074
How do VP1 and VP2 interact in norovirus assembly?
VP1 forms the structural framework of the capsid, while VP2 interacts with VP1 and the viral RNA to complete virion assembly.
1075
What is the significance of the self-assembly property of VP1?
VP1 can spontaneously form virus-like particles (VLPs), which are used in vaccine research.
1076
When do symptoms of norovirus infection typically appear?
Symptoms appear 12–48 hours post-infection.
1077
How long do norovirus symptoms usually last?
Symptoms last between 2–3 days.
1078
What are the primary symptoms of norovirus infection?
Symptoms include:
* Nausea
* Vomiting
* Diarrhea
* Abdominal cramps and pain
1079
What is the primary route of transmission for norovirus?
Oral-fecal route.
1080
What are the specific ways norovirus is transmitted through the oral-fecal route?
* Consumption of contaminated food.
* Person-to-person or fomite-to-person contact.
* Airborne droplets from vomiting.
1081
How can vomiting contribute to the transmission of norovirus?
Vomiting releases airborne droplets containing the virus, which can infect individuals nearby.
1082
Which groups are primarily affected by astroviruses?
Young children, the elderly, and institutionalized patients.
1083
What is known about astrovirus immunity?
Determinants of immunity are not well understood, but generated immunity is generally long-lasting, though it wanes with age.
1084
What percentage of children aged 5–10 years have antibodies against astroviruses (AstV)?
Over 80% of children in this age group have antibodies.
1085
What diagnostic methods are used to detect astroviruses?
* Electron Microscopy (EM)
* Enzyme-Linked Immunosorbent Assay (ELISA)
* Nucleic Acid Amplification Tests (NAATs)
1086
Why might sequence variability be a challenge in diagnosing astroviruses?
Sequence variability can complicate nucleic acid-based diagnostics like NAATs.
1087
What is the initial step for rotavirus to attach to host cells?
Rotavirus uses its VP4 spike protein to bind to sialic acid residues on the surface of host intestinal epithelial cells.
1088
How does rotavirus gain access to the host cell after attachment?
Proteolytic cleavage of VP4 by enzymes (e.g., trypsin) in the gut enhances viral binding and penetration.
1089
What is the role of VP4 in rotavirus entry?
VP4 facilitates both attachment to the host cell and penetration of the plasma membrane.
1090
After entering the host cell, where does the rotavirus uncoat?
Rotavirus uncoats in the cytoplasm, releasing its double-layered particle (DLP), which protects the dsRNA genome while enabling transcription.
1091
What receptor does norovirus use to attach to host cells?
Norovirus binds to histoblood group antigens (HBGAs) on the surface of intestinal epithelial cells.
1092
How do histoblood group antigens (HBGAs) facilitate norovirus entry?
HBGAs serve as attachment factors, allowing the virus to interact with the host cell and initiate internalization.
1093
What mechanism does norovirus use to enter the host cell?
Norovirus enters the host cell through receptor-mediated endocytosis.
1094
Where does norovirus release its genome after entering the host cell?
Norovirus releases its single-stranded positive-sense RNA genome into the cytoplasm for translation and replication.
1095
What is a key difference between rotavirus and norovirus entry?
Rotavirus relies on proteolytic activation of VP4 for penetration, while norovirus uses receptor-mediated endocytosis facilitated by HBGAs.
1096
What is a common feature in both rotavirus and norovirus entry mechanisms?
Both viruses require specific host cell surface molecules (sialic acid for rotavirus, HBGAs for norovirus) to initiate attachment and entry.
1097
What is the genome structure of adenoviruses?
Adenoviruses have a double-stranded DNA (dsDNA) genome, approximately 36–38 kB in size.
1098
What is the Baltimore classification group for adenoviruses?
Adenoviruses belong to Group I (dsDNA viruses).
1099
What is the morphology of adenoviruses?
They are non-enveloped, icosahedral viruses with a very distinctive structure, making them easily identifiable by electron microscopy (EM).
1100
How many serotypes of adenoviruses have been identified?
There are more than 50 serotypes.
1101
Which adenovirus serotypes are specialized for intestinal infection?
Serotypes 40 and 41 are specialized for infecting intestinal cells and are referred to as enteric adenoviruses.
1102
What other infections are adenoviruses commonly associated with?
Many serotypes are strongly linked to respiratory and eye infections.
1103
Which population is most commonly affected by adenoviruses?
Adenoviruses primarily affect children under 2 years old.
1104
What is the seroprevalence of adenoviruses in children?
Up to 50% seroprevalence is observed, which decreases as they age.
1105
How are adenoviruses transmitted?
They are transmitted through the oral-fecal route and are found robustly in water.
1106
What is the difference in adenovirus transmission compared to other gastroenteritis viruses?
Adenoviruses are primarily waterborne, not foodborne.
1107
Why are adenoviruses considered indicators of fecal contamination?
Their presence in water systems reflects contamination with fecal matter.
1108
What is the infectious dose (ID) of adenovirus?
The ID for adenovirus is not known.
1109
What is the incubation period of adenovirus?
5–7 days.
1110
What are the symptoms caused by adenovirus?
Watery diarrhea.
1111
How long do adenovirus symptoms typically last?
5–7 days.
1112
What is the infectious dose (ID) of astrovirus?
Less than 1000 viral particles.
1113
What is the incubation period of astrovirus?
3–4 days.
1114
What symptoms are caused by astrovirus?
Diarrhea and vomiting, with diarrhea being the predominant symptom.
1115
How long do astrovirus symptoms typically last?
4–7 days.
1116
What is the infectious dose (ID) of rotavirus?
10–100 viral particles.
1117
What is the incubation period of rotavirus?
2–4 days.
1118
What symptoms are caused by rotavirus?
Diarrhea and vomiting.
1119
How long do rotavirus symptoms typically last?
4–7 days.
1120
What is the infectious dose (ID) of norovirus?
Less than 10 viral particles.
1121
What is the incubation period of norovirus?
0.5–1 day.
1122
What symptoms are caused by norovirus?
Diarrhea and vomiting, with vomiting being more predominant.
1123
How long do norovirus symptoms typically last?
2–4 days.
1124
will infected hosts always show symptoms?
no, some hosts can be infected and spread a virus without showing any symptoms
1125
why does Virus exchange between donor
and recipients take place by chance?
Virus exchange between donor
and recipients
Takes place by chance because
Recipient cells need to have the
right receptors
1126
what hosts are most susceptible to viral spillover?
Recipient cells need to have the right receptors
Closest host genetically have more chance to
get similar cell receptors
1127
when does a spillover event occur?
when the person is infected and brings the virus back to the rest of the population
1128
when is spillover transmission complete?
Infected person transmit viruses
to other people.
The jump from animal to human
is complete
1129
what is the one health initiative being used by the WHO
The One Health Initiative is a global, interdisciplinary approach adopted by organizations like the World Health Organization (WHO) to address health challenges at the intersection of human, animal, and environmental health. This initiative emphasizes the interconnectedness of these domains and the need for collaborative, multi-sectoral efforts to prevent and control health threats.
1130
what can be a problem caused by variations in surface proteins?
this can affect the efficacy of vaccines
1131
is Nipah a respiratory virus?
yes
1132
what is unique about the Hyalomma tick species?
they chase their victims and are very aggressive
1133
What is spillover?
Spillover is the transmission of a pathogen from an animal to a human.
1134
Does spillover always result in human-to-human transmission?
No, in most cases, spillover does not cause the human to get sick or allow the pathogen to be transmitted to other humans.
1135
What does shedding mean in virology?
