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Viruses Flashcards

1
Q

What is a viral envelope?

A

Partially host-derived lipid membrane that has an inner protein layer and glycoprotein spikes

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2
Q

What is a capsid?

A

Protein coat composed of symmetrically-arranged structural units (capsomeres) that surround the viral genome

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3
Q

Give the stages of viral entry into cells

A

Attachment or adsorption via receptor

Penetration / entry via phagocytosis or pinocytosis

Uncoating via removal of envelope and capsid

Replication - Exact steps differ based on the kind of nucleic acid virus has. There is reproduction of viral copies, including the viral genome as well as the proteins required to make up the capsid.

Assembly, maturation, release. Virions bud out through the cell membrane.
There can either be budding or there can be rupture (lysis)

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4
Q

Positive vs. Negative stranded RNA viruses?

A

Positive -> Viral ssRNA directly translated into viral proteins. RNA-dependent RNA Polymerase (RDRP) synthesises progeny RNA and mRNA templates

Negative -> Viral RNA needs to be transcribed to mRNA by the enzyme VIRAL RDRP.

Side note -Retroviruses have RNA-dependent DNA polymerase. Integrates proviral DNA into host genome

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5
Q

What are 3 effects of viruses on cells

A

Latency

CPE - Cytopathic effect

Cellular transformation - Normal to malignant

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6
Q

Effect of temperature on viruses?

A

Can be stored at -70C or lower

Most at inactivated by 56C for a few minutes, 100C for seconds

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7
Q

What is the effect of UV on viruses

A

Inactivates them

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8
Q

What do ether and chloroform do for viruses

A

Inactivates ENVELOPED viruses because of the lipid membrane

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9
Q

Name some chemical agents that inactivate viruses

A

Reducing and Oxidising agents like chlorine, iodine, hydrogen peroxide, formaldehyde

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10
Q

What ingredient in household bleach inactivates viruses?

A

Hypochlorite.

Glutaraldehyde as well, though that isn’t really found in bleach

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11
Q

Where does viral multiplication tend to occur?

A

Local epithelium and lymphoid tissue before spreading to the regional lymph nodes and causing transient viraemia

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12
Q

What is Guillan-Barre syndrome?

A

Post-infectious neurological syndrome whereby anti-viral (anti-bacterial as well!) antibodies attack neurological tissue

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13
Q

What points to note in isolating a virus infection?

A

Collect in the first few days of illness because viraemia is transient

Use specific virus transport medium

If blood, heparinise it to prevent clotting. If CSF or stool sample, it can be sent plain

Can be stored in freezer, except respiratory syncytial virus

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14
Q

What is the concept of paired sera for IgM?

A

IgM indicates acute infection

Paired:
First - Acute, at the start of the illness
Second - Convalescent, 2-3 weeks later

Look out for change in antibody titre

Do not freeze the blood collected

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15
Q

How can microscopes look at viruses?

A

Electron microscopes

Inclusion bodies in cells

Immunofluorescent monoclonal antibodies that detect viral antigens

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16
Q

Viruses can be cultivated in what kinds of media?

A

Cell cultures, organ cultures, hen eggs, animals

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17
Q

What rise in titre is significant to show recent infection?

A

IgM in paired sera increases fourfold

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18
Q

What are some common tests done to identify / detect viruses?

A

ART

PCR

Paired sera

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19
Q

Measles is part of what kind of group?

A

Paramyxovirus!

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20
Q

Outline measles

A

Paramyxovirus

Children would get it by age 5 if unvaccinated.

Viraemia is common

Replicates in the skin and respiratory epithelium

R0 = 15
95-97% immunity is the target

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21
Q

Outline disease caused by measles

A

Prodromal - Characteristic Koplik’s spots (salt and pepper appearance) around parotid duct. This precedes maculopapular rash that spreads from face to, eventually, the entire body

Hypopigmentation of skin, but not permanent. Only lasts the duration of infection

Infection of the mucosa - Conjunctivitis, otitis media

Respiratory - Bronchopneumonia, giant cell pneumonia (rare but very bad in immunocompromised or malnourished pts)

GI - Diarrhoea. Could be because of the virus itself, or a secondary bacterial infection

CNS - Encephalitis that has high mortality

Sub-acute Sclerosing Panencephalitis (SSPE) - Develops over months or years after an apparent recovery. Likely due to latent measles virus in the neurones that reinfects when the immune system weakens. This leads to myoclonic seizures, intellectual deterioration, SUPPRESSION BURST pattern in EEG. RAPIDLY FATAL

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22
Q

Diagnosis of measles?

