Hepatitis B overview
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Hepatitis B |
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Hepatitis B overview On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jolanta Marszalek, M.D. [2]; João André Alves Silva, M.D. [3]
Overview
Hepatitis B virus(HBV) is a double stranded DNA virus belonging to the family Hepadnaviridae. It is responsible for hepatitis B virus infection in humans that attacks the liver and causes both acute and chronic disease.
Historical Perspective
The earliest record of an epidemic caused by HBV was made by Lurman in 1885 after an outbreak of smallpox led to the vaccintation of shipyard employees with prepared material from human lymph. Several weeks to 8 months later, some of the workers became ill with jaundice while unvaccinated workers remained healthy. Similar outbreaks of serum hepatitis were reported throughout the early 20th century in clinics treating diabetes, syphilis, and tuberculosis. These outbreaks were most likely due to the transmission of the virus through the the use of contaminated needles and syringes. During World War II, jaundice epidemics occurring amongst military personnel led to studies that differentiated hepatitis B from hepatitis A. The virus itself was not discovered until 1965 by Baruch Blumberg, who identified the Australia antigen(later known to be hepatitis B surface antigen or HBsAg) in blood collected from Australian aborigines. The virus particle was identified in 1970 with electron microscopy by D.S. Dane et al. By the early 1980's the virus' genome had been sequenced, and in 1982, a vaccine against HBV was available.
Pathophysiology
Hepatitis B virus is a non-cytopathic, intracellular virus that causes little or no damage to the cell.[1] The host immune response to the virus is responsible for the hepatocellular damage seen in HBV infection. The HBV virion binds to a receptor at the surface of the hepatocyte and enters the cell, where it uses the host's cell mechanisms to replicate its genome and proteins.[1] The following viral antigens and antibodies are detected in serum throughout the course of the disease: HBsAg, HBcAg, HBeAg, anti-HBs, anti-HBC and anti-HBe. Transmission occurs from exposure to infectious blood or body fluids. Immune complexes, such as surface antigen-antibody, are important in the pathogenesis of hepatitis B. Hepatitis B is associated with the development of hepatocellular carcinoma.
Causes
The hepatitis B virus is responsible for causing hepatitis B. HBV is a double stranded DNA virus belonging to the family Hepadnaviridae. The viral particle consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. The nucleocapsid encloses the viral DNA. HBV DNA polymerase has reverse transcriptase activity. It shows tropism for hepatocytes. Humans are the only natural reservoir.
Differentiating Hepatitis B from other Diseases
Hepatitis B must be differentiated from other diseases that cause fever, nausea, vomiting, jaundice, hepatomegaly, icteric sclera, elevated ALT, AST, such as viral hepatitis(caused by other etiologic agents), alcoholic hepatitis, and autoimmune hepatitis.
Epidemiology and Demographics
Chronic Hepatitis B (HBV) is a major global health problem. According to the World Health Organization (WHO), more than 2 billion people have been infected with HBV. It is a major cause of chronic liver disease worldwide, affecting an estimated 1.25 million persons in the U.S., and more than 240 million people world wide.[1] [2]
Risk Factors
Generally, the highest risk for HBV infection is associated with lifestyles, occupations, or environments in which contact with blood from infected persons is frequent. High-risk populations include immigrants/refugees from areas of high HBV endemicity, clients in mental health institutions, injection drug users, and homosexually active men, patients of hemodialysis, and household contacts of HBV carriers. Perinatal transmission from mother to infant at birth is very efficient. If the mother is positive for both HBsAg and HBeAg, 70%–90% of infants will become infected in the absence of postexposure prophylaxis.[3]
Screening
High risk groups should be tested for HBV infection. These include immigrants/refugees from areas of intermediate or high endemicity, persons with chronically elevated aminotransferases, immunocompromised individuals, and persons with a history of injection drug use(IDU).
Screening for hepatocellular carcinoma should extend to Asian men over 40 years and Asian women over 50 years of age, persons with cirrhosis, persons with a family history of HCC, Africans over 20 years of age, and any HBV carrier over 40 years with persistent or intermittent ALT elevation and/or high HBV DNA level >2,000 IU/mL.
Natural History, Complications and Prognosis
The course of hepatitis B may be extremely variable. Hepatitis B has different clinical manifestations depending on the patient’s age at infection, immune status, and the stage at which the disease is recognized.[1] During the incubation period patients may experience flu-like symptoms, such as nausea, vomiting, and headaches. A person infected with hepatitis B virus may recover completely, become an asymptomatic carrier of the virus, develop chronic disease, or develop fulminant hepatitis. In acute hepatitis B, the incubation period may range from 45 to 120 days, depending on the amount of virus in the inoculum, host factors, and mode of transmission. These patients may experience the following symptoms: fatigue, nausea, vomiting, anorexia, abdominal discomfort, and jaundice. In most cases, no special diet or treatment are necessary. The risk of developing chronic hepatitis decreases with age, with infants having the highest risk. Chronic hepatitis may progress to: cirrhosis, liver failure, or hepatocellular carcinoma. In most cases the prognosis of acute hepatitis is good, with symptoms lasting 2 to 3 weeks. However, in infants and immunocompromised persons, the risk of developing chronic disease is increased.
Treatment
Surgery
The treatment of hepatitis B usually involves no surgical procedures. However, among patients with advanced liver damage secondary to HBV infection or liver failure in fulminant hepatitis, liver transplantation may be beneficial.
References
- ↑ 1.0 1.1 1.2 1.3 "Hepatitis B" (PDF).
- ↑ Center for Disease Control and Prevention. Guidelines for Hepatitis Sureveillance and Case Management 2009.http://www.cdc.gov/hepatitis/Statistics/SurveillanceGuidelines.htm
- ↑ Center for Disease Control and Prevention. Epidemiology and Prevention of Vaccine-Preventable Diseases. Hepatitis B 2012.http://www.cdc.gov/vaccines/pubs/pinkbook/hepb.html