Shedding refers to the release of a virus from an infected person into the environment.
1136
How does shedding contribute to the spread of a pathogen?
Pathogens shed into the environment can often remain infectious and facilitate transmission from one person to another.
1137
What is zoonosis?
Zoonosis is when a pathogen or virus spreads from animals to humans.
1138
Are all pathogens zoonoses?
No, not all pathogens are zoonoses.
1139
What is a reservoir in terms of pathogen biology?
A reservoir is the place where a pathogen normally lives and reproduces.
1140
Give an example of a pathogen reservoir.
Bats, deer, or other wildlife can serve as reservoirs for various pathogens.
1141
What is a vector in pathogen transmission?
A vector is an organism that transmits a pathogen to other organisms.
1142
Can you provide an example of a vector?
Mosquitoes are vectors for diseases like malaria and dengue.
1143
What is a host in the context of infectious diseases?
A host is a human or animal that acts as a carrier for a pathogen.
1144
How is a host different from a reservoir?
While a host can carry a pathogen, a reservoir is the natural habitat where the pathogen lives and reproduces.
1145
What environmental data is important for understanding spillover?
Reservoir host distribution and reservoir host density.
1146
How do bat roost distribution and behavior influence pathogen transmission?
They affect the prevalence of pathogens and the likelihood of pathogen release into the environment.
1147
What role does pathogen prevalence play in spillover?
Higher pathogen prevalence in bat populations increases the chances of excretion and spillover events.
1148
How does infection intensity in bats impact pathogen release?
Greater infection intensity increases the amount of pathogen excreted, raising exposure risk.
1149
What happens during the release of a pathogen from the reservoir host?
The pathogen is excreted into the environment, potentially contaminating surfaces, food, or water.
1150
How do pathogens survive outside reservoir hosts?
They adapt to survive and spread in the external environment, waiting for a susceptible recipient host.
1151
What determines whether humans are exposed to the pathogen?
Pathogen survival in the environment and human behaviors that increase contact, such as handling animals or contaminated materials.
1152
What are structural barriers in recipient hosts?
These include physical and molecular defenses that prevent pathogens from binding, replicating, or spreading in host cells.
1153
What processes occur in the recipient host that allow spillover to succeed?
Viral binding, fusion, replication, assembly, and dissemination occur in the recipient host cells.
1154
What host factors influence the success of spillover?
The innate immune response and molecular compatibility between the virus and host cells play a crucial role.
1155
What conditions lead to complete replication and dissemination cycles in recipient hosts?
Overcoming innate immune responses and completing viral replication allow the pathogen to establish and spread.
1156
What is the final step in the spillover process?
Successful transmission routes and established human infectivity result in spillover.
1157
How does close contact with animals increase the risk of spillover?
Frequent interaction with pets, livestock, or wild animals can increase the chances of zoonotic pathogen transmission.
1158
Give an example of close contact with animals that may lead to spillover.
Handling domestic pets or working on farms where animals are present.
1159
Why do wet markets pose a risk for spillover?
Wet markets bring live animals, raw meat, and humans into close proximity, creating an ideal environment for pathogen transmission.
1160
What conditions in wet markets amplify the risk of spillover?
Poor sanitation, overcrowding, and the mixing of multiple animal species in close quarters.
1161
How does animal husbandry contribute to spillover risk?
Intensive farming practices often house large numbers of animals in confined spaces, facilitating the spread of pathogens.
1162
What are examples of husbandry-related spillover risks?
Livestock outbreaks like swine flu and avian influenza in crowded farming setups.
1163
How does the destruction of natural environments increase spillover risk?
Habitat destruction forces wildlife into closer contact with human populations, increasing opportunities for pathogen transmission.
1164
What human activities contribute to habitat destruction and spillover risk?
Deforestation, urbanization, and agricultural expansion.
1165
How does wildlife hunting increase the risk of spillover?
Hunters are exposed to blood, tissues, and pathogens carried by wild animals during handling and consumption.
1166
Give an example of zoonotic spillover linked to wildlife hunting.
The transmission of Ebola virus through the handling and consumption of bushmeat.
1167
Why does the illegal wildlife trade increase the risk of spillover?
Animals are kept in cramped, stressed conditions, often alongside other species, allowing pathogens to jump between species and to humans.
1168
What is a key example of a pathogen linked to the wildlife trade?
SARS-CoV, believed to have emerged from animals sold in wildlife markets.
1169
What does R0 represent in infectious diseases?
R0, or the basic reproduction number, represents the average number of people that one infected person will transmit the virus to in a completely susceptible population.
1170
What are other names for R0?
R0 is also called R naught or R zero.
1171
Is R0 the same for all viruses?
No, R0 is different for all viruses, even if they have the same transmission mode.
1172
What factors influence the R0 value of a virus?
Factors include the virus's transmissibility, population density, host susceptibility, and environmental conditions.
1173
What is the R0 range for COVID-19?
2–2.5, meaning one infected person infects 2–2.5 others on average.
1174
What is the R0 range for H1N1 influenza?
1.2–1.6, indicating lower transmissibility compared to COVID-19.
1175
What is the R0 range for Ebola virus?
1.6–2, slightly higher than H1N1 but lower than COVID-19.
1176
Why is R0 important in public health prioritization?
It helps assess the transmissibility of a virus and prioritize control measures to prevent outbreaks.
1177
What does an R0 value greater than 1 indicate?
The infection can spread in the population, leading to an outbreak or epidemic.
1178
What does an R0 value less than 1 signify?
The infection is likely to die out over time without causing widespread transmission.
1179
How does R0 influence the prioritization of a virus?
The higher the R0 (basic reproduction number), the more transmissible the virus is, increasing its priority for control measures.
1180
Why is the case fatality rate important in prioritizing a virus?
Viruses with high case fatality rates, such as Hendra virus (60%), pose a significant threat to human health and require urgent attention.
1181
How does spillover potential affect prioritization?
Viruses with a high likelihood of jumping from animals to humans (spillover potential) are prioritized because of the risk of novel outbreaks.
1182
What is evolutionary potential, and why is it significant?
It refers to the virus’s ability to mutate and adapt, potentially increasing its transmissibility, virulence, or resistance to countermeasures.
1183
Why are available countermeasures like vaccines and antivirals critical in prioritizing a virus?
Viruses without effective vaccines or antivirals pose a greater challenge to public health and are given higher priority.
1184
How does detection difficulty impact prioritization?
Viruses that are hard to detect early, either due to asymptomatic transmission or inadequate diagnostic tools, are more likely to cause large outbreaks.
1185
How does the public health infrastructure of an affected area influence virus prioritization?
Areas with poor healthcare and research infrastructure are more vulnerable to outbreaks, making these viruses a higher priority for control.
1186
Why is the potential scope of an outbreak important in prioritization?
Viruses with the potential to spread across large geographic areas or infect a significant proportion of the population demand more resources and attention.
1187
How do societal impacts influence the prioritization of a virus?
Viruses that could disrupt economies, cause panic, or overwhelm healthcare systems are prioritized for containment.
1188
Why is there a strong case for integrated controls in rabies eradication?
Rabies requires a multi-sectoral approach involving human, animal, and environmental health to effectively manage and eliminate the disease.
1189
What is a key public health intervention for rabies management?
Management of rabies in animals is critical for preventing transmission to humans.
1190
What tools are available for rabies eradication?
Vaccines for both animals and humans are available but must be properly applied.
1191
What role do policymakers play in rabies eradication?
Policymakers need to acknowledge the problem and prioritize resources and strategies for eradication.
