L49: Medically Important Viruses Flashcards

1
Q

Picornavirus (big family)

A
  1. Enterovirus:
    - Rhinovirus (Respiratory route, URT infection)
    - Enterovirus (GI/faecal-oral route, systemic infection e.g. poliovirus)
  2. Paraechovirus
  3. Hepatovirus
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2
Q

Pathogenesis of Enterovirus

A
  • no lipid envelope
  • Stability in environment: can survive external environment, gastric acidity and faecal enzyme
  • Asymptomatic infection (Iceberg effect): multiply in intestinal lymphoid tissue, remain undetected and can still transmit from asymptomatic persons
  • Flu-like illness: viraemia —> fever
  • Full disease syndrome: organ dysfunction: poliomyelitis, meningitis, encephalitis, myocarditis
  • DO NOT cause diarrhoea
  • Once recover immunity is lifelong, no mechanisms for persistence
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3
Q

Enterovirus 71

A

Hand,foot and mouth disease

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4
Q

Polio vaccine

A

Type 1, 2, 3 (type 2 + 3 now eradicated)

Multivalent (Type 1, 2, 3)

  1. Oral live attenuated (one live virus each time, at least 3 doses)
    - easy to administer, mucosal immunity —> block transmission
    - virulence reversion
    - now type 2 oral vaccine removed —> IPV only
  2. Killed (3 dose: primary, secondary and booster)
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5
Q

Pathogenesis of Herpesviridae

A
  • double stranded DNA virus
  • Enveloped
  • Virus latency (within any level of spinal cord): Once infected —> always infected
  • Viral genome: integrated / episomal
  • Genome not completely expressed
  • Viral antigens not visible on cell surface: evade host immune mechanism
  • Trigger from latency to full replication (from time to time): Lysogenic cycle —> Lytic cycle —> can spread to others
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6
Q

Herpes simplex type 1 vs Herpes simplex type 2

A

HSV1 (above waist)

  • Often asymptomatic
  • Mild oral lesions to severe stomatitis
  • Herpetic whitlow
  • macule vs papule
  • vesicle vs pustule
  • ulcer

HSV2 (below waist)
- genital herpes

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7
Q

Primary infection and recurrence of HSV and VZV

A

Primary
HSV: mild pharyngitis, fever, genital herpes
VZV: chickenpox

Recurrence (depends on latency in which level of spinal cord)
HSV: cold sore, genital herpes
VZV: shingles / herpes zoster

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8
Q

Pathogenesis of Influenza virus

A
  • Type A, B, C
  • RNA virus (single stranded, negative sense)
  • segmented genome
  • Haemagglutinin H1-H16: bind to sialic acid on host cells
  • Neuraminidase N1-N9: cleaves Terminal sialic acid —> virus release
  • Antigenic drift and Antigenic shift
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9
Q

Antiviral drugs (4 classes)

A
  1. Amantadine/ Rimantadine: Block virus uncoating
  2. Oseltamivir, Zanamivir: Neuraminidase inhibitor
  3. Baloxavir marboxil: cap-dependent endonuclease inhibitor (interfere with replication process)
    (4. Favipiravir: polymerase inhibitor)
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10
Q

Symptoms of flu

A

Often caused by cytokines by host immune system (not the virus going to different body parts)

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11
Q

Host immunity

A
  • Cell-mediated response: helps recovery

- Humoral response: Antibody bind to Neuraminidase and Haemaglutinin —> neutralises infectivity

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12
Q

Antigenic Drift vs Antigenic Shift

A

Drift: Minor antigenic change from MUTATION since RNA polymerase lack proof reading mechanism

Shift: Complete change of H and N antigen due to GENETIC REASSORTMENT: mixing of 2 viral genes (human and animals)

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13
Q

Prevention of influenza

A
  1. Vaccine: need to identify new antigenic drift variants
  2. Antiviral: Oseltamivir / Zanamivir (Amantadine / Rimantadine not used anymore)
  3. Hygiene
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