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Hepatitis B Virus (HBV)

Genome: DNA Virus, dsRNA Virus Structure: Enveloped Virus
  • Hepatitis B Virus (HBV) is a hepatitis virus which can result in either acute or chronic infection of the liver. The probability of developing either syndrome is largely dependent on the immune status of the patient. A variety of serological markers are often used to determine if patients have been recently infected or are chronic carriers.
  • HBV can be transmitted parenterally, sexually, or from mother-to-child.
Viral Components
  • Surface Antigen (HBsAg)
    • This is viral envelope protein and is shed by actively infected hepatocytes often on its own independent of intact virions. The presence of HBsAg in the serum always indicates active infection.
  • Core Antigen (HBcAg)
    • This is a viral core protein and is released only as part of intact virions. Therefore, HBcAg cannot be detected during serologies as it is either sequestered in the viral envelope or inside Hepatocytes.
  • E Antigen (HBeAg)
    • This is a nucleocapsid protein present in naked form in the serum and is thus serologically detectable. The presence of serum HBeAg in the serum indicates an active infection which is highly contagious.
Serology of Acute Infection
  • Incubation Period
    • Following initial infection there is an asymptomatic period when all serologies may be negative for anywhere between 1-12 weeks.
  • Acute Disease
    • Acute Disease is heralded by the signs and symptoms of acute viral hepatitis including jaundice. During this period HBsAg and HBeAg will be present in the serum.
  • Initial Immune Response
    • Anti-HBcAg IgM and Anti-HBeAg IgG indicate the initial immune response. These developments coincide with a dramatic drop in HBeAg levels, marking significantly lowered infectivity. Levels of serum HBsAg also begin to decline but more slowly.
  • Mature Immune Response
    • As the immune response to the virus matures, Anti-HBcAg switches to IgG and an Anti-HBsAg IgG also begins to develop. Development of Anti-HBsAg is the definitive marker of immunity as it provides excellent protection against the virus.
Serology of Chronic Infection
  • For the chronically infected, Anti-HBsAg IgG is totally absent or present only at low levels and some HBsAg will be detectable. However, in chronically infected patients Anti-HBcAg will have switched to the IgG subtype. Therefore, the presence of HBsAg, absent/low Anti-HBsAg IgG, and Anti-HBcAg IgG is indicative of a chronically infected state. The presence of HBeAg in the chronically infected indicates a highly infective state whereas those without HBeAg and displaying Anti-HBeAg IgG indicate a chronically infected state with low infectivity.
Clinical Consequences
  • Immunocompetent Adults
    • Nearly all immunocompetent adults develop a syndrome of acute viral hepatitis with attendant jaundice upon initial infection with Hepatitis B Virus. Nearly 95% of these adults will develop strong Anti-HBsAg IgG and thus clear the infection after several months. In a small minority of cases high levels of Anti-HBsAg will not develop, allowing for chronic viral hepatitis to ensue.
  • Children and Immunocompromised Adults
    • Because these individuals have weak immune systems they may or may not develop significant symptomology associated with acute viral hepatitis. The insufficient immune response does not result in strong Anti-HBsAg antibodies and allows for chronic viral hepatitis to ensue.
  • Fulminant Hepatitis: A rare response that may occur in immunocompetent adults who have an excessively exuberant immune response to acute infection
  • Hepatocellular Carcinoma: Occurs in some patients with chronic infection
  • Cirrhosis: Occurs in some patients with Chronic Infection