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Hepatitis B (HBV) has been known to be separate from Hepatitis A since the 1940´s. Verification is by specific serologic test since the signs and symptoms are the same for all types of acute hepatitis. Once called serum hepatitis, the virus is blood-borne and is transmitted by percutaneous and mucosal exposure to infectious body fluids. Hepatitis B is caused by infection with the hepatitis B virus (HBV), a double stranded DNA hepadnaviridae virus. The virus is replicated in the liver and high concentrations of the virus are found in the blood. The surface of the virus contains the hepatitis B antigen (HBsAg). Antibody to HBsAg is available and protects against infection. Finding antibody to the core antigen confirms HBV infection. The incubation period ranges from 45 to 160 days with an average of 120 days. Clinical manifestations are somewhat age-dependent with symptoms occurring more often in adults. Still, approximately 50% of adults with acute HBV infection are asymptomatic. In general, newborns do not develop any clinical signs and infection produces typical illness in only 5% to 15% of children aged 1 to 5 years. Fulminant hepatitis occurs in 1 to 2% of acute cases and those have a case-fatality rate of 63% to 93%. When symptoms do present, the clinical course can be described in three phases; the preicteric (pre-jaundice) phase, the icteric phase, and convalescence. The preicteric phase is characterized by insidious onset with malaise, anorexia, nausea, vomiting, right upper quadrant abdominal pain, fever, headache, myalgias, shin rashes, arthralgieas and arthritis, and dark urine beginning 1 to 2 days before the onset of jaundice. The icteric phase last 1 to 3 weeks and is characterized by jaundice, light or gray stools, hepatic tenderness and hepatomegaly. During convalescence, malaise and fatigue often persist for weeks or months as jaundice, anorexia, and other symptoms disappear. In adults, most acute infections will result in complete recovery and immunity from future infection. Although acute hepatitis B consequences can be very serious, most of the serious complications of HBV infection are due to chronic infection. Persons with chronic infections are often detected in screening programs such as blood donors, pregnant women and refugees. Any person testing positive for HBsAg is potentially infectious to both household and sexual contacts. Those contacts should receive appropriate immunization. There are 1.0 to 1.25 million people in the United States with chronic HBV infection with nearly 5,000 deaths each year from HBV-induced chronic liver disease. HBV is the most common cause of chronic viremia known, with an estimated 200 to 300 million chronic carriers worldwide. Chronic HBV infection is found in 0.5% of adults in North America and in 0.1% to 20% of people from other parts of the world. After acute HBV infection, the risk of developing chronic infection varies inversely with age. Chronic HBV occurs in about 90% of infants infected at birth; 20% to 50% of children infected at 1 & 5 years of age, and about 1% - 10% of persons infected as older children and adults. An estimated 15% - 25% of persons with chronic HBV infection will die prematurely from either cirrhosis or hepatocellular carcinoma. HBV may be the cause of up to 80% of all cases of hepatocellular carcinoma worldwide, second only to tobacco among human carcinogens. HBV is a small, double-shelled virus in the class Hepadnaviridae. It contains numerous antigenic components including, HBsAg, hepatitis B core antigen (HBcAg), and hepatitis B e antigen (HBeAg). It is a 42-nm partially double-stranded DNA virus composed of a 27-nm nucleocapsid core (HBcAg) surrounded by an outer lipoprotein coat containing the surface antigen HBsAg. HBsAg is an antigenic determinant found on the surface of the virus. It also makes up subviral 22-nm spherical and tubular particles. It can be identified in serum 30 to 60 days after exposure to HBV. Only the complete virus is infectious (HBsAg alone is not) however, when HBsAg is in the blood, the complete virus is as well. During replication, excess HBsAg is produced. Antibody to HBsAg protects against infection. HBsAg is the most commonly used test for diagnosing acute HBV infection or for detecting carriers. NOTE: Drawing page 208 and movement of HBsAg off virus. HBcAg, the nucleocapsid protein
core of HBV, is not detectable in serum although the presence of
antibody to HBcAg indicates infection.
HBeAg is a soluble protein in the core of HBV and, when detected
in the serum of persons with high virus titers, indicates high infectivity.
During convalescence or after hepatitis B vaccination, the
antibody to HBsAg, or anti-HB, develops.
The presence of HBcAg antibody indicates immunity to HBV.
Antibody to HBcAg (Anti-HBc) indicates infection with HBV
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