Explain the characters and laboratory diagnosis of Hepatitis B virus

Hepatitis B Virus is a member of the Hepadnaviridae family. It is the only DNA virus among the agents which commonly cause viral hepatitis. The viral particle (dane particle) is 42 nm in diameter.
The lipoprotein (HBsAg) which  encoats the virus is seen not only as a viral envelope but also by electron microscopy as free non-infectious tubular and spherical structures. These forms of HBsAg circulate in considerable excess compared with the virion and may play a permissive role in viral persistence.  Therefore, the presence of HBsAg does not necessarily imply contagiousness.However, HBsAg may be present in blood when replication cannot be documented.
HBV replicates in hepatocytes and possibly in peripheral blood mononuclear cells. Its genome is the smallest of all known animal DNA viruses. The replicative process is unusual in several aspects;
  1. it has an efficient genomic design of four overlapping open reading frames,
  2. it utilizes successive strand synthesis and reverse transcription similar to retroviruses, and
  3. it has both glucocorticoid- and hepatocyte-specific enhancing elements.

Viral replication can be documented by measuring HBeAg (a component of the core gene product) or HBV-DNA (by a non-PCR method) in serum.

Laboratory diagnosis of Hepatitis B virus infection

  1. Detection of Viral Markers:Diagnosis of Hepatitis B infection rests on serological demonstration of the viral markers and can be carried out by detection of HBsAg, anti-HBs, HBeAg, anti HBe, IgM anti-HBc, IgG-anti-HBc and HBV DNA in the serum.
    1. HBsAg is the most important serological marker for identifying infection.  It is the first marker to appear in the blood after infection. It is usually detectable 2-6 weeks in advance of clinical and biochemical evidence of hepatitis and persists throughout the clinical course of disease. It  disappears with resolution of infection and persists in chronic infection.
    2. IgM anti-HBc is essential for the diagnosis of acute infection, but is also seen occasionally in very active chronic hepatitis.
    3. Anti-HBc antibodies develop and persist after all HBV infections. The loss of HBsAg and development of anti-HBc signals resolution of acute infection.
    4. Anti-HBs also occurs post vaccination, but anti-HBc will not be present in such cases.

Chronic infection is manifested by persistent HBsAg. Markers of viral replication such as HBeAg and HBV-DNA (non-PCR method) are detectable during the early high replication phase, but are not detectable during the later quiescent low replication phase. HBeAg is not a reliable marker of HBV replication when a precore variant is responsible for the infection. Such cases will be HBeAg negative, anti-HBe positive, but HBV-DNA (by a non-PCR method) positive

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