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21 Cards in this Set
- Front
- Back
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HAV
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Picornavirus
Naked Accute Fulminant |
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HBV
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Hepadnavirus
Envelope Accute to Chronic Fulminant |
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HCV
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Flavivirus
Envelope Accute to Chronic Fulminant |
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HDV
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Deltavirus
Envelope Accute to Chronic Fulminant |
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HEV
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Calicivirus
Naked Accute Fulminant |
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HGV etc
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Flavivirus
Envelope Chronic ? if fulminant |
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HAV structure
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- 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) |
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HAV genome
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- + sense, ssRNA that functions as mRNA
- translated as one ORF into polyprotein then processed by viral-coded proteases |
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HAV translation
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- 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 |
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HAV-infected hepatocyte
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- 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 |
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HAV Diagnosis
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- serology for anti-HAV specific IgM
- detection of an immune response at same time as onset of clinical symptoms implies immunopathogenesis |
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HAV pathogenesis
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- 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 |
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HAV immune response
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- 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?? |
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HAV epi
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- 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 |
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HAV treatment
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- 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 |
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HEV structure
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- + sense ssRNA; three ORFs - one translated as a polyprotein processed by a viral protease
- classified as a calicivirus (general similarity to HAV) |
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HEV clinical features
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- fecal-oral spread - similar to HAV
- much higher incidence of fulminant hepatitis, with an especially high mortality (20%) in pregnant woman |
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HEV Pathogenesis
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- no chronic carrier state
- no progression to hepatocellular carcinoma |
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HEV Epi
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- 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 |
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HEV Diagnosis
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- clinical signs combined with history and exclusion
- serology requires special tests (available through CDC) |
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HEV Treatment
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- supportive treatment only (no anti-viral therapy)
- recombinant vaccines are still under development |