1192
What is the role of diagnosis and surveillance in rabies eradication?
Continuous monitoring of rabies in both wildlife and humans helps track the spread and implement timely interventions.
1193
How do vaccination campaigns contribute to rabies eradication?
Vaccination campaigns involve veterinarians and medical doctors working together to vaccinate animals and humans at risk.
1194
Why is studying rabies virology important for eradication?
Understanding the virology of rabies helps to predict epidemics and plan preventive measures.
1195
What is essential for eradicating rabies epidemics?
Collaboration among human health, veterinary, and environmental sectors is critical to achieving rabies eradication.
1196
How is Ebolavirus classified?
Ebolavirus is an enveloped, negative-sense, single-stranded RNA (ssRNA) virus, classified under the order Mononegavirales and family Filoviridae.
1197
What is the family and genus of Ebolavirus?
Family: Filoviridae
Genus: Ebolavirus
1198
How many main strains of Ebolavirus are identified?
There are 6 main strains.
1199
How are Ebolavirus strains named?
They are named after the place of discovery, such as Tai Forest Ebolavirus and Zaire Ebolavirus.
1200
What is the sequence variation observed between Ebolavirus strains?
Strains show 30–40% variations in their sequences.
1201
What type of genome does Ebolavirus have?
A negative-sense RNA genome consisting of one segment.
1202
How many proteins are encoded by the Ebolavirus genome?
The genome encodes 7 proteins.
1203
What types of proteins are encoded by the Ebolavirus genome?
4 non-structural proteins and 3 structural proteins.
1204
What structural protein is responsible for forming the viral capsid?
The Nucleoprotein (NP).
1205
What is the role of VP24 and VP40 in Ebolavirus structure?
VP40: Forms the viral matrix and regulates assembly and budding.
VP24: Inhibits host immune responses by interfering with interferon signaling.
1206
What glycoprotein allows Ebolavirus to attach to and enter host cells?
GP1 is responsible for attachment, and GP2 facilitates membrane fusion.
1207
What role does VP35 play in the virus lifecycle?
VP35 acts as a polymerase cofactor and also antagonizes host immune responses.
1208
How does Ebolavirus produce multiple proteins from its genome?
The genome undergoes mRNA editing, resulting in the production of various proteins like GP1, GP2, and sGP.
1209
What enzyme cleaves the Ebolavirus glycoprotein?
Host protease furin cleaves the glycoprotein.
1210
What is the function of the Delta peptide in Ebolavirus?
It modulates host immune responses and affects viral infectivity.
1211
How does Ebolavirus attach to host cells?
Ebolavirus attaches to host cells using receptors like HAVCR1 (TIM1), facilitated by its glycoprotein (GP).
1212
What process allows Ebolavirus to enter the host cell?
Macropinocytosis, a non-specific endocytic process.
1213
What process allows Ebolavirus to enter the host cell?
Macropinocytosis, a non-specific endocytic process, is used for entry.
1214
What role do cathepsins play in Ebolavirus entry?
Cathepsin B and cathepsin L process the viral glycoprotein in the endosome, triggering membrane fusion and releasing the viral genome into the cytoplasm.
1215
What happens after the viral genome is released into the cytoplasm in the ebolavirus cycle?
The viral negative-sense RNA genome undergoes transcription by the viral RNA-dependent RNA polymerase (L) to produce mRNAs for protein synthesis.
1216
What is the significance of mRNA editing in Ebolavirus replication?
mRNA editing allows the production of multiple viral proteins, including structural and non-structural proteins.
1217
Which viral protein facilitates transcription of the negative-sense RNA genome in the ebolavirus cycle?
The polymerase cofactor VP30 facilitates transcription.
1218
How does Ebolavirus evade host immune detection during replication?
The viral protein VP35 suppresses host antiviral RNA sensors, preventing immune activation.
1219
Where does genome replication occur in the host cell during the ebola virus cycle?
Replication occurs in cytoplasmic viral factories, where new copies of the negative-sense RNA genome are synthesized.
1220
How does VP24 contribute to immune evasion in the ebola virus cycle?
VP24 inhibits interferon signaling by disrupting host nuclear transport mechanisms.
1221
What structural proteins are involved in viral assembly in the ebola virus cycle?
Structural proteins like VP40 (matrix protein) and GP (glycoprotein) assemble at the host cell membrane.
1222
How does Ebolavirus exit the host cell?
It buds from the host cell using the ESCRT (Endosomal Sorting Complex Required for Transport) machinery.
1223
What transport mechanism helps viral components reach the membrane for budding in the ebola virus cycle?
Actin-dependent outward transport directs viral components to the assembly site.
1224
What is the role of sGP (secreted glycoprotein) in Ebolavirus infection?
sGP modulates the host immune response, reducing the effectiveness of immune cells targeting the virus.
1225
How does VP35 aid in immune evasion in the ebola virus cycle?
VP35 inhibits antiviral RNA sensors, helping the virus evade immune detection.
1226
What host mechanism is disrupted by VP24 to block immune responses in the ebola virus cycle?
VP24 blocks interferon signaling, hindering the antiviral response.
1227
What are the key steps of the Ebolavirus lifecycle?
* Attachment via GP to receptors like HAVCR1 (TIM1).
* Entry through macropinocytosis.
* Fusion and genome release in the cytoplasm.
* Replication of the genome and protein synthesis.
* Assembly of new virions.
* Budding from the host cell using ESCRT machinery.
1228
What is the incubation period for Ebola virus disease?
The incubation period ranges from 3 days to 3 weeks.
1229
What are the non-specific symptoms of Ebola virus disease?
* Fever
* Sore throat
* Muscle pain
* Headaches
1230
What symptoms are seen in severe cases of Ebola virus disease?
* Vomiting
* Diarrhea
* Rash
* Decreased liver and kidney function
1231
How does Ebola virus disease often lead to death?
Death is often caused by shock from fluid loss, occurring 6 to 16 days after the first symptoms appear.
1232
What percentage of people infected with Ebolavirus die from the disease?
Ebolavirus kills 50% of those infected.
1233
How is Ebola virus transmitted?
The virus spreads through direct contact with:
* Body fluids of an infected human or animal.
* Fomites (contaminated surfaces or objects).
1234
What does 'enzootic' mean?
'Enzootic' means native to the place. It refers to infections that are maintained in a population without external inputs.
1235
How does the enzootic cycle relate to Ebolavirus?
The enzootic cycle involves bats as reservoir hosts, where the virus is maintained and transmitted among bat populations.
1236
What human term is analogous to an enzootic disease?
Enzootic diseases are similar to endemic diseases in human populations.
1237
Which Ebolavirus strains are implicated in the enzootic cycle?
* Ebola virus (formerly Zaire virus)
* Sudan virus
* Tai Forest virus
* Bundibugyo virus
* Reston virus (non-human)
1238
What does 'epizootic' mean?
'Epizootic' comes from the Greek words 'epi' (upon) and 'zoon' (animal). It refers to outbreaks in animals in a specific place.
1239
How does the epizootic cycle relate to Ebolavirus?
Ebolaviruses cause high mortality outbreaks among non-human animals, such as duikers and gorillas, which can precede human epidemics.
1240
What human term is analogous to an epizootic disease?
Epizootic diseases are similar to epidemic diseases in human populations.
1241
How does an epizootic event lead to human infection?
Humans become infected through contact with infected animals, such as bats or other wildlife, initiating human-to-human transmission.
1242
What is the primary feature of human epidemics of Ebolavirus?
Human-to-human transmission is the predominant feature of Ebolavirus epidemics.
1243
How does Ebolavirus spread between humans?
