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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
Q

Disease caused by Mumps?

A

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
Q

Diagnosis of mumps?

A

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
Q

Outline the MMR vaccine

A

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
Q

Outline Rubella

A

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
Q

Outline disease caused by Rubella

A

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
Q

How do you diagnose rubella?

A

RT-PCR
Serology 1 month after the rash appears

Included in the TORCH panel

31
Q

What is the TORCHES panel of tests?

A

Toxoplasma
Rubella
CMV (Cytomegalovirus)
Herpes
Syphilis

32
Q

How do you manage rubella?

A

Aside from the MMR vaccine, quarantine and screen close contacts, ESPECIALLY pregnant women antenatally

33
Q

Who is C/I for the MMR vaccine?

A

PREGNANT WOMEN
IMMUNOCOMPROMISED

Women should avoid getting pregnant within 3 months of getting the vaccine

34
Q

What are the 3 complications of mumps aside from the bullneck and salivary gland enlargement

A

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
Q

What virus has only one phenotype?

A

Rubella

36
Q

Difference between Koplik’s spots and Forschheimer’s spots?

A

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
Q

Aside from CRS, what are the complications of Rubella?

A

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
Q

Outline HIV structure

A

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
Q

How many HIV genotypes?

A

HIV1 - Most parts of the world
HIV2 - Western Africa

40
Q

HIV is linked closely to which virus?

A

Simian immunodeficiency virus

41
Q

GP120 binds to _ receptor

A

CD4 receptor

42
Q

What is the receptor on T cells that detects MHCII?

A

T Cell Receptor

NOT CD4, though that is a molecule expressed by the cell

43
Q

Dengue is part of what family?

A

Flavivirus

44
Q

Outline structure of dengue

A

Flavivirus
4 serotypes (1,2,3,4)

Spherical, enveloped

ssRNA

45
Q

What is characteristic of dengue fever?

A

Abrupt onset, high fever
UNDIFFERENTIATED FEVER
Muscle and joint pains
Rash

Pain behind eyes is very classical of dengue

46
Q

What are different manifestations of dengue?

A

Asymptomatic

Symptomatic:
- Undifferentiated fever
- Dengue fever
- DHF / DSS

47
Q

Outline haemorrhagic manifestations of dengue

A

Petechiae, Purpura, Ecchymosis

Epistaxis, Gum bleeding

Haematemesis, Melaena

POSITIVE TOURNIQUET TEST! (Pump a BP cuff between systolic and diastolic; Downstream petechiae will form)

48
Q

What is the pulse pressure in DSS?

A

_<20mmHg or general hypotension

The pulse is rapid and weak because of cold, clammy skin as well restlessness

49
Q

Outline DSS

A

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
Q

Outline severe dengue

A

DSS
Fluid accumulation with respiratory distress

Severe bleeding

LIVER DAMAGE! Raised AST ALT

CNS - Impaired consciousness

Heart also affected by drop in perfusion

51
Q

How do you manage DHF / DSS

A

Infusion of plasma / plasma expander / electrolyte solution

AVOID salicylates for pain / pyrexia such as aspirin. Give paracetamol instead

52
Q

First infection vs. Second infection of dengue?

A

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
Q

Why does DHF / DSS occur?

A

Some strains of dengue just cause more severe complications because they are more virulent
OR
Immune enhancement by INFECTION-ENHANCING ANTIBODIES

54
Q

In what group of patients does DSS occur?

A

Babies <1y/o that are on their first infection

Children >1y/o incl. adults that are on their second infection

MicroB (4 decks)

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