virology exam 3 Flashcards
1
Q
- What structure does Picornavirus have? =
A
- small, naked, icosahedral
2
Q
- What is the genome of Picornavirus?
A
- ss+RNA, linear and capped with VPg
3
Q
- What are some medically important viruses of Picornavirus?
A
- Rhinoviruses (common cold), Enteroviruses (Poliovirus & Coxsackie A and B), Heparnavirus/Hepatovirus (Hepatitis A)
4
Q
- During replication of Picornavirus the whole genome is translated.
A
– P1 goes to VP1,2,3,4 (structural proteins) and P3 goes to polymerase and VPg
5
Q
- What is the major protease during Picornavirus replication?
A
- 3c (2a is also one)
6
Q
- What is the polymerase used during Picornavirus replication?
A
- 3D
7
Q
- The plus sense (+ssRNA) of Picornavirus is?
A
– directly translated to polypeptide
8
Q
- The negative sense of Picornavirus is?
A
– is the template to make more copies of plus sense; exits by lysis in intestinal cells
9
Q
- How is Poliovirus transmitted?
A
- fecal-oral transmission
10
Q
- Are there still outbreaks of Poliovirus? =
A
– Yes. It has been eradicated from North America, but there are still outbreaks elsewhere in the world
11
Q
- What does Poliovirus target in the paralytic form?
A
- the anterior horn motor neurons
12
Q
- What happens to intestinal cells and neuronal cells in the paralytic form of Poliovirus?
A
- intestinal cells explode and come back, but neuronal cells explode and do come back so it is permanent paralysis (these neurons literally explode which do not regenerate and spinal cord damage is now permanent)
13
Q
- Typical presentation of Polio:
A
- asymptomatic, fever of unknown origin (FUO), meningitis, paralytic polio, and bulbar meningitis
14
Q
- What are the symptoms of Paralytic Polio?
A
– fever and diarrhea; paralysis of one side of the body, usually legs before arms
15
Q
- Paralytic polio can lead to?
A
– post polio
16
Q
- What is Post-polio syndrome?
A
– inflammation of the spinal cord; partial paralysis’ paraplegic
17
Q
- Post-polio can lead to?
A
– bulbar myelitis
18
Q
- What is Bulbar myelitis?
A
– inflammation of the brainstem where neurons are killed and patient can’t walk, move arms, or no longer breathe unless with “iron lungs”
19
Q
- What is the vaccine/treatment for Poliovirus?
A
– Dead Salk and Alive Sabin. Salk vaccine (killed) and Sabin vaccine (live, attenuated–no longer used in US)
20
Q
- Salk vaccine - also called
A
inactivated polio vaccine (IPV); shot, killed vaccine
21
Q
- Sabin vaccine - also called
A
oral polio vaccine (OPV); not a shot, originally was placed on a sugar cube
22
Q
- What is the benefit of the Sabin vaccine?
A
provides the best immunity
23
Q
- What is the problem with the Sabin vaccine?
A
because it is live attenuated it is able to replicate, hence causing paralysis
24
Q
- What is the chance that the live, attenuated strain reverts back to original paralytic polio?
A
1 in one million
25
25. What is the transmission of Coxsackie A & B?
fecal-oral
26
26. What is the treatment/vaccine for Coxsackie A & B?
– no effective antiviral treatments, use handwashing for the best preventive mechanism
27
27. Coxsackie A causes
- meningitis, herpangina (red/white blisters back of mouth) & hand, foot, and mouth disease (Blisters on mouth hurt the most making it hard to eat)
28
28. What strain of Coxsackie causes hand, foot, and mouth disease?
- A 16
29
29. What is the difference between Herpangina and Herpes?
– herpes is blisters on lips, gums, and tip of tongue whereas Herpangina is blisters on the back of throat and root of tonsils
30
30. Coxsackie A 16 is typically seen in
babies; usually a little kid presents with a fever and gets blisters in 3 locations: palms, soles, and back of throat & tongue
31
31. Coxsackie B causes:
meningitis, viral myocarditis, Bornholm's disease (Devil's grip)
32
32. Viral Myocarditis is the number one cause of?
heart failure in patients under the age of 50 years old
33
33. Bornholm's disease (Devil's grip) is what type of disease?
a respiratory disease/pulmonary infection breathe in horrible sharp pain in chest (feels like a piece of chest is being gripped)