Transmission occurs through contact with bodily fluids of infected individuals.
1244
What role do bats play in the ecology of Ebolavirus?
Bats are considered reservoir hosts, maintaining the virus within their populations without external inputs.
1245
What is the key difference between enzootic and epizootic cycles?
* Enzootic cycle: Maintains the virus within a population (native and stable).
* Epizootic cycle: Causes outbreaks in animal populations and potentially humans.
1246
What are the key methods for diagnosing Ebolavirus?
Diagnosis involves:
* Isolating the virus.
* Detecting its RNA using PCR (Polymerase Chain Reaction).
* Detecting viral proteins using ELISA (Enzyme-Linked Immunosorbent Assay).
* Detecting antibodies against the virus in a person's blood.
1247
What does PCR detect in Ebolavirus diagnosis?
PCR detects the RNA of the Ebolavirus.
1248
What does ELISA detect in Ebolavirus diagnosis?
ELISA detects viral proteins or antibodies produced against the virus.
1249
How is the Ebolavirus vaccine developed using the GP protein?
The gene encoding the GP protein is extracted from the Ebolavirus and inserted into the genome of a vesicular stomatitis virus (VSV).
1250
What is the role of vesicular stomatitis virus (VSV) in vaccine production?
VSV acts as a vector to deliver the Ebolavirus GP gene, allowing the production of Ebolavirus-like particles that trigger an immune response.
1251
Why is the Ebolavirus GP protein important for vaccine development?
The GP protein is essential for attachment and entry into host cells, making it a key target for eliciting protective immunity.
1252
What is the name of the Ebolavirus vaccine produced using this method?
The vaccine is called VSV-Ebola vaccine (VSV-ZEBOV).
1253
How does the VSV-Ebola vaccine work in humans?
The vaccine stimulates the production of antibodies against the Ebolavirus GP protein, which protect against future infections.
1254
What immune component is measured to confirm vaccine efficacy?
Antibodies against the GP protein are measured to assess vaccine efficacy.
1255
What are the two main strategies used in Ebolavirus control?
* Accurate diagnosis using PCR, ELISA, and antibody detection.
* Vaccination using the VSV-Ebola vaccine targeting the GP protein.
1256
why can it be hard to tell if a tick is biting you?
thye have immune factors which can suppress your immunse system and prevent a reaction to their bites
1257
What is the natural host of the Nipah virus?
The Pteropodidae family of fruit bats.
1258
Where and when did the Nipah virus first appear?
It first appeared in Malaysia in 1998.
1259
What led to the initial identification of Nipah virus?
The outbreak was associated with contact with infected pigs and fruit bats.
1260
Which countries have reported Nipah virus infections?
Malaysia, Singapore, Bangladesh, India.
1261
Which regions have been most affected by Nipah virus outbreaks?
Outbreaks have been concentrated in South and Southeast Asia.
1262
How many people have died from Nipah virus infections worldwide since 1998?
More than 260 people.
1263
Why is Nipah virus considered a public health concern?
It has a high case fatality rate and has caused recurrent outbreaks in densely populated regions.
1264
What is the role of fruit bats in Nipah virus transmission?
Fruit bats are the reservoir host, and the virus can be transmitted through contact with bat saliva, urine, or partially eaten fruits.
1265
How is the Nipah virus classified?
Nipah virus is an enveloped, negative-sense single-stranded RNA (ssRNA) virus classified under:
* Order: Mononegavirales
* Family: Paramyxoviridae
* Genus: Henipavirus
1266
What are the key viral strains included in the Henipavirus genus?
Nipah virus (Malaysia), Hendra virus (Australia).
1267
What diseases are associated with Henipavirus strains?
Nipah virus causes severe encephalitis and respiratory illnesses in humans, while Hendra virus is associated with respiratory and neurological diseases.
1268
What type of genome does the Nipah virus have?
Nipah virus has a negative-sense RNA genome.
1269
How many proteins are encoded by the Nipah virus genome?
One segment (genome) encodes 9 proteins.
1270
What is the distribution of the proteins encoded by the Nipah virus genome?
The genome encodes:
* 5 non-structural proteins.
* 4 structural proteins.
1271
What is the function of the glycoprotein (G) in Nipah virus?
The glycoprotein (G) facilitates attachment to host cell receptors.
1272
What is the role of the fusion protein (F)?
The fusion protein (F) allows membrane fusion between the virus and host cell, enabling entry.
1273
What does the matrix protein (M) do?
The matrix protein (M) provides structural integrity and is involved in viral assembly and budding.
1274
What is the role of the nucleoprotein (N) in the Nipah virus?
The nucleoprotein (N) encapsulates the viral RNA genome, protecting it and facilitating replication.
1275
What is the function of the polymerase (L) protein?
The polymerase (L) catalyzes RNA synthesis, including replication and transcription.
1276
What is the incubation period for Nipah virus disease?
The incubation period is 4 to 14 days.
1277
How is Nipah virus transmitted?
Nipah virus is transmitted through:
* Contact with infected bats or pigs.
* Consumption of contaminated food.
* Human-to-human contact.
1278
What are the non-specific symptoms of Nipah virus disease?
Flu-like symptoms, fever, sometimes diarrhea and vomiting.
1279
What are the severe symptoms of Nipah virus disease?
Pneumonia, encephalitis, meningitis, can cause bleeding in the brain.
1280
Can Nipah virus disease affect animals?
Yes, it can also be observed in pigs.
1281
What percentage of infected individuals progress to critical illness with Nipah?
60% of infected people progress to critical illness.
1282
What is the case fatality rate of Nipah virus?
Nipah virus kills 40% to 75% of infected patients.
1283
Is there a specific treatment or vaccine available for Nipah virus?
No, there is currently no treatment or vaccine available for Nipah virus.
1284
What is the primary treatment for Nipah virus infection?
The primary treatment is supportive care for infected individuals.
1285
Why is the diagnosis of Nipah virus often delayed?
The initial signs and symptoms of Nipah virus infection are nonspecific, and the diagnosis is often not suspected at the time of presentation.
1286
What diagnostic test is used to detect viral RNA in Nipah virus cases?
Real-time polymerase chain reaction (RT-PCR) is used to detect viral RNA from bodily fluids.
1287
What method is used for antibody detection in Nipah virus diagnosis?
Antibodies are detected via enzyme-linked immunosorbent assay (ELISA).
1288
What bodily fluids are typically tested for Nipah virus RNA?
Bodily fluids such as blood, cerebrospinal fluid, or respiratory secretions are tested using RT-PCR.
1289
What are the primary hosts for Crimea-Congo Hemorrhagic Fever (CCHF)?
Goats and cattle are the primary hosts.
1290
Who are the dead-end hosts for CCHF?
Humans are considered dead-end hosts.
1291
What is the vector responsible for transmitting CCHF?
Hyalomma Ticks are the vectors responsible for transmitting the virus.
1292
How many people are at risk of infection with CCHF globally?
Approximately three billion people are at risk globally.
1293
How many infections and deaths occur due to CCHF each year?
There are 10,000 to 15,000 infections and around 500 deaths annually.
1294
Which regions were recent hotspots for CCHF in 2023?
Hotspots include Turkey, Albania, and Georgia.
1295
In which regions is CCHF endemic according to the distribution map?
CCHF is endemic across parts of Africa, the Middle East, Eastern Europe, and Asia.
1296
What is a significant cause of the spread of this virus?
Global warming is allowing these ticks to spread across greater environments because the ticks like hot, dry climates.
1297
What type of genome does the CCHF virus have?
