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Hepatitis Viruses


VIRUS:
  • Hepatitis A, B, C


GENERAL CONCEPTS:
  • Type A hepatitis virus (HAV) is a member of the enterovirus group of Picornaviruses; Hepatitis B virus (HBV) is distinctly different and contains a DNA genome; Hepatitis C virus (HCV, also referred to as non-A, non-B or NANBH) is not well characterized but appears to contain an RNA genome and may belong in the Flavivirus group.
  • The disease caused by these agents is hepatitis, a generalized infection with inflammation and necrosis of the liver. The course of hepatitis may range from inapparent disease to chronic liver disease.


DISTINCTIVE PROPERTIES:
  • Hepatitis A: As a member of the Enterovirus group, HAV contains a linear, positive strand RNA genome. It is also known as Enterovirus type 72 and is resistant to heat and acid.
  • Hepatitis B: HBV contains a circular, partly double-stranded DNA genome 3200 nucleotides in length. Interestingly, a 600-2100 single-stranded region is contained in the DNA molecule. The particle contains a DNA-dependent DNA polymerase and a reverse transcriptase and replicates via an RNA intermediate. HBV possesses several antigens; the "Australian antigen" is associated with the surface (HBsAg), the "core antigen" (HBcAg) is internal and the "e antigen" (HBeAg) is part of the same capsid polypeptide as the HBcAg. All of these antigens elicit specific antibodies.
  • Hepatitis C: HCV (or NANBH) contains a positive stranded RNA genome and is related to the Flaviviruses.


PATHOGENESIS:
  • Hepatitis A: Clinical presentation of HAV infection varies from subclinical and mild in children to jaundice in adults. The virus usually enters by intestinal infection (fecal-oral transmission), spreads via the blood to the liver, which is its target organ. HAV is detectible in the feces during the incubation period (average 4 weeks), preceding a rise in serum levels of aminotransferase enzymes and the occurrence of pathologic changes in the liver. Most disease resolves within two weeks. Chronicity or fulminant hepatitis is rare.
  • Hepatitis B: HBV, in contrast, may produce a persistent carrier state in addition to liver damage. Infection early in life often produces a carrier state, but only about 5-10% of cases if infection occurs later. Most disease is acquired via the parenteral route (blood transfusions. There are generally two patterns of HBV-associated disease:
    1. Chronic persistent: Infections are generally asymptomatic with a mild elevation of serum alanine transaminase (ALT) and little liver fibrosis.
    2. Chronic active: Infections produce jaundice with elevated ALT levels, liver damage and cirrhosis. Liver failure may predispose those affected to cancer.
  • Hepatitis C: HCV may also produce a persistent carrier state, a higher level of chronic disease and cirrhosis. At least 50% of HCV infections result from blood transfusion.
  • The following table outlines some of the differences between the Hepatitis viruses:
Hepatitis A Hepatitis B Hepatitis C
Genome +RNA DNA +RNA
Onset Abrupt Insidious Insidious
Transmission Fecal-Oral Parenteral Parenteral
Incubation (days) 15-40 60-180 28-112
Asymptomatic infection usual common common
Carrier State no yes yes
Chronicity 0% 10% 30-60%
Sequelae no cirrhosis cirrhosis

HOST DEFENSES:
  • Hepatitis A: Antibody usually develops late in the infection; IgM after a week, IgG later. These help to clear virus from the body via complement and antibody-dependent cell-mediated cytotoxicity, which may account for some of the liver damage.
  • Hepatitis B: Antibody and the cell-mediated responses are induced but do not seem to protect against infection and probably cause autoimmune responses (liver damage may relate to the host immune response). The possibility of immune complexes with surface antigen can also lead to immune complex disease.
  • Hepatitis C: Little is known about host defenses against this agent but immune serum does not seem to be an effective prophylactic remedy. Probably a combination of humoral and cell-mediated defenses are important.


EPIDEMIOLOGY:
  • Infectious hepatitis (HAV) is endemic throughout the world, but the incidence is difficult to estimate because many cases are subclinical. HAV has a low mortality but patients may be incapacitated for several weeks. It is spread via the fecal-oral route, person to person and reflects conditions of poor sanitation and overcrowding. The virus may be shed in the feces but there is no carrier state or progression to chronic liver disease.
  • Serum hepatitis (HBV, HCV) is generally passed via blood, unsterile syringes, transfusions, etc. A carrier state can occur; in North America and Europe, the rate is about 0.1%. The rate increases to about 25-30% in Africa, Asia and the Pacific.


DIAGNOSIS:
  • Clinical: Clinical diagnosis depends on the symptomology, which may include fever, malaise, headache, dark-colored urine and jaundice.
  • Laboratory: Serology is the best method for determining infection.


CONTROL:
  • Sanitary: HAV infection may be prevented by ensuring a safe water supply; HBV and HCV may be prevented by testing the blood supply.
  • Immunological: Human immunoglobulin prevents or attenuates HAV and vaccines are under study. A vaccine for HBV is available and effective. A vaccine against HCV is under study.
  • Chemotherapeutic: None.

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