34
34. What is another name for Enterovirus 68 and 71?
Nonpolio Acute Paralysis Syndrome
35
35. Enterovirus 68 and 71 are not?
– polio or coxsackie
36
36. Enterovirus 68 and 71 were initially identified in?
1960s California, again in 2008-2009, 2010, 2015,2018
37
37. Enterovirus 68 and 71 were typically seen in?
kids and caused paralysis
38
38. What is the difference between paralytic polio and Enterovirus 68 and 71?
paralytic is paralysis of one side of the body and Enterovirus 68 and 71 paralysis is more widespread, progressive, and rapid
39
1. What is the structure of Herpesvirus?
large, icosahedral, enveloped
40
2. What is the genome of Herpesvirus?
linear dsDNA
41
3. What does the tegument layer of Herpesvirus contain?
- proteins that regulate host processes as well as early viral replication
42
4. Where are the different places the envelope of Herpesvirus comes from?
first layer is from the nucleus, pulls from the plasma membrane, and also the ER; buds from nucleus, ER, Golgi/plasma membrane
43
5. What family would a virus belong to if the envelope has been determined to contain nuclear proteins?
Herpesvirus
44
6. Tegument is the layer between
- nucleocapsid and actual virion to pack something inside of it
45
7. How is Herpesvirus similar to Poxvirus?
large in structure, brings lots of things with it for replication, has its own DNA polymerase
46
8. Herpes virus uses its own DNA polymerase. What is the benefit of the fact that Herpesvirus doesn't hijack the host's polymerase when it replicates in the nucleus?
We can make drugs that hurt the virus' polymerase without hurting host polymerase
47
9. How many different genome isomers of Herpesvirus is possible and why?
4; due to rearrangements around terminal and internal repeats on the long and short genome regions
48
10. latency associated transcripts (LAT) allows the herpesvirus
to go latent until infection
49
11. What is one thing that is true for all Herpesviruses?
Once you get a particular Herpes, you can have it for life ("the gift that keeps on giving")
50
12. What does Herpesvirus bind to get into the cell?
- binds to extracellular matrix (heparans & chondroitin proteoglycans)
51
13. concatemeric DNA is DNA that
is just copies of itself
52
What Are Gamma proteins
late proteins, structural proteins (nucleocapsid, glycoproteins etc.)
53
16. During both productive and latent infection of herpes what is the shape of the genome?
–linear.
54
17. Why does herpesvirus go through all these steps of immediate-early gene replications in productive infection?
– IE turns on E. E activates replication and forms concatemeric DNA, which is the template for L expression
55
18. What happens to the viral DNA or herpesviridae during latent infection?
- vDNA circularizes and is associated with host nucleosomes
56
19. LAT latency associated transcripts is produced during latent infection and two things can happen ?
– RNA translated to protein called LAT protein OR RNA is maintained in nucleus: exons splice together: introns spliced out, but 1 maintains in RNA called the stable intron in Lariat configuration
57
20. what is a lariat loop -
a loop formed when LAT mRNA is made
58
21. Once the cell becomes permissive what occurs? –
reactivation, now active or productive infection
59
22. What are some things that can cause herpesvirus to reactivate and go back to active infection? -
trauma to cell, hormone alterations, physiological stress, immunosuppression
60
23. HSV1 is associated with? -
cold sore and gingivostomatitis (looks like herpanagina but is inflammatory condition of the gums inside the mouth)
61
24. The initial infection of HSV1?
clinically unapparent
62
25. Where does HSV1 lay dormant before reinfection?
- trigeminal nerve root ganglia (retrograde, dynein)
63
Reactivation of HSV1 leads to?