The CCHF virus has an enveloped, negative-sense, single-stranded RNA (ssRNA) genome.
1298
What is the taxonomic classification of the CCHF virus?
Order: Bunyavirales, Family: Nairoviridae, Genus: Orthonairovirus.
1299
How is the genetic diversity of CCHF virus strains linked?
The genetic diversity is linked to geographic localization.
1300
In which protein do CCHF viral strains show the greatest amino acid diversity?
The greatest diversity is observed in the glycoprotein precursor (GPC).
1301
How many segments does the CCHF virus genome have?
The genome is composed of 3 segments.
1302
How many proteins are encoded by the CCHF virus genome?
The genome encodes 4 proteins.
1303
What are the types of proteins encoded by the CCHF genome?
1 non-structural protein, 3 structural proteins.
1304
What role does the L (large) segment of the CCHF genome play?
It encodes the RNA-dependent RNA polymerase (L) for viral replication.
1305
What does the M (medium) segment encode in the CCHF virus?
The M segment encodes the glycoprotein precursor (GPC), which is cleaved into mature glycoproteins.
1306
What does the S (small) segment encode in the CCHF virus?
The S segment encodes the nucleocapsid protein (NP), which encapsidates the viral RNA.
1307
What structural features are indicated in the CCHF virus illustration?
The illustration includes:
* Glycoprotein precursor (GPC).
* RNA-dependent RNA polymerase (L).
* Nucleocapsid protein (NP).
* Negative-sense RNA genome.
1308
What is the incubation period for CCHF?
The incubation period is approximately 7 days.
1309
What are the non-specific symptoms of CCHF?
Fever, fatigue, myalgia (muscle pain), diarrhea, vomiting.
1310
What are the severe symptoms of CCHF?
Thrombocytopenia (low platelet count causing bleeding), hemorrhagic manifestations, such as ecchymosis (bruising).
1311
How does CCHF present in humans?
CCHF causes mild to severe hemorrhagic fever, occurring exclusively in humans who are dead-end hosts.
1312
What factors contribute to the symptoms of CCHF?
High viremia (high viral load in the blood), low antibody counts, high pro-inflammatory cytokines, multi-organ infection causing organ failure.
1313
What is the case fatality rate of CCHF outbreaks?
The case fatality rate can reach up to 40%.
1314
What is the role of Ixodid (hard) ticks in the CCHF enzootic cycle?
Ixodid ticks act as both reservoirs and vectors for the CCHF virus.
1315
How is the CCHF virus maintained in nature through ticks?
The virus is maintained through transovarial (from mother to eggs) and transstadial (through life stages) transmission in ticks.
1316
What are the life stages of ticks involved in the enzootic cycle?
Eggs, Larva, Nymph, Adult.
1317
During which seasons do most CCHF cases occur?
Most cases occur during the warmer parts of the year, primarily in spring and summer, with no cases typically observed during the winter.
1318
What types of animals serve as hosts for ticks and amplify the CCHF virus?
Wild and domestic animals such as cattle, goats, sheep, birds, and hares serve as hosts and amplifiers for the virus.
1319
How do humans become infected during the epizootic-epidemic cycle?
Humans become infected through:
* Tick bites
* Direct contact with infected animal blood or tissues.
1320
What activities increase the risk of CCHF transmission to humans?
Slaughtering infected animals, veterinary procedures, hospital settings where proper protective equipment and disinfection procedures are lacking.
1321
Why are hospital settings a high-risk area for CCHF transmission?
Improper use of protective equipment and insufficient disinfection protocols can facilitate the spread of the virus.
1322
What preventive measures can reduce the risk of CCHF transmission?
Using protective equipment during handling of animals or animal products, proper tick control on animals and in tick-infested areas, disinfection protocols in veterinary and healthcare settings.
1323
Why is the diagnosis of CCHFV difficult?
Diagnosis is difficult because there are low to no antibodies detected in patients.
1324
What are the main methods of detecting CCHFV?
RT-PCR to detect viral RNA, microscopy to detect the virus in blood samples.
1325
Why is patient testing for CCHFV considered hazardous?
Testing is hazardous because of the high risk associated with handling the virus. It must be done in a high containment laboratory.
1326
What biosafety level is required for handling CCHFV?
Testing requires a BSL-4 (biosafety level 4) facility.
1327
Is there a vaccine available for humans or animals for CCHFV?
No, there is no vaccine available for humans or animals.
1328
Is there a specific treatment available for CCHFV?
No, there is no specific treatment for CCHFV.
1329
What antiviral drug can be used for CCHFV treatment?
Ribavirin, an antiviral drug that inhibits viral RNA synthesis, is used.
1330
Where must CCHFV testing and handling be performed globally?
In BSL-4 facilities worldwide, as shown in the map on the slide.
1331
What are some tips to prevent tick bites that can transmit CCHFV?
Wear a long-sleeve shirt and long pants tucked into shoes, wear closed-toe shoes, shower and wash hair after being outdoors, stay on trails away from tall grass, use insect repellent, wear light-colored clothing to easily spot ticks.
1332
Why is understanding tick-virus interaction important for CCHFV prevention?
It helps researchers develop methods to stop viral transmission from ticks to vertebrates.
1333
What is one innovative approach being developed to prevent CCHFV transmission?
The development of an anti.
1334
What should you wear to protect your feet from ticks?
Wear closed-toe shoes.
1335
What should you do after being outdoors?
Shower and wash hair after being outdoors.
1336
What is a recommended practice when hiking?
Stay on trails away from tall grass.
1337
What should you use to prevent tick bites?
Use insect repellent.
1338
What type of clothing is recommended to spot ticks easily?
Wear light-colored clothing to easily spot ticks.
1339
What is one innovative approach being developed to prevent CCHFV transmission?
The development of an anti-tick vaccine targeting tick saliva proteins.
1340
How does the anti-tick vaccine work?
It attracts immune cells to the site of tick feeding to reduce the risk of infection.
1341
Why is prevention considered the best tool for CCHFV control?
Due to the lack of specific treatments and vaccines, preventing tick bites and reducing vector transmission is crucial.
1342
do protazoa have cell walls?
no
1343
what are the 4 fungi groups?
Phycomycetes, Ascomycetes, Basidiomycetes, Deuteromycetes
1344
# [](http://)
what fungi groups cause the most illness in humans?
Ascomycetes, Basidiomycetes
1345
what are the benifits on fungi?
* Nutrient cycling
* Food
* Beverages
* Medicine such as penicillin
1346
what problems can fungi cause?
* Food spoilage
* Toxins
1347
why may some mushrooms produce psychoactive substances?
Psilocybin mushrooms are the most well-known for
hallucinogenic properties- this may have evolved to disorient preditors and stop them eating the mushrooms
1348
1349
What is an example of a fungus classified under Phycomycetes?
Rhizopus
1350
What is an example of a fungus classified under Ascomycetes?
Neurospora
1351
What is an example of a fungus classified under Basidiomycetes?
Agaricus (a type of mushroom)
1352
What is an example of a fungus classified under Deuteromycetes?
Fusarium.
1353
What are the three main types of fungi?
* Mushroom (a)
* Yeast (b)
* Filamentous fungi (c)
1354
What distinguishes mushrooms, yeasts, and filamentous fungi?
* Mushroom: Multicellular fungi with a reproductive structure visible above ground.
* Yeast: Single-celled fungi capable of fermentation and asexual reproduction.
* Filamentous fungi: Form hyphae and mycelium, with multicellular thread-like structures.
1355
What does 'dimorphic fungi' mean?
