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Infection & Immunity > Viruses > Flashcards

Viruses Flashcards

0
Q

Outline the steps of viral replication of enveloped and non-enveloped viruses.

A

Enveloped viruses:

  1. Attachment
  2. Uncoating (removal of envelope)
  3. Replication (in host nucleus)
  4. Assembly
  5. Budding (bud contains new virus particles)

Non-enveloped viruses:

  1. Entry
  2. Uncoating
  3. Replication
  4. Assembly
  5. Rupture (host cell bursts, releasing viral particles)
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1
Q

Define virus. How are viruses classified?

A

Infectious agent that is minimally constructed from a genome (RNA or DNA) and a capsid, capable of replication only in living cells

i.e. obligate intracellular parasite

Baltimore classification: type & structure of viral nucleic acid, strategy used in replication, symmetry of capsid (helix or icosahedron), presence of lipid envelope

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2
Q

What is the structure of HIV? How is it transmitted?

A

ss+ RNA retrovirus (integrates genome into host cell DNA randomly using reverse transcriptase)

Transmission: sexual, percutaneous - blood, IV drug use, sharps, tattoos, vertical transmission

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3
Q

Outline the pathogenesis of HIV infection.

A
  1. Long incubation with rapid seroconversion - production of specific antibodies (within weeks).

Usually asymptomatic but is evident in some patients -> AIDS seroconversion illness (usually resolves in 2-3 weeks, possibly indicates an increased risk for an accelerated disease progression)

S&S:

  • acute viral infective indicative symptoms e.g. fever, malaise, arthralgia, headache, sore throat, lymphadenopathy
  • neurological (early invasion of nervous system): meningitis, encephalitis, peripheral neuropathy, myelopathy
  • non-specific erythematous maculopapular rash (flushed, has flat areas of altered skin colour and small raised spots) on the palms and soles (25% of AIDS seroconversion illness patients)
  • exanthema (rash/eruption) on soft palate
  1. Progressive loss of CD4+ T-cells causing immunodeficiency - AIDS which exposes the patient to opportunistic infections & malignancies

e.g. Kaposi’s sarcoma (malignant tumour of blood vessels in skin)
e.g. advanced oral hairy leukoplakia (OHL)
e.g. oral pseudomembranous candidiasis
etc.

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4
Q

How can HIV be diagnosed?

A

Culture from circulating mononuclear cells
Antigen detection by PCR (can be detected prior to seroconversion)
ELISA
Western blot/immunoassay (risk of false-positive e.g. antibodies released in pregnancy/immune disease)

Total anti-HIV antibody indicates presence of HIV

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5
Q

What is the treatment and management of HIV+ve patients?

A

HAART = highly active anti-retroviral therapy

  • NRTIs: nucleoside reverse transcriptase inhibitors
  • non-NRTIs (NNRTIs)
  • protease inhibitors
  • fusion inhibitors
  • integrase inhibitors
  • co-receptor/entry inhibitors (prevent binding to/fusion with membrane of CD4+ cells)

note: new anti-retrovirals often required due to rapid recombination of genome by HIV (although this can sometimes reverse drug resistance or reduce the replication rate of the virus)
note: drug resistant HIV “archived” in body (HIV strains remain latent in lymph nodes and can be reactivated)

note: impossible to cure someone of HIV after the virus has integrated its genome into host cell DNA (drugs will just slow the spread of infection and reduce the replication rate)
* Berlin patient cured by bone marrow transplantation from an individual with a mutation of their WBC receptors (but the virus can mutate and start using a different receptor to circumvent this)

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6
Q

What are elite controllers of HIV?

A

Able to maintain a high CD4+ count & low (but detectable) viral load for many years without antiretroviral therapy

Also known as longterm non-progressors

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7
Q

What is the structure and mode of transmission of hepatitis B?

A

enveloped ds DNA (but uses reverse transcriptase)

Transmission: vertical, sexual, percutaneous (blood, IV drug use, sharps, tattoos)

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8
Q

Outline the pathogenesis of hepatitis B.

A

Incubation period: 2-6 months (can be acute only, or can progress to chronic)

ACUTE:

  • febrile: fever, malaise, nausea, myalgia,
  • anorexia
  • liver: jaundice, bilirubinuria, enlarged & tender liver

CHRONIC: ?

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9
Q

How is hepatitis B diagnosed, and how is acute differentiated from chronic in terms of biomarkers?

A

anti-HBe antibodies = how infective you are

anti-HBc IgG = marker of presence of infection (or vaccination)

anti-HBc IgM = acute infection (disappears after period of acute infection, reappears in chronic active hepatitis)

HBsAg = infectious (decreases over time in acute, remains high in chronic)

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10
Q

What form is the vaccination for hepatitis B?

A

3 doses of recombinant version of HBsAg

PEP: HBIg (hyperimmunoglobulin) (given for needle-stick injuries/newborns born from HBsAg+ve mothers)

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11
Q

What is the treatment/management for hepatitis B?

A

Antivirals (reduce Hep. B DNA & initiates seroconversion to anti-HBe)

  • interferon-alpha
  • entecavir
  • terofovir
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12
Q

Outline the pathogenesis of hepatitis D?