classical vesicle formation on lips. "dew drop on a rose bud" serous-filled vesicle on an erythematous base (anterograde, kinesin)
64
27. What is the vaccine and treatment for HSV 1? -
no vaccine; treated with Acyclovir and derivatives
65
28. What percentage of time is a cold sore or oral presentation caused be HSV1?
- 80%
66
29. What percentage of the time is a cold sore or oral presentation caused by HSV2?
- 20%
67
30. HSV2 is associated with?
– genital herpes
68
31. The initial infection of HSV2?
– clinically unapparent OR inflammation
69
32. Where does HSV2 lay dormant before reinfection?
- sacral nerve root ganglia (retrograde, dynein)
70
33. Reactivation of HSV2 leads to?
- classical vesicle formation on lips. "dew drop on a rose bud" serous-filled vesicle on an erythematous base (anterograde, kinesin)
71
34. What is the vaccine and treatment for HSV2? -
no vaccine; treated with Acyclovir and derivatives
72
35. What percentage of time is genital herpes is caused by HSV2?
80%
73
36. What percentage of the time genital herpes is caused by HSV1? -
20%
74
37. The initial infection of HHV3?
– chickenpox; technical name is varicella
75
38. What makes chickenpox different from Poxvirus?
– asynchronous rash
76
39 What makes chickenpox different from measles or rubella?
- Usually rash begins on chest or trunk and works its way out
77
40. Reactivation of HHV3 leads to?
- shingles, technical name zoster. With unilateral dermatome expression
78
41. What is the vaccine and treatment for HHV3?
– live attenuated vaccine; treated with Acyclovir and derivatives in immunocompromised patients
79
42. What percentage of people actually catch Herpes when patients shows no symptoms?
- 70%
80
43. Aseptic meningitis is the most common cause of –
viral meningitis and encephalitis and involves the temporal lobe
81
44. Herpetic whitlow is due to-
touching herpetic sores
82
45. Herpes gladiatorum is often associated with -
wrestlers using inoculated mats
83
46. Herpetic keratitis/ocular involvement leads to
– blindness in usually children
84
Where does HHV3 lay dormant before reinfection?
in dorsal root nerve ganglia
85
48. HHV4 is associated with –
Epstein-Barr
86
49. What does HHV4/EBV infect and where does it go latent before reinfection?
- the B-cells (entry via CD21) and can also act as a B-cell mitogen
87
50. In HHV4/EBV because B-cells proliferate leading to non-specific antibody response (heterophile antibody), what needs to happen?
T-cells need to control the infection
88
51. How many percent of us are exposed to HHV4 (EBV) as a child?
- 95%
89
52. What is the clinical presentation of HHV4 if infected as a child?
- clinically unapparent infection
90
53. What is the clinical presentation of HHV4 if exposed later?
- tired, fatigue that can last for months, swollen lymph nodes, swollen spleen
91
54. What are you looking for when you perform a Monospot Test? -
looking for presence of heterophile antibodies
92
55. What are the multitudes of presentations that HHV4/EBV can present as in later reactivation? -
Burkitt's Lymphoma, Nasopharyngeal carcinoma, Hodgkin's lymphoma, Oral hairy leukoplakia
93
56. Burkitt's Lymphoma in
Africa; a reactivation of HHV where lymph nodes in face start swelling, sometimes can knock teeth out and make it very difficult to eat; starts at the head; jaw dislocated and tonsils grow outwards
94
57. Nasopharyngeal carcinoma in
Asia; a reactivation of HHV/EBV; starts in nose and back of throat
95
58. Hodgkin's lymphoma in
America; a reactivation of HHV/EBV; lymphoid on neck (can start in armpit or groin)
96
59. Oral hairy leukoplakia in
AIDS patients; a reactivation of HHV/EBV; white and hairy plaques present on the tongue & inside of mouth and cannot be scraped off
97
60. What is the treatment of HHV4/EBV? -
no vaccine, can use acyclovir in complicated cases but pretty rare
98
61. HHV5 is associated with -
Cytomegalovirus
99
62. The only difference between HHV5 from HHV4 is?
– HHV4 causes heterophile antibody positive infectious mononucleosis and HHV5 causes heterophile antibody negative infectious mononucleosis.
