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Review
. 2007 Jan 7;13(1):82-90.
doi: 10.3748/wjg.v13.i1.82.

Pathogenesis of hepatitis B virus infection

Thomas F Baumert  1 , Robert Thimme, Fritz von Weizsäcker
Affiliations
Review

Pathogenesis of hepatitis B virus infection

Thomas F Baumert et al. World J Gastroenterol. .

Abstract

Infection with hepatitis B virus (HBV) leads to a wide spectrum of clinical presentations ranging from an asymptomatic carrier state to self-limited acute or fulminant hepatitis to chronic hepatitis with progression to cirrhosis and hepatocellular carcinoma. Infection with HBV is one of the most common viral diseases affecting man. Both viral factors as well as the host immune response have been implicated in the pathogenesis and clinical outcome of HBV infection. In this review, we will discuss the impact of virus-host interactions for the pathogenesis of HBV infection and liver disease. These interactions include the relevance of naturally occurring viral variants for clinical disease, the role of virus-induced apoptosis for HBV-induced liver cell injury and the impact of antiviral immune responses for outcome of infection.

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Figures

Figure 1
Figure 1
Cytopathic and non-cytopathic T cell responses against HBV infection.
See this image and copyright information in PMC

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References

    1. Nassal M. Hepatitis B virus replication: novel roles for virus-host interactions. Intervirology. 1999;42:100–116. - PubMed
    1. Hollinger FB, Liang TJ. Hepatitis B virus. In: Knipe DM, Howley PM, editors. Fields Virology. Philadelphia: Lippincott Williams and Wilkins; 2001. pp. 2971–3036.
    1. Summers J, Mason WS. Replication of the genome of a hepatitis B--like virus by reverse transcription of an RNA intermediate. Cell. 1982;29:403–415. - PubMed
    1. Bartenschlager R, Schaller H. The amino-terminal domain of the