Structure and selection of hepatitis B virus variants during the natural course of infection and interferon therapy.
The consequences of hepatitis B virus (HBV) infection range from asymptomatic transient and chronic infections to mild and severe forms of hepatitis up to the development of liver cirrhosis and hepatocellular carcinoma. Immune-mediated destruction of infected liver cells plays a major role in HBV pathogenesis. Escape from immune-recognition by changing the antigenic make-up of HBV or by preventing the expression of some viral proteins leads to the emergence of viral variants. Variants can harbor mutations in the pre-core/core gene (pre C/C) or the preS/S gene, either of which can play a role in immune escape, viral persistence, and pathogenesis. A novel method has been developed to facilitate identification and functional analysis of full-length variant genomes of HBV, with implications for HBV diagnosis and therapy.
Günther
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S
Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Hamburg, Germany.
Miska
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S
Meisel
H
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Will
H
H
D014644:Genetic Variation; D016679:Genome, Viral; D006509:Hepatitis B / Q000821:virology*; D006512:Hepatitis B Core Antigens / Q000235:genetics; D006514:Hepatitis B Surface Antigens / Q000235:genetics; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D011498:Protein Precursors / Q000235:genetics
D006512:Hepatitis B Core Antigens; D006514:Hepatitis B Surface Antigens; D011498:Protein Precursors; C050807:presurface protein 2, hepatitis B surface antigen