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(+) 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

(+) Stranded RNA Viruses III

Hepatitis A, Hepatitis C, Hepatitis E, Hepatitis G

RNA Hepatitis Viruses

http://www.mgm.ufl.edu/faculty/dbloom.htm

hepatitis a hav
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
hepatitis a hav5
Hepatitis A (HAV)

Pathogenesis

  • Enters through the mouth (ingestion)
  • Multiplies in intestional epithelial cells
  • Bloodstream
  • Liver
hepatitis a hav7
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
hepatitis a hva
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)
hepatitis a hav9
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
hepatitis a hav10
Hepatitis A (HAV)

Clinical diagnosis

  • Based on time course of clinical symptoms
  • Anti-HAV IgM
hepatitis a hav11
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
hepatitis c hcv
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”
hepatitis c hcv16
Hepatitis C (HCV)

Pathogenesis

  • Bloodstream
  • Liver
hepatitis c hcv18
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
hepatitis c hcv19
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)
hepatitis c hcv20
Hepatitis C (HCV)

80% assymptomatic

20 % symptomatic

cirrhosis

  • In the U.S. HCV is a more important cause of cirrhosis than alcoholism
hepatitis c hcv21
Hepatitis C (HCV)

Clinical diagnosis

  • Based on time course of clinical symptoms
  • Anti-HCV IgM
hepatitis c hcv22
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
hepatitis e hev
Hepatitis E (HEV)

General Features

  • Calicivirus
    • Very labile virion
  • Fecal-oral transmission (mainly water-borne)
  • Mainly seen in under-developed countries
hepatitis e hev26
Hepatitis E (HEV)

Pathogenesis

  • Enters through the mouth (ingestion)
  • Multiplies in intestional epithelial cells
  • Bloodstream
  • Liver
hepatitis e hev28
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
hepatitis e hev29
Hepatitis E (HEV)

Pathogenesis (con’t)

  • Normal case-fatality rate is 0.5 - 3%
    • But 10- 20% in pregnant women
  • No chronic carrier state
hepatitis e hev30
Hepatitis E (HEV)

Clinical diagnosis

  • Exclusion of HAV and HBV
hepatitis e hev31
Hepatitis E (HEV)

Treatment/Prevention

  • Cook foods and avoid contaminated water when traveling to endemic regions
  • Ig from western countries not helpful
  • Vaccine?
hepatitis g hgv
Hepatitis G (HGV)

General Features

  • Flavivirus
  • Parenteral transmission (esp. i.v. drug use)
    • Sexual transmission?
  • Newly characterized NANBH
hepatitis g hgv35
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
hepatitis g hgv36
Hepatitis G (HGV)

Risk groups

  • Transfusion recipients
  • Injection drug users
  • Frequent co-infection with hepatitis C
hepatitis g hgv37
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