A

Coinfects with hepatitis B (requires envelope)

Causes severe acute disease (coinfection) or severe chronic liver disease (superinfection)

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13
Q

What is the structure and method of transmission of hepatitis C? What is the post-exposure prophylaxis? Outline the pathogenesis.

A

enveloped, ss+ RNA

Transmission: vertical, sexual, percutaneous (blood, IV drug use, sharps, tattoos)

PEP: immunoglobulin X (no vaccine)

Acute = mild/asymptomatic 
Chronic = liver cirrhosis & hepatocellular carcinoma
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14
Q

Outline the structure, replication, transmission, diagnosis, clinical presentation, and treatment of adenovirus infection.

A

STRUCTURE: non-enveloped dsDNA

REPLICATION: lytic; in epithelial cells usually

TRANSMISSION:

  • direct e.g. conjunctiva
  • faecal-oral —> GI disease
  • aerosol —> respiratory disease
  • exposure to infected tissue/blood

DIAGNOSIS:

  • antigen detection
  • PCR assay
  • virus isolation serology

CLINICAL:

  • pharyngo(conjunctival) fever = pharyngitis +/- conjunctivitis —> viral pneumonia
    (note: Centor score calculates probability that pharyngitis is Streptococcal according to age and symptoms)
  • follicular conjunctivitis/epidemic keratoconjunctivitis
  • viral diarrhoeal disease (children)
    etc.

Treatment: none (vaccine only available in U.S. military)

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15
Q

Outline the structure, replication, transmission, diagnosis, clinical presentation, and treatment of infleunza A infection.

A

STRUCTURE = enveloped RNA, ss-ve

REPLICATION = budding

TRANSMISSION = direct contact, aerosol, fomite (object capable of carrying infectious organism)

DIAGNOSIS = gold standard is isolation of virus from nasopharyngeal washings, or can detect viral RNA by RT-PCR, or can detect viral antigens

CLINICAL PRESENTATION =

  • non productive cough
  • chills
  • high fever
  • muscle aches
  • drowsiness
  • runny nose is unusual (differentiate ‘flu and common cold)

TREATMENT =

  • early: amantadine/rimantadine (prevent viral uncoating)
  • zanamivir/oseltamivir (inhibit viral neuraminidase)
  • ‘flu vaccine (children, elderly, healthcare workers)

note: Reye syndrome is a rare complication in children that can manifest (e.g. if you give aspirin - therefore give acetaminophen to children with fevers of unknown origin)

16
Q

How can influenza A be subtyped?

A

Antigens associated with outer viral proteins

Haemagglutinin

Neuraminidase

e.g. H1N1 = swine flu

17
Q

What is antigenic drift? How does it compare to antigenic shift?

A

Antigenic drift = minor antigenic changes in haemagglutinin & neuraminidase proteins due to random mutations in viral RNA
(occurs every year, viral subtype does not change, antibodies will not work as well due to change in binding sites)

Antigenic shift = combination of viral strains in cell infected by two viruses which creates a new strain/subtype due to the reassortment of viral RNA
(infrequent, e.g. H1N1, H5N1)

18
Q

Outline the structure, replication, transmission, diagnosis, clinical presentation, and treatment of varicella-zoster virus.

A

STRUCTURE = enveloped dsDNA (herpes virus)

REPLICATION =

  • primary round of replication: infect respiratory mucosa and spread to regional lymph nodes and through bloodstream
  • secondary round of replication: multiply in liver and spleen; disseminated throughout body by infected mononuclear leukocytes

TRANSMISSION = aerosol

DIAGNOSIS = usually based on clinical presentation, but can use DNA PCR

CLINICAL PRESENTATION = 
Chickenpox (primary infection):  
- fever 
- malaise 
- headache 
- abdominal pain
- exanthem (vesicular rash) -> itchy

Shingles (secondary infection - latent virus in dorsal root ganglia reactivated):

  • dermatomal distribution of vesicular lesions
  • postherpetic neuralgia (pain)

TREATMENT = (shingles)
IV acyclovir/famciclovir/valacyclovir to reduce healing time/lesion formation (therefore reduce postherpetic neuralgia burden)

19
Q

What is impetigo? How is it treated?

A

Highly infectious skin disease commonly affecting the face and limbs

Causative organism classically Strep. pyogenes (but Staph. aureus more commonly implicated now)

Topical agent e.g. mupirocin or penicillin/cephalosporin

20
Q

Give some examples of diseases caused by Staph. aureus infection.

A

Septicaemia (toxic shock syndrome)
Pneumonia
Localised skin infections e.g. folliculitis, furuncles (boils), impetigo
Deep localised infections e.g. septic joint, bone marrow
Acute endocarditis
Gastroenteritis
Scalded skin syndrome

21
Q

What are some of the virulence factors of Staph. aureus?

A

Fibronectin binding proteins (promotes binding to mucosal cell matrices)

Enzymes inc. coagulase, catalase, hyaluronidase, fibrinolysin

Slime production

Cytolytic exotoxins (haemolysins)

Antiphagocytic binding to IgG

Superantigen exotoxins (bind to T-cell receptor-MHCII complex —> enhances T-lymphocyte response —> large amount of T-cell cytokines released —> toxic shock syndrome)

Infection & Immunity (13 decks)

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