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21 Cards in this Set

  • Front
  • Back
HAV
Picornavirus
Naked
Accute
Fulminant
HBV
Hepadnavirus
Envelope
Accute to Chronic
Fulminant
HCV
Flavivirus
Envelope
Accute to Chronic
Fulminant
HDV
Deltavirus
Envelope
Accute to Chronic
Fulminant
HEV
Calicivirus
Naked
Accute
Fulminant
HGV etc
Flavivirus
Envelope
Chronic
? if fulminant
HAV structure
- same as poliovirus (but does NOT inactivate host cell protein that associates with capped mRNAs)
- Non-enveloped, icosahedral
- 60 capsomers ( w/ VP1, VP2, VP3, VP4)
HAV genome
- + sense, ssRNA that functions as mRNA
- translated as one ORF into polyprotein then processed by viral-coded proteases
HAV translation
- NTRs at the 5’ and 3’ ends.
- 5’ end not capped
- translation from ribosomes that enter at IRES in 5’ NTR
- Viral protein VPg covalently linked at 5’ and does RNA replication, and packaging, uncoating and penetration
HAV-infected hepatocyte
- translation of host mRNAs by usual cap-dependent process
- translation of viral mRNAs by CAP-independent process via IRES in 5’ NTR
- not cytolytic
- replication doesn't overstress the hepatocyte
- IRES not efficient at loading host ribosomes
HAV Diagnosis
- serology for anti-HAV specific IgM
- detection of an immune response at same time as onset of clinical symptoms implies immunopathogenesis
HAV pathogenesis
- likely a GI site for primary replication ⇒ liver by viremia
- hepatocytes probably damaged by cytotoxic T and leads to release of virus into blood,
- no chronic carrier state, lifelong immunity
- no progression to carcinoma
HAV immune response
- humoral IgM - later supplanted by IgG
- CMI responds with cytotoxic lymphocytes
- clinical symptoms after viral shedding stops(immune response) - serum ALT, AST rise
- all infected cells cleared from liver and replaced by new
- resolution ⇒ recovery ⇒ immunity
- in young, asymptomatic ⇒ response of less mature CMI??
HAV epi
- HUMANS ONLY RESERVIOR
- hard to control since virus SHEDS IN FECES FOR 2 WEEKS BEFORE SYMPTOMS
- most mild or asymptomatic
- STABLE IN ENVIRONMENT
- spread person to person via FECAL-ORAL spread during sex, esp anal sex
- problem day care centers
- fecal contam of source, esp water w/ shellfish
- in food if poor hygene or uncooked fruits or gebbies
HAV treatment
- practice proper hygiene
- Vaccine, need 2-3 doses of killed - recommended for travelers
- required for some school entry, given to children at ≥ age 2
- no drugs available
- used to give immune serum globulin to prevent effects, but now pooled gamma globulin is becoming low in anti-HAV
HEV structure
- + sense ssRNA; three ORFs - one translated as a polyprotein processed by a viral protease
- classified as a calicivirus (general similarity to HAV)
HEV clinical features
- fecal-oral spread - similar to HAV
- much higher incidence of fulminant hepatitis, with an especially high mortality (20%) in pregnant woman
HEV Pathogenesis
- no chronic carrier state
- no progression to hepatocellular carcinoma
HEV Epi
- similar to HAV
- endemic in 3rd world from contamination of water
- uncommon in US, only from going abroad
- important to ask about pregnancies
- its been found in US pigs, be careful w/ hog farms near water
HEV Diagnosis
- clinical signs combined with history and exclusion
- serology requires special tests (available through CDC)
HEV Treatment
- supportive treatment only (no anti-viral therapy)
- recombinant vaccines are still under development