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(+) Stranded RNA Viruses III

(+) Stranded RNA Viruses III. Hepatitis A, Hepatitis C, Hepatitis E, Hepatitis G. RNA Hepatitis Viruses. http://www.mgm.ufl.edu/faculty/dbloom.htm. Comparison of Hepatitis Viruses. Hepatitis A (HAV). General Features. Picornavirus Acid stable, non-cytolytic

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(+) Stranded RNA Viruses III

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  1. (+) Stranded RNA Viruses III Hepatitis A, Hepatitis C, Hepatitis E, Hepatitis G RNA Hepatitis Viruses http://www.mgm.ufl.edu/faculty/dbloom.htm

  2. Comparison of Hepatitis Viruses

  3. Hepatitis A (HAV) General Features • Picornavirus • Acid stable, non-cytolytic • Enterically transmitted (fecal/oral route) • Often referred to as “infectious hepatitis” • Only a single serotype exists • Estimated to be the cause of 40% of acute hepatitis cases

  4. Hepatitis A (HAV) Pathogenesis • Enters through the mouth (ingestion) • Multiplies in intestional epithelial cells • Bloodstream • Liver

  5. Hepatitis A (HAV) Pathogenesis (con’t) • Virus is abundant in the feces (with some culturable from throat and saliva as well) • Incubation time is 4 weeks • Abrupt onset of symptoms (15 to 50 days p.I.) and intensify 4 to 6 days before icteric phase • By the time “dark urine” appears, most of the virus is gone • Clinical symptoms very similar to HBV (malaise, lethargy) but may be less severe

  6. Hepatitis A (HVA) Pathogenesis (con’t) • Most infections occur in children who are asymptomatic or anicteric(symptomatic without jaundice) • By the time “dark urine” appears, most of the virus is gone • Severity of the disease increases with age (2/3 of adult infections are icteric)

  7. Hepatitis A (HAV) Pathogenesis (con’t) • Overall case fatality rate is 0.5% (from liver failure) • 1/1000 will get fulminant liver disease (80% of these cases will be fatal) • Illness typically lasts 4 weeks (from onset of symptoms) • Virus is shed prior to onset of symptoms • There is no chronic carrier state

  8. Hepatitis A (HAV) Clinical diagnosis • Based on time course of clinical symptoms • Anti-HAV IgM

  9. Hepatitis A (HAV) Treatment/Prevention • Interruption of fecal-oral spread • Avoidance of contaminated water or food (undercooked shell fish) • Proper handwashing in day care and healthcare facilities • Prophylaxis with immune globulin before or early in incubation (< 2wks post exposure) is 80 - 90% effective • Killed vaccine is available for those at risk

  10. Hepatitis C (HCV) General Features • Flavivirus • One of the first NANBH viruses to be characterized • Parenteral transmission (esp. i.v. drug use) • Originally referred to as “non-A, non-B hepatitis”

  11. Hepatitis C (HCV) Pathogenesis • Bloodstream • Liver

  12. Hepatitis C (HCV) Pathogenesis (con’t) • Acute hepatitis C is clinically similar to HBV and HAV • Primarily spread via blood (and to lesser extent via sexual contact

  13. Hepatitis C (HCV) Differences: • 6 - 8 week incubation period • 75% of infections are sub-clinical • clinical infections are generally less severe than HBV • HVC has a higher incidence of chronic liver disease than HBV(50% of patients remain viremic for more than 1 year)

  14. Hepatitis C (HCV) 80% assymptomatic 20 % symptomatic cirrhosis • In the U.S. HCV is a more important cause of cirrhosis than alcoholism

  15. Hepatitis C (HCV) Clinical diagnosis • Based on time course of clinical symptoms • Anti-HCV IgM

  16. Hepatitis C (HCV) Treatment/Prevention • Poor homologous immunity makes a vaccine unlikely • Immune globulin not helpful • Alpha-interferon is the only reliable treatment and only moderately successful

  17. Hepatitis E (HEV) General Features • Calicivirus • Very labile virion • Fecal-oral transmission (mainly water-borne) • Mainly seen in under-developed countries

  18. Hepatitis E (HEV) Pathogenesis • Enters through the mouth (ingestion) • Multiplies in intestional epithelial cells • Bloodstream • Liver

  19. Hepatitis E (HEV) Pathogenesis (con’t) • 2 - 8 week incubation • Mostly sub-clinical in children • Acute hepatitis C is clinically similar to HAV • Except: • Bilirubin levels higher • Juandice is deeper and more prolonged

  20. Hepatitis E (HEV) Pathogenesis (con’t) • Normal case-fatality rate is 0.5 - 3% • But 10- 20% in pregnant women • No chronic carrier state

  21. Hepatitis E (HEV) Clinical diagnosis • Exclusion of HAV and HBV

  22. Hepatitis E (HEV) Treatment/Prevention • Cook foods and avoid contaminated water when traveling to endemic regions • Ig from western countries not helpful • Vaccine?

  23. Hepatitis G (HGV) General Features • Flavivirus • Parenteral transmission (esp. i.v. drug use) • Sexual transmission? • Newly characterized NANBH

  24. Hepatitis G (HGV) Pathogenesis • Estimated to cause 0.3% of acute viral hepatitis • 900 - 2000 infections per year, mostly asymptomatic • Chronic disease rare or may not occur

  25. Hepatitis G (HGV) Risk groups • Transfusion recipients • Injection drug users • Frequent co-infection with hepatitis C

  26. Hepatitis G (HGV) Prevention/treatment “Confirmation of disease association, determination of routes of transmission, and development of serologic screening assays are necessary before prevention measures can be considered” --CDC, August 1, 2000

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