100
63. Where does the HHV5 virus go latent before reinfection? -
in B-cells
101
64. Cytomegalovirus can initially infect what and can cause what
– lymph nodes and salivary glands; pneumonitis
102
65. What can occur if exposed to HHV5/CMV during late uterine or early postnatal life? -
Cytomegalic inclusion disease of the newborn; can be life-threatening
103
66. HHV5 reactivation or representation is because of
– radiation/cancer, organ transplant, AIDS
104
67. In immunocompromised hosts, HHV5 reactivation can lead to what?
- CMV retinitis which can lead to blindness; damaged liver; inflamed lungs
105
68. What is the problem with HHV5/CMV in women who are pregnant?
- if never got exposed to it as a child, the initial infection can now cross the placenta, go to the baby and cause inclusion disease of the newborn & can kill the baby
106
69. Why can't you give patients with HHV5/CMV acyclovir as a treatment?
- does not encode thymidine kinase, so acyclovir is useless
107
70. What are the treatments for HHV5?
ganciclovir and derivatives, and foscarnet
108
71. HHV5/CMV has something called perinuclear halo
– described as owl eyes where there is a double nuclei associated with lungs (perinuclear halo is usually associated with HPV at the cervical level)
109
72. HHV6 and HHV7 are associated with –
roseola, 1 of the 5 rash-causing childhood diseases
110
73. What is roseola technically known as?
- exanthem (erythema) subitum ("subtle rash")
111
74. How is HHV6 &HHV 7 (roseola) characterized by?
- a fever for a few days, followed by a faint rash that spreads from the trunk to the extremities
112
75. Where does HHV6 & HHV7 virus lay latent before reactivation?
in T-cells; may reactivate in transplant patients leading to bone marrow failure
113
76. What is the treatment and vaccine for HHV6 & HHV7?
no vaccine available; apparently can be treated with ganciclovir & derivatives (acyclovir useless because does not encode thymidine kinase)
114
77. HHV8 is associated with –
Kaposi’s sarcoma
115
78. What is Kaposi’s sarcoma?
- a rare cancer in the general population, but relatively common in AIDs patients
116
79. Where does the primary and late infection occur for HHV8? -
in B-cells (no apparent disease); in tumor cells
117
80. What is the treatment for HHV8/KSHV? -
no specific treatment available, but reversal of immunosuppression often causes regression of the tumors (chemo & radiation if continues to grow)
118
81. Where did you hear of KSHV/Kasposi Sarcoma prior to late 1970s? -
in patients who were old men, who were usually Jewish & particularly in the Mediterranean area
119
82. For a long time Kasposi sarcoma was known as what? -
the "gay cancer" (essentially seen secondary to AIDS)
120
83. What is the clinical presentation of Kaposi’s sarcoma?
- vascular bruises purplish-brown in color that can swell & get larger--not just on the skin: gums & tongues, rectum, in serious cases heart, liver, lungs
121
84. What are the divisions of why a patient could have Kaposi’s sarcoma? -
infected with AIDS, recent organ transplant, old Jewish guy, etc.
122
85. How likely is it for someone to contract HHV8/KSHV?
- most people carry this virus but not clinically seen UNTIL you become immunocompromised
123
86. Which herpesviruses are usually transmitted through saliva & respiratory secretions?
3, 4, 5, 6, 7
124
87. Which herpesviruses are usually transmitted by direct contact?
1 & 2
125
88. What is the structure of Hepadnavirus?
- enveloped, icosahedral/spherical
126
89. What is the genome of Hepadnavirus?
- partial dsDNA/ partial --ssDNA (capped by nucleic acid)
127
90. What is the medically important virus of Hepadnavirus?
- Hepatitis B
128
91. In Hepadnavirus, the virus overproduces?
– surface antigen (s, m, l) non-infectious polymers of surface antigens are found in blood during infection
129
92. In Hepadnavirus - fully-formed infectious particle of Hepatitis B (core DNA & surface proteins) is called -
"Dane particle"
