Hepatitis B virus (HBV) is a DNA virus with a compact genomic structure. The clinical presentation may vary from being asymptomatic and inapparent to fulminant and fatal acute infections on one hand and from subclinical persistent infections to rapidly progressive chronic liver disease with cirrhosis and even hepatocellular carcinoma. It belongs to hepadnaviruses type 1. The envelope protein expressed on the outer surface of the virion is referred to as Hepatitis B surface antigen (HBsAg), this is a product of the S gene of HBV. Another antigen on the surface of the nucleocapsid core is referred to as Hepatitis B Core antigen (HBcAg). A third HBV antigen is Hepatitis Be antigen (HBeAg), it is a product of the C gene of HBV. Within the nucleocapsid core is present a DNA polymerase which directs replication and repair of HBV DNA. HBcAg particles remain in the hepatocyte. Therefore naked core particles do not circulate in the serum.
Diagnosis: The first viral marker detectable in the serum is HBsAg, followed by elevation of serum aminotransferase and clinical symptoms and remains detectable during the entire symptomatic phase of Hepatitis B and beyond. HBsAg becomes undetectable in two months after the onset of jaundice. After HBsAg disappears, anti HBsAg becomes detectable in the serum and remains thus indefinitely. HBcAg is never seen freely in the serum. Anti HBcAg is detectable in the serum one to two weeks after appearance of HBsAg. During the window period between HBsAg disappearance and appearance of anti HBsAg the anti HBcAg is the only serological evidence for detection of HBV infection. IgM anti HBcAg indicates a current or recent acute HBV infection. IgG anti HBcAg indicates an infection in the remote past as well as a chronic HBV infection. In persons who have recovered from Hepatitis B, anti HBs and anti HBc persists indefinitely. HBeAg appears shortly after HBsAG. During this phase there is a high viral replication and detectable levels of HBV DNA. Individuals who remain HBsAg positive for atleast 6 months are considered to HBV carriers. HBeAg is a convenient and readily detectable qualitative marker of HBV replication. HBsAg positive serum containing HBeAg is likely to be highly infectious and to be associated with the presence of HBV DNA. HBeAg appears shortly after HBsAg. During the course of Hepatitis B, HBeAg may disappear and anti HBeAg will appear in the serum. When this happens there is a concurrent decline in the viral load. PCR tests have been developed to measure levels of HBV DNA, called the viral load.
Transmission: It is transmitted mainly through sexual contact, blood transfusions, reuse of contaminated needles and syringes and vertical transmission from mother to child.
Symptoms: It has an incubation period of 4 to 12 weeks. Acute infection begins with lethargy, weakness, loss of appetite, nausea, vomiting, fever, dark coloured urine, jaundice. In most cases it is a self limiting illness. However few patients may progress to development of fulminant disease which proves fatal. Chronic infection may be asymptomatic or may be associated with chronic inflammation of the liver and progress to cirrhosis and finally hepatocellular carcinoma.
Treatment: Acute Hepatitis B infection does not require treatment in most cases as it is self limiting. Only immunocompromised hosts may require antiviral therapy. Chronic carriers require antiviral drugs like interferons, lamivudine, tenofovir, adefovir, entecavir. Treatment may last for 6 months to a year depending on the medication used.
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