A

RT-PCR (Reverse Transcriptase)

Serology (IgM for acute, IgG for retrospective)

Once infected, the immunity is lifelong

Cell culture -> Isolate virus from the pharynx or conjunctiva and then infect monkey kidney cells -> Look for giant cells

23
Q

Treatment of measles?

A

MMR LIVE VACCINE (C/I in malnoursihed and immunocompromised children. C/I in pregnant women!!!)

Highly effective vaccine but if you cannot take it, immune gammaglobulin is a good way to get passive immunity

24
Q

Outline mumps

A

Paramyxovirus that can hit between 5-15y/o in unvaccinated kids

Incubation of 2-3weeks

25
Disease caused by Mumps?
Tender cervical lymphadenopathy usually bilateral that gives a bull-neck appearance Enlarged and painful salivary gland, worsened by eating. Particularly the parotid gland Fever and malaise Other complications that occur more commonly in adults: - Aseptic meningitis that is common but mild. It is called aseptic because you can’t grow bacteria from it - Orchitis. Painful testicular swelling in 10-25% of post-pubertal mumps. May cause subfertility if bilateral but if unilateral it’s usually fine - Pancreatitis in 10% of cases!
26
Diagnosis of mumps?
RT-PCR from the saliva, throat washings, urine, CSF IgM / IgG for acute / retrospective diagnosis Under a microscope, CPE may also be observed like rounding of cells and eosinophilic inclusions Cultures can be grown with cell lines or hen eggs, though uncommon
27
Outline the MMR vaccine
Live, attenuated vaccien that is given at 12 months with a second dose at 15 months Covers Measles, Mumps, Rubella It is recommended for pre-adolescents who are unimmunised and HAVEN’T BEEN INFECTED BEFORE C/I in immunocompromised because the vaccine is live!
28
Outline Rubella
Rubivirus from the togavirus family Has a small RNA. Enveloped and cubic symmetry Rubella has ONE phenotype. You only get infected once and then have lifelong immunity. Transmission via inhalation of respiratory droplets; Replicates later in the respiratory epithelium + lymph nodes to go on to cause viraemia 2-3 week incubation
29
Outline disease caused by Rubella
Prodrome of malaise, headache, fever, conjunctivitis, cough, LYMPHADENOPATHY, coryza (nasal congestion) Forschheimer’s spots are characteristic spots on the palate that precede a maculopapular skin rash that extends from the face to the trunk. The rash can vary from discrete to a geographic pattern distribution The rash moves from upper body then to the lower body after 3 days After the rash subsides, there is painful arthritis that involves the knee, wrist, finger joints. Encephalitis - Uncommon, but occasionally fatal Purpura because of thrombocytopenia and increased haemorrhaging tendency **Congenital Rubella Syndrome** Highly teratogenic, especially if mother caught the virus in first trimester of pregnancy (1/3 chance of CRS; odds drop as the months go on) CRS = Virus crosses placenta to dmaage any organ. Can lead to: Ocular lesions - Cataracts, retinopathy, micro-ophthalmia Ototoxicity - Sensorineural deafness CNS - Microcephaly, mental retardation CVSRESPI - PDA, VSD, Pulmonary stenosis, inflamed lung Pancreatic damage resulting in DM! Hepatosplenomegaly Ostitis Thrombocytopaenia Stillbirth / Spontaneous abortion
30
How do you diagnose rubella?
RT-PCR Serology 1 month after the rash appears Included in the TORCH panel
31
What is the TORCHES panel of tests?
Toxoplasma Rubella CMV (Cytomegalovirus) Herpes Syphilis
32
How do you manage rubella?
Aside from the MMR vaccine, quarantine and screen close contacts, ESPECIALLY pregnant women antenatally
33
Who is C/I for the MMR vaccine?
PREGNANT WOMEN IMMUNOCOMPROMISED Women should avoid getting pregnant within 3 months of getting the vaccine
34
What are the 3 complications of mumps aside from the bullneck and salivary gland enlargement