130
93. How many open reading frames does Hepadnavirus have & what do they produce?
- 4 open-reading frames produce 4 major proteins
131
94. PreC+C=?
E antigen
132
95. Pre-S2+S=? -
medium surface
133
96. Pre-S1+Pre-S2+S=?
- large surface
134
97. X protein - regulatory protein -
associated with risk of cirrhosis/HCC
135
98. How does Hepadnavirus enter the cell and what is its target? -
enters by binding NTCP; target organ is the liver
136
99. When the genome of Hepadnavirus enter the nucleus what does the host do?
– elongates +DNA strand and creates covalently closed circular DNA (cccDNA)
137
100. When the genome of Hepadnavirus enter the nucleus what does your liver stop doing
– finishes copying DNA
138
101. In Hepadnavirus where does mRNA go for translation; surface proteins?
cytoplasm; mainly Golgi (can ER)
139
102. In Hepadnavirus host transcribes mRNA using –
DNA dep RNA poly
140
103. In Hepadnavirus after the host transcribes mRNA using DNA dep RNA poly, Full length mRNA is converted to –
DNA in cytoplasm via – viral polymerase (RT Activity)
141
104. In Hepadnavirus after the host transcribes mRNA using DNA dep RNA poly, Full length mRNA is converted to –DNA in cytoplasm via viral polymerase, DNA is then partially made –
double stranded by viral polymerase (DNA dep DNA poly activity)
142
105. How is Hepatitis B transmitted? -
exchange of blood, sexual contact, probably other body fluids
143
106. In Hepatitis B infected hepatocytes are targeted for –
destruction by CTL
144
107. How many percent of people clear the Hepatitis B infection if contracted as an adult? -
90-95% of adults
145
108. How many percent of people develop chronic Hepatitis B if contracted as an adult?
- 5-10% of adults
146
109. How many percent of people clear the Hepatitis B infection if contracted during childhood? -
5-10%
147
110. How many percent of people develop chronic Hepatitis B if contracted during childhood? -
90-95%
148
111. Chronic hepatitis B: - increases
risk of liver cancer 100-150 fold
149
112. What is the prevention of Hepatitis B? -
a molecular vaccine (HBsAg);
150
113. What is the treatment of Hepatitis B for acute cases?
symptomatic treatment only
151
114. What is the treatment of Hepatitis B for chronic cases - antiviral medications are available pill:
Lamivudine, tenofovir, adefovir, (L,T 1st treatment A least effective) AND shot: PEGasys [interferon])
152
115. What is the problem with PEGasys, an injection of interferons, in patients with Hepatitis B? - common side effects are flu-like symptoms;
if have an auto immune disorder can't take this medicine; in depression or mental illness, depression & suicide are relatively common
153
116. What is primarily used as a marker of infectivity in Hepatitis B?
HBeAg
154
117. What does "at risk" mean in terms of Hepatitis B?
someone who has never had Hepatitis B before and also has never been vaccinated before
155
118. HBsAg never infected, never vaccinated
susceptible so you should get vaccinated
156
119. HBeAg vaccinated –
protected against disease
157
120. Anti-HBes had infection before ad cleared it –
won’t get it again
158
121. Anti Core protein (IgM early and IgG late) has infection now –
tells about infectivity or contagious
159
122. Deltavirus is also known as: - "delta agent"
Deltavirus - the cause of hepatitis D
160
124. Why is Deltavirus known as a defective virus or a satellite virus?
- because it requires hepatitis B for replication (does not encode its own surface antigen, steals HBsAg)
161
125. What is the structure of Deltavirus?
- enveloped, icosahedral
162
126. What is the genome of Deltavirus? -
-ssRNA (but not contain its own polymerase)
163
128. What is the good thing about Hep D?
if you have been vaccinated against Hep B or had previous infection but cleared of Hep B, you cannot get Hep D (immune protection)
164
129. What is the initial shape of the genome of Deltavirus –
circularized with significant base pairing
165
130. Deltavirus: host RNA polymerase reads genome as dsDNA and then what is made –
mRNA which is used to make small D-antigen
166
131. Deltavirus: antigenomic RNA is made and is used as a template for genome production –
rolling strand formation, 85bp sequence functios as a ribozyme
167
132. When is the large antigen of Deltavirus produced – when host adenine deaminase ADA1 converts UAG stop codon to UCG serine;