Dimorphic fungi can exist in two forms: as a yeast at body temperature (37°C) and as a mold (filamentous form) at cooler environmental temperatures (25°C).
1356
What are some examples of dimorphic fungi?
* Blastomyces dermatitidis
* Coccidioides immitis
* Histoplasma capsulatum
* Paracoccidioides brasiliensis
1357
At what temperature does Blastomyces dermatitidis exist as a mold?
At 25°C, it exists as a mold.
1358
At what temperature does Histoplasma capsulatum take its yeast form?
At 37°C, it exists as a yeast.
1359
Why are dimorphic fungi significant in infections?
Dimorphic fungi are pathogenic and can switch forms to adapt to host environments, often causing systemic fungal infections.
1360
How does the environment influence dimorphic fungi?
They grow as molds in the environment (25°C) and transition to yeast in the host body (37°C), aiding infection and immune evasion.
1361
What type of infections are typically caused by dimorphic fungi?
Dimorphic fungi often cause systemic mycoses that can affect multiple organ systems.
1362
Why are dimorphic fungi a focus in medical mycology?
Their ability to switch forms makes them adaptable and harder for the immune system to combat, increasing their virulence.
1363
What key medicinal product is derived from Penicillium spp.?
Penicillin, a widely used antibiotic.
1364
What is the primary use of penicillin?
It is used to treat bacterial infections by inhibiting bacterial cell wall synthesis.
1365
What antibiotic is derived from the genus Acremonium?
Cephalosporins, a group of broad-spectrum antibiotics.
1366
What is the significance of cephalosporins in medicine?
Cephalosporins are effective against both Gram-positive and Gram-negative bacteria and are often used for patients allergic to penicillin.
1367
What immunosuppressive drug is derived from Trichoderma polysporum?
Cyclosporin A.
1368
What is the primary medical use of Cyclosporin A?
It is used to prevent organ rejection in transplant patients by suppressing the immune response.
1369
What is Cephalexin, and which fungal genus contributes to its production?
Cephalexin is a cephalosporin antibiotic derived from Acremonium (Cephalosporium spp.).
1370
What infections is Cephalexin commonly used to treat?
It is used to treat infections of the respiratory tract, skin, bones, and urinary tract.
1371
Why are fungi important in medicine?
Fungi produce bioactive compounds such as antibiotics (e.g., penicillin, cephalosporins) and immunosuppressants (e.g., cyclosporin).
1372
Name three fungal genera that are significant for medicinal products.
* Penicillium (antibiotics)
* Acremonium (cephalosporins)
* Trichoderma (immunosuppressants)
1373
What kind of infections are caused by Tinea spp.?
Tinea infections, such as ringworm and athlete's foot.
1374
What is a characteristic symptom of Tinea infections?
Red, scaly, and ring-like lesions on the skin.
1375
What disease is caused by Pneumocystis jirovecii?
Pneumonia, specifically in immunocompromised individuals.
1376
Who is at higher risk for Pneumocystis jirovecii infections?
People with weakened immune systems, such as those with HIV/AIDS or undergoing immunosuppressive therapies.
1377
How do fungi like Batrachochytrium dendrobatidis impact ecosystems?
By reducing populations of certain species, fungi can disrupt ecosystem balance.
1378
What types of organisms do fungal pathogens affect?
* Plants (e.g., Ophiostoma novo-ulmi).
* Animals (e.g., Batrachochytrium dendrobatidis).
* Humans (e.g., Tinea spp. and Pneumocystis jirovecii).
1379
What are the four main types of fungal diseases?
* Superficial
* Cutaneous
* Subcutaneous
* Systemic/Invasive
1380
Which type of fungal disease affects the skin, nails, and hair?
Cutaneous fungal diseases.
1381
What type of fungal disease involves deeper layers of the skin and tissues?
Subcutaneous fungal diseases.
1382
What are systemic fungal infections?
Infections that spread throughout the body and can invade internal organs.
1383
What is a primary fungal pathogen?
A pathogen that can cause infection regardless of the host's immunity or commensal flora.
1384
Give an example of a primary fungal pathogen.
Histoplasma capsulatum, which is dimorphic.
1385
What does 'dimorphic' mean in the context of fungal pathogens?
Dimorphic fungi can grow in two forms: one in the host and one in the external environment.
1386
What are opportunistic fungal pathogens?
Fungi that cause disease in hosts with weakened immune systems or disrupted commensal flora.
1387
What are some risk factors for opportunistic fungal infections?
* Antibiotics
* Disruption of commensal flora
* Immune suppression
* Diabetes
1388
Are most fungal pathogens primary or opportunistic?
Most fungal pathogens are opportunistic.
1389
Why is the dimorphic nature of fungi like Histoplasma capsulatum significant?
It allows the fungus to adapt to both host environments and external environments, increasing its pathogenicity.
1390
Why do immunosuppressant drugs increase the risk of fungal infections?
Immunosuppressants weaken the immune system, making it harder to fight off infections, including systemic fungal infections.
1391
Name two types of immunosuppressants that increase the risk of fungal infections.
* Corticosteroids (e.g., Prednisolone)
* TNF inhibitors (used for rheumatoid arthritis).
1392
What is a common use for corticosteroids like Prednisolone?
Long-term treatment for inflammatory conditions.
1393
What is a TNF inhibitor, and what condition is it used for?
A tumor necrosis factor inhibitor used as an anti-inflammatory for conditions like rheumatoid arthritis.
1394
What type of cells do superficial fungal infections typically infect?
Dead cells on the surface of the skin.
1395
What is the host immune response to superficial fungal infections?
The host does not mount a cell-mediated immune response.
1396
What is the risk of superficial fungal infections in immunocompromised individuals?
There is a risk of the infection spreading systemically or invasively.
1397
What is Piedra, and what does it affect?
Piedra is a fungal growth on hair.
1398
What is Pityriasis, and what causes it?
Pityriasis is a skin rash caused by fungus, specifically Malassezia furfur.
1399
What type of fungi are associated with superficial infections like Piedra and Pityriasis?
Keratinophilic (keratin-digesting) fungi.
1400
What type of fungus is Malassezia furfur?
A dimorphic Basidiomycete.
1401
What condition does Malassezia furfur cause, and where does it feed?
It causes Pityriasis and feeds on oils in the skin and hair follicles.
1402
How does Malassezia furfur spread?
It spreads directly or via fomites, such as hairbrushes.
1403
Define 'Keratinophilic.'
Keratinophilic fungi can digest keratin, allowing them to infect hair, skin, and nails.
1404
What causes cutaneous fungal infections?
Dermatophytes, which affect the skin, hair, nails, and mucous membranes.
1405
What type of immune response is generated in cutaneous fungal infections?
A cell-mediated immune response.
1406
What are common symptoms of cutaneous fungal infections?
* Tinea pedis (Athlete’s foot): Cracking, redness, and itching of the skin between toes.
* Tinea corporis (Ringworm): Circular, red, scaly lesions on the skin.
1407
Name the three genera of dermatophytes responsible for cutaneous fungal infections.
* Trichophyton
* Microsporum
* Epidermophyton
1408
Which pathogen is commonly associated with ringworm?
Trichophyton rubrum.
1409
What condition is commonly referred to as Athlete’s foot?
Tinea pedis, caused by dermatophytes.
1410
What is Ringworm, and how does it present on the skin?
Tinea corporis, presenting as circular, red, scaly lesions.
1411
How are cutaneous fungal infections transmitted?
* Direct contact with infected individuals or animals.
* Indirect contact through fomites like towels or clothing.
1412
Who is at higher risk of developing cutaneous fungal infections?
Individuals with weakened immune systems, excessive sweating, or prolonged exposure to moisture.
1413
Why is microscopy important in diagnosing superficial and cutaneous mycoses?
Dermatophytes grow very slowly on agar (can take weeks), so microscopy provides faster detection.
1414
What types of samples are used for diagnosing dermatophyte infections?
Clippings or scrapings of hair, nails, or skin.
1415
What is the purpose of a 10% KOH preparation in fungal diagnostics?
It breaks down keratin, allowing fungal structures like hyphae to be observed under a microscope.
1416
What does the Periodic Acid-Schiff (PAS) stain highlight in fungal cells?
It stains fungal cell walls, making fungal structures more visible.
1417
What dye is used for cultured fungi to enhance visibility?
Lacto blue dye.
1418
Which fungus is commonly associated with onchomycosis (diseased nails)?
Trichophyton mentagrophytes, Fusarium species.
1419
What structures are observed in Trichophyton mentagrophytes under microscopy?
Septate hyphae (observed in KOH and PAS), microconidia clustered on septate hyphae, coiled spiral hyphae on slide culture.
1420
What unique structures are seen in Fusarium species?
Alkaline septate hyphae, sickle- or canoe-shaped macroconidia along septate hyphae, transparent looking hyphae (observed in KOH).
1421
What are the main diagnostic tools for confirming fungal nail infections?
Clinical examination, KOH preparation, PAS staining, culture for fungal growth.
1422
How do the KOH and PAS results differ in their observations for fungal infections?
KOH: Reveals the fungal hyphae by breaking down keratin. PAS: Stains the fungal cell walls for detailed visualization.
1423
What are subcutaneous mycoses?
Fungal infections that cause cysts and granulomas of varying severity in the subcutaneous tissue.
1424
Where are subcutaneous mycoses most commonly found?
In tropical and sub-tropical regions.
1425
Are subcutaneous mycoses primary pathogens or opportunistic?
They are typically opportunistic pathogens.
1426
What condition does Sporothrix schenckii cause, and what system does it affect?
It causes lymphocutaneous sporotrichosis, which affects lymph drainage.
1427
What is zygomycosis, and which demographic groups does it affect?
Affects limbs in children, affects facial structures in adults, caused by the mucormycete group.
1428
What condition is caused by eumycotic mycetoma, and what does it involve?
Eumycotic mycetoma causes destructive granulomas.
1429
Which tissue layers are primarily affected by subcutaneous mycoses?
Epidermis, dermis, subcutaneous tissue.
1430
What are granulomas in the context of subcutaneous mycoses?
Granulomas are localized inflammatory responses caused by fungal infection, often leading to tissue damage.
1431
What defines an opportunistic pathogen?
An organism that causes infection primarily in immunocompromised hosts or under specific conditions.
1432
How do pathogens causing eumycotic mycetoma enter the body?
Pathogens enter through skin lesions.
1433
What type of exposure increases the risk of eumycotic mycetoma?
Environmental or occupational exposure, with the feet being commonly affected sites.
1434
Is eumycotic mycetoma caused by a single pathogen or multiple genera?
A number of genera may be responsible for the disease.
1435
What are the key symptoms of eumycotic mycetoma?
Swelling at the site of infection, formation of granulomas, discharge of pus containing fungal granules.
1436
In which regions is eumycotic mycetoma most prevalent?
It is prevalent in tropical and sub-tropical regions, often in areas with poor sanitation.
1437
Is eumycotic mycetoma considered an opportunistic infection?
It is typically not opportunistic but associated with direct environmental exposure.
1438
What is the first step in diagnosing eumycotic mycetoma?
Appearance and clinical features are often diagnostic.
1439
What laboratory methods can confirm the diagnosis?
Microscopy to visualize fungal structures, cultures to identify the specific pathogen.
1440
What antifungal treatment is commonly used for eumycotic mycetoma?
Itraconazole is often effective.
1441
When might surgical treatment be necessary for eumycotic mycetoma?
In severe cases, surgical intervention or even amputation may be required.
1442
Why are feet commonly affected in eumycotic mycetoma?
Due to frequent environmental exposure and lack of proper foot protection in endemic areas.
1443
What are examples of primary fungal pathogens that are respiratory dimorphic fungi?
Blastomyces dermatitidis, Coccidioides immitis, Histoplasma capsulatum.
1444
Where are Blastomyces dermatitidis and Coccidioides immitis geographically found?
In the Americas.
1445
Where is Histoplasma capsulatum found?
It is globally widespread.
1446
What type of infection is caused by Histoplasma capsulatum?
Respiratory infection.
1447
Where are Histoplasma spores typically found?
In soil, and in bird/bat droppings.
1448
Is histoplasmosis usually severe or mild?
It is usually self-limiting.
1449
What can occur in acute, disseminated histoplasmosis?
It may affect skin and other organs if disseminated, it can lead to granuloma formation.
1450
What do fungal cells of histoplasmosis look like under the microscope?
They have halos and are present in granuloma formations.
1451
What immune cells are involved in granuloma formation during histoplasmosis?
Histocytes.
1452
What are key features of acute disseminated histoplasmosis in immunocompromised individuals?
Severe skin involvement (as shown in the clinical image), dissemination to multiple organs, respiratory symptoms.
1453
What are major risk factors for disseminated histoplasmosis?
AIDS, organ transplant, cancer chemotherapy.
1454
Why is histoplasmosis more severe in immunocompromised individuals?
The immune system cannot adequately contain the fungal infection, leading to dissemination.
1455
How does Histoplasma capsulatum transform in the host?
It rapidly transforms into the yeast form in the host.
1456
What happens to H. capsulatum upon entering the host?
It is engulfed by macrophages.
1457
How does H. capsulatum modify the macrophage environment to survive?
It adjusts the pH from ~4.5 to 6.0–6.5 within the macrophage.
1458
Why does H. capsulatum need to maintain the pH between 6.0 and 6.5?
pH > 6.0 is too high for macrophage respiratory burst to function effectively, pH > 6.5 is too high for H. capsulatum to access iron molecules.
1459
What is the role of apoptosis in the pathogenesis of H. capsulatum?
Apoptosis allows the yeast to spread to new cells, it also activates the adaptive immune response.
1460
How does H. capsulatum appear inside macrophages under a microscope?
The yeast cells can be seen within macrophages, as shown in a bone marrow aspirate stained with May-Grünwald Giemsa.
1461
What key structures are visible in macrophages infected with H. capsulatum?
The nucleus of the macrophage, H. capsulatum yeast cells inside the macrophage.
1462
What is Candida albicans, and where is it commonly found?
Candida albicans is part of the commensal flora and is commonly found on mucosal surfaces and damp, warm areas of the skin. Can cause infections in oral-genital areas.
1463
Under what conditions can Candida albicans overgrow and invade tissues?
It can overgrow when conditions such as impaired mucosal barriers or disruption to commensal flora occur.
1464
What are some factors that impair mucosal barriers and increase the risk of Candida infections?
Use of cosmetics, soaps, antibiotics.
1465
Is candidiasis a sexually transmitted infection (STI)?
No, candidiasis is not an STI, but yeasts may be transmitted during sexual contact through mucosal surfaces.
1466
Why is Candida albicans considered an important nosocomial infection?
Because it can cause infections associated with catheters and lead to bloodstream infections.
1467
What areas of the body are commonly invaded during Candida infections in hospital settings?
Mucosal surfaces, bloodstream, and areas associated with invasive medical devices.
1468
What mechanisms does Candida spp. use to bind to host cells?
It uses adhesins for ligand binding on host cells and invasins for invasion.
1469
What types of forces are involved in Candida spp. binding to host cells?
It utilizes electrostatic and van der Waals forces for binding.
1470
How does Candida spp. damage host tissues?
It damages tissues via proteases and phospholipases.
1471
What are the key enzymes involved in Candida spp. pathogenicity?
Hydrolytic enzymes like secretory aspartyl proteases, phospholipases.
1472
What are the major components of the Candida spp. cell wall?
β-(1-3) glucan, chitin, mannoproteins.
1473
To what structures does Candida spp. adhere?
Epithelial cells, endothelial cells, extracellular matrix, C3b (complement protein).
1474
What is the significance of dimorphism in Candida spp.?
Candida spp. can transition between yeast and hyphal forms, aiding in colonization and pathogenesis.
1475
What is thigmotropism in Candida albicans?
It is a 'sense of touch,' enabling Candida albicans to grow along grooves and through pores.
1476
Where is thigmotropism commonly seen, and how is it related to Candida albicans?
Thigmotropism is commonly seen in climbing plants and is utilized by Candida albicans for growth in structured environments like tissues.
1477
How does sugar concentration affect bacteria growth differently to fungal growth?
bacteria can be inhibited by high sugar concentrations whilst high sugar concentration can increase fungal growth
1478
1479
What is Candida auris?
It is an invasive nosocomial (hospital-acquired) pathogen known for its antifungal resistance.
1480
When and where was Candida auris first identified?
It was first identified in 2009 in Japan and has since spread worldwide.
1481
What makes Candida auris a concern in healthcare settings?
Its resistance to antifungal treatments, its ability to persist on multiple body sites, and its ease of spread require robust infection control measures.
1482
What are the key settings where Candida auris infections occur?
In high-dependency healthcare settings, such as intensive care units.
1483
What are some characteristics of Candida auris infections?
Persistent carriage on multiple body sites, easily spread despite control measures, and an unknown environmental source.
1484
What does Candida auris join as an emerging fungal infection?
It joins Candida glabrata and Candida parapsilosis as emerging drug-resistant fungal infections.
1485
Where are Candida auris cases documented globally?
Cases are reported worldwide, primarily in regions such as Asia, Europe, the Americas, and Africa.
1486
Where is Aspergillus spp. commonly found?
It is a soil microbe.
1487
How does Aspergillus spp. infect the lungs?
Conidia are inhaled, bind to lung laminin and fibrinogen, and germinate in the alveoli.
1488
What enzymes does Aspergillus spp. produce for cell invasion?
Proteases and elastases.
1489
What conditions can Aspergillus spp. cause?
Sinusitis, Aspergilloma (fungal ball in the lungs), and invasive infections involving skin, GI tract, lungs, heart, brain, and kidneys.
1490
What complication occurs if Aspergillus spp. invades blood vessels?
Thrombosis.
1491
How does the immune system respond to Aspergillus spp.?
Macrophages and neutrophils attack the fungus. Those that escape infect pulmonary tissue and blood vessels.
1492
What is the role of catalase and gliotoxins in Aspergillus spp.?
These are factors that may aid in immune evasion and tissue damage.
1493
What is an aspergilloma?
It is a fungal ball that colonizes in a healed lung scar or abscess from a previous disease.
1494
What types of tissues and organs can Aspergillus spp. invade?
Lungs, skin, GI tract, heart, brain, and kidneys.
1495
What type of infection is pulmonary aspergillosis?
A lung infection caused by Aspergillus spp., leading to significant tissue invasion.
1496
What is the primary diagnostic tool for fungal infections?
Microscopy of clinical or cultured samples.
1497
Which microscopy stains are used for fungal diagnosis?
* Gram stain (fungi don't react like bacteria).
* Haematoxylin and Eosin (H&E).
* Germ tube test for Candida albicans.
1498
How does the Gram stain work with fungi?
While fungi don't react to Gram stain like bacteria, it can still highlight Candida spp.
1499
What is the germ tube test used for?
It is used to identify Candida albicans by forming a germ tube after incubation in serum for 3 hours.
1500
How do pseudohyphae and hyphae differ in the germ tube test?
* Pseudohyphae: Shows constrictions between cells.
* Hyphae: No constrictions.
1501
What does the image of Candida albicans with Gram stain reveal?
It reveals the purple-stained fungal cells, distinguishing them from bacterial forms.
1502
What are the challenges of treating fungal infections with drugs?
* Poor drug access to infection sites (e.g., epidermis, nails, hair).
* Less scope for selective toxicity compared to prokaryotic drug targets.
1503
What is the key structural difference between mammalian and fungal cells in terms of the cell wall?
* Mammalian cells: No cell wall.
* Fungal cells: Have cell walls made of chitin, mannans, and glucans.
1504
What is the difference in membrane sterols between mammalian and fungal cells?
* Mammalian cells: Contain cholesterol.
* Fungal cells: Contain ergosterol.
1505
Which enzyme is present in fungal cells but not in mammalian cells, making it a drug target?
Cytosine deaminase.
1506
What is the role of squalene epoxidase in fungal cells?
It is involved in ergosterol synthesis, making it a target for antifungal drugs.
1507
How do DNA synthesis processes differ between fungi and mammals in terms of drug targeting?
Some agents are selectively activated in fungi over yeast cells, exploiting unique fungal pathways.
1508
What are some of the prokaryotic drug target sites that make selective toxicity easier in bacteria compared to fungi?
* Cell wall/membrane: Targeted by beta-lactams, vancomycin, etc.
* Protein synthesis: Targeted by aminoglycosides, macrolides, etc.
* Nucleic acid synthesis: Targeted by quinolones.
* Anti-metabolites: Targeted by sulphonamides, trimethoprim.
1509
What is the target of many antifungal drugs?
Ergosterol biosynthesis.
1510
What type of infections do allylamines treat?
Dermatophyte infections.
1511
What are azoles used to treat?
* Candidiasis.
* Onychomycosis.
* Skin infections.
1512
What is the primary use of morpholines in antifungal therapy?
Onychomycosis treatment.
1513
What infections are treated with polyenes?
* Mucocutaneous infections.
* Invasive infections in immunocompromised people.
1514
What is the function of azole antifungal drugs?
They target ergosterol biosynthesis by inhibiting the Erg11 enzyme, which prevents the conversion of lanosterol into ergosterol.
1515
Name two examples of azole antifungal drugs.
Clotrimazole and fluconazole.
1516
What happens when ergosterol synthesis is disrupted by azole drugs?
Toxic sterols accumulate, leading to membrane stress and loss of membrane integrity.
1517
What is the role of the Erg11 enzyme in fungi?
Erg11 is involved in the conversion of lanosterol into ergosterol during ergosterol synthesis.
1518
Why are 'toxic sterols' significant in azole antifungal treatment?
Toxic sterols accumulate due to the inhibition of ergosterol synthesis, disrupting membrane integrity and causing membrane stress in fungal cells.
1519
What is Griseofulvin primarily used for?
It is a topical treatment for dermatophyte infections such as ringworm and athlete’s foot.
1520
What organism produces Griseofulvin?
Penicillium griseofulvum.
1521
How does Griseofulvin function?
It binds to tubulins, inhibiting mitotic spindle formation and preventing the separation of daughter nuclei, resulting in a fungistatic effect.
1522
What role does keratin play in Griseofulvin treatment?
The drug binds to keratin, making it effective in targeting skin and nail infections.
1523
When might Griseofulvin be prescribed in tablet form?
If the infection does not respond to topical treatment.