Aseptic meningitis Orchitis (no problem in unilateral, subfertility in bilateral) in 10-25% of postpubertal mumps Pancreatitis in 10% (Acronym: PAO. You get fat from SALIVATING before eating PAO and therefore a double chin hence the bullneck)
35
What virus has only one phenotype?
Rubella
36
Difference between Koplik’s spots and Forschheimer’s spots?
Koplik’s spots are salt and pepper around the parotid glands. Characteristic of Measles Forschheimer’s spots are rose spots on the palate that precede a maculopapular skin rash in Rubella
37
Aside from CRS, what are the complications of Rubella?
Arthritis and joint pain that follows the maculopapular rash Encephalitis - Uncommon and mainly hits adults but can be fatal Purpura - Thrombocytopenia and increased hemorrhagic tendency
38
Outline HIV structure
Retrovirus Enveloped 2 x Positive ssRNA Envelope has GP120 (glycoprotein) exposed to the external environment and GP41 embedded in the membrane. Together they make GP160! There’s a capsid inside the envelope with 2x positive ssRNA, integrase enzyme, reverse transcriptase, protease
39
How many HIV genotypes?
HIV1 - Most parts of the world HIV2 - Western Africa
40
HIV is linked closely to which virus?
Simian immunodeficiency virus
41
GP120 binds to _ receptor
CD4 receptor
42
What is the receptor on T cells that detects MHCII?
T Cell Receptor NOT CD4, though that is a molecule expressed by the cell
43
Dengue is part of what family?
Flavivirus
44
Outline structure of dengue
Flavivirus 4 serotypes (1,2,3,4) Spherical, enveloped ssRNA
45
What is characteristic of dengue fever?
Abrupt onset, high fever UNDIFFERENTIATED FEVER Muscle and joint pains Rash Pain behind eyes is very classical of dengue
46
What are different manifestations of dengue?
Asymptomatic Symptomatic: - Undifferentiated fever - Dengue fever - **DHF / DSS**
47
Outline haemorrhagic manifestations of dengue
Petechiae, Purpura, Ecchymosis Epistaxis, Gum bleeding Haematemesis, Melaena POSITIVE TOURNIQUET TEST! (Pump a BP cuff between systolic and diastolic; Downstream petechiae will form)
48
What is the pulse pressure in DSS?
_<20mmHg or general hypotension The pulse is rapid and weak because of cold, clammy skin as well restlessness
49
Outline DSS
Occurs between day 3 - 7 and comes after the fever. There is shock due to widespread increase in vascular permeability and increased extravasation of plasma BE CONCERNED ABOUT DSS WHEN THERE’S ACUTE ABDOMINAL PAIN SHORTLY BEFORE ONSET OF SHOCK (also see - restlessness, lethargy, cold extremities, oliguria, skin congestion) Pt may die within 12-24 hours of developing DSS or recover if you give the right therapy Thrombocytopaenia usually occurs too (100,000/mm3 or less), as well as a rise in haematocrit
50
Outline severe dengue
DSS Fluid accumulation with respiratory distress Severe bleeding LIVER DAMAGE! Raised AST ALT CNS - Impaired consciousness Heart also affected by drop in perfusion
51
How do you manage DHF / DSS
Infusion of plasma / plasma expander / electrolyte solution AVOID salicylates for pain / pyrexia such as aspirin. Give paracetamol instead
52
First infection vs. Second infection of dengue?
First - IgM produced transiently at first. This is a neutralising antibody. Rise in IgG titre later on. Partial protection to other dengue serotypes for 3-6 weeks Second - The infecting serotype is different from the first infection! There is consequently an IgG antibody that may enhance the infection After 2nd infection the patient is well protected against the disease
53
Why does DHF / DSS occur?
Some strains of dengue just cause more severe complications because they are more virulent OR Immune enhancement by INFECTION-ENHANCING ANTIBODIES
54
In what group of patients does DSS occur?
Babies <1y/o that are on their first infection Children >1y/o incl. adults that are on their second infection

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