increases length of small antigen by 19 AA; rewuired for viron assembly
168
133. What is the structure of Flaviviridae?
- icosahedral, enveloped
169
134. What is the genome of Flaviviridae?
ss+RNA (some capped with nuclotide, some with VPa)
170
135. Major medically important viruses of Flaviviridae: -
- Hepatitis C & Arboviruses
171
136. The whole genome of flavivirus is:
translated to form one polyprotein, which is then later cleaved
172
137. What is the initial part of the genome of flavivirus? -
structural proteins (C capsid, M membrane, E envelope proteins)
173
138. What is the latter part of the genome of flavivirus? -
non-structural proteins; NS3 is the important one (protease); when bound to others becomes helicase and RTPase
174
139. What is the function of NS4 – helper proteins
140. NS4a is important for – NS3 to work
| 141. NS4b is important for – NS5 to work
175
142. What is the function of NS5 –
RNA dependent RNA polymerase
176
143. What protein is critical for attachment in Flavivirus? -
E-protein
177
144. How is Hepatitis C transmitted?
- parental (blood mix) or sexual
178
147. What percent of Hep C cases progress to chronic hepatitis? -
80% of cases
179
148. What percent of cases of hepatocellular carcinoma is caused by Hepatitis C? -
25%
180
149. Why is Hepatitis C so hard to diagnose? -
because it is an acute infection, which is usually subclinical; never know you are sick
181
150. What basis is the diagnosis for Hepatitis C made? -
based on antibody against HCV; if positive a PCR is performed to determine if it is chronic
182
151. What percentage of patients with Hep C will develop cirrhosis? -
20% of patients
183
152. What is the treatment and vaccine for Hep C? -
no vaccine; treatment may include interferon and ribavirin combo; drugs maverick and harvoney
184
153. What is the difference between the ribavirin medication given to Hep C patients rather than in RSV patients? -
it is a pill
185
154. Telapravir - NS3 protease inhibitor;
75% chance of clearing the infection
186
155. Flavivirus (Hep C) eascapes Golgi by -
budding
187
156. What virus causes Hepatitis A? –
picornavirus; heparnavirus
188
157. How is Hepatitis A transmitted? -
fecal-oral transmission
189
158. What are the classic hepatitis symptoms caused by Hepatitis A? -
fever, malaise, anorexia, jaundice
190
159. How is Hepatitis A in healthy individuals compared to immunocompromised?
- relatively mild, not chronic, no long-term complications; immunocompromised patients may have fulminant hepatitis
191
160. How is Hep A diagnosed? -
look at antibodies for IgM against HAV antigens
192
161. What is the treatment or vaccine for Hep A? -
both a killed & live vaccine are available & used in the US
193
162. What are the recommendations for the Hepatitis A vaccines?
- for all children over 1 year old to get vaccine (been around only since early 2000s)
194
163. What is the structure of Hepeviridae? -
icosahedral, naked
195
164. What is the genome of Hepeviridae?
- ss+RNA (capped by nucleic acid, not protein)
196
165. What is the medically important virus of Hepeviridae? -
Hepatitis E virus
197
166. What other virus did Hepeviridae used to be classified with?
- Calicivirus (Norwalk virus); lytic infection
198
167. How is Hepatitis E transmitted?
- fecal-oral transmission; often from contaminated drinking water
199
168. Hepatitis E: often asymptomatic, no chronic state; can lead to -
fulminant hepatitis in immunocompromised or pregnant patients
200
169. Where is Hepatitis E not common or not endemic?
U.S.
201
170. Where is Hepatitis E common?
- Mexico, East Africa, & India have high prevalence
202
171. Where is hepatitis endemic?
– south America, mexico, central America
203
172. What is the treatment and prevention for Hepatitis E? -
no vaccine, no specific antiviral treatment available; ensure sanitary food & water sources, handwashing
204
173. If you had a patient with recent travel to Mexico who is pregnant, got a fever, turned yellow, & dropped dead, the most likely cause is? -
Hepatitis E
