Hepatitis A Virus (HAV)

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Viruses - RNA Viruses

Key Points

Hepatitis A virus (HAV)
- Transmission
  - Fecal oral
    - Occurs in crowded areas with poor sanitation (travelers, daycare)
      - Think: standard pattern for a lot of fecal-oral infections
    - Undercooked contaminated shellfish most commonly implicated in US
- Presentation
  - Acute Hepatitis
    - Occurs after short incubation period (~30 days)
    - Fever, jaundice, elevated ALT and AST, nausea/vomiting, abdominal pain
    - Aversion to smoking may be observed
    - Usually self-limiting in adults and asymptomatic in children
      - Usually resolves completely within 2 months
      - No carrier state
    - Good prognosis → no HCC risk
- Diagnosis
  - Anti-HAV IgM
    - indicates acute infection
    - RT-PCR of HAV RNA also used
  - Anti-HAV IgG
    - indicates recovery/immunity
    - Due to prior HAV infection and/or vaccination
  - Liver biopsy
    - All viral hepatitis produce a similar histopathological pattern
    - Hepatocyte swelling (necrosis)
      - “Ballooning degeneration”, thought to be caused by ATP depletion and disruption of cytoskeleton
      - Hyperplasia may also occur due to regeneration of tissue (active cell replication) lost to viral damage
    - Monocyte infiltration
      - Occurs due to viral infection and hepatocyte necrosis
    - Councilman bodies
      - Apoptotic bodies form round pink (eosinophilic) bodies known as Councilman bodies
- Treatment
  - None; Usually self-limiting
- Vaccination
  - killed (inactivated) vaccine