Pathophysiology

Hepatitis A

Hepatitis A is a nonenveloped single-stranded RNA virus classified as the Hepatovir-us genus under the Picornaviridae family.1'4 The only host for the HAV is humans, with hepatic cells as the primary site for viral replication. As part of the viral degradation process, the HAV is released into the biliary system causing elevated concentrations of the virus in the feces.

Hepatitis B

Hepatitis B (also known as the Dane particle) belongs to the Hepadnaviridae family The HBV is a partially double-stranded DNA virus with a phospholipid layer containing hepatitis B surface antigen (HBsAg) that surrounds the nucleocapsid. The nuc-leocapsid contains the core protein that produces hepatitis B core antigen (HBcAg), which is undetectable in the serum. Hepatocellular injury from HBV is thought to be due to a cytotoxic immune reaction that occurs when HBcAg is expressed on the surface of the hepatic cells. Fortunately, antibodies against hepatitis B core antigen (anti-HBc) are measurable in the blood, where anti- HBc to immunoglobulin M (IgM) indicates active infection and anti-HBc to IgG relates to either chronic infection or possible immunity against HBV.

Viral replication occurs when hepatitis B envelope antigen (HBeAg) is present and circulating in the blood. The serum HBV DNA concentration is a measure of viral infectivity and quantifies viral replication. Once the hepatitis B infection resolves, antibodies against hepatitis B envelope (anti-HBe) and antibodies against hepatitis B surface antigen (anti-HBs) develop, and HBV DNA levels become undetectable. However, if these antibodies do not develop, then the likelihood of developing chronic hepatitis B increases. This is primarily dependent on the host's immune system at the time the infection was attained. In immunocompetent individuals, the disease resolves spontaneously in most cases with no further sequelae. In immunocompromised

persons, the infection is less likely to be eradicated. Natural History of Hepatitis B

The natural history of hepatitis B depends on the age at which infection is acquired. Chronic HBV occurs in less than 5% of those who are older than 5 years of age, whereas the rate is more than 90% in infants born to mothers infected with HBV. Approximately 90% of adults infected with HBV develop anti-HBs, which results in lifelong immunity. About 30% of adults with initial symptoms of HBV present with

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jaundice or fatigue, and about 0.5% exhibit fulminant hepatitis. ' Cirrhosis and HCC are the two major complications associated with chronic hepatitis B infections. Patients who develop cirrhosis have a higher mortality rate than those without this complication.11

Hepatitis C

Hepatitis C, first known as non-A, non-B hepatitis, is a bloodborne infection caused by a single-stranded RNA virus belonging to the Flaviviridae family and the Hepa-

civirus genus.13,16 It is theorized that structural and nonstructural (NS) peptides may be responsible for RNA viral replication, specifically the NS5 peptide. There are 11

genotypes (numbered 1-11) and more than 90 subtypes (genotypes 1a, 1b, 2a, 3b, etc.)

that are unique to hepatitis C.

Antibodies against HCV (anti-HCV) in the blood indicate infection with the HCV. If the infection persists for more than 6 months and viral replication is confirmed by HCV RNA levels, then the person has chronic hepatitis C. Chronic disease may be due to an ineffective host immune system against the HCV. Cytotoxic T lymphocytes are ineffective in eradicating the HCV, thus allowing persistent damage to hepatic cells. Therefore, immunocompromised individuals are less likely to eradicate the HCV.16

Natural History of Hepatitis C

Only 10% to 15% of patients have acute hepatitis C that resolves without any further sequelae. In more than 70% of cases, hepatitis C develops into a chronic disease that is asymptomatic in about 60% to 80% of patients.12,13 Approximately 70% of chronic HCV cases progress to mild, moderate, or severe hepatitis. Cirrhosis and its complications occur in 15% to 20% of patients infected with HCV. In 10% to 20% of cases, 20 to 40 years may elapse between the time of exposure and the development of cir-rhosis.12 Once cirrhosis is confirmed, the rate of developing HCC increases by 1% to 4% per year.12 Approximately 25% of patients infected with the HCV who develop cirrhosis ultimately die from the disease.13

Hepatitis D

Hepatitis D (originally called delta hepatitis) belongs to the genus Deltavirus of the Deltaviridae family.1 ,19 The HDV virion is a defective single-stranded circular RNA

virus that requires the presence of HBV for HDV viral replication. This is because the hepatitis D virus antigen (HDVAg) is coated by the HBsAg.

The mechanism of hepatic damage induced by HDV is undetermined, but it is known that replication of HDV cannot occur without HBV being present causing either coinfection (both hepatitis B and D infection occurring simultaneously) or superinfection (acquiring HDV after having longstanding disease with HBV).1 ,19

Hepatitis E

Hepatitis E is a nonenveloped single-stranded messenger RNA virus of unclassified genus.21 The HEV is similar to HAV in that the virus is found in contaminated feces, thus infecting people via the fecal-oral route. High HEV levels in the bile often prompt viral shedding in the feces. The severity of hepatic damage is dependent on

the HEV strain: Mex 14, Sar 55, or the US 2 strain. No cases of chronic hepatitis E have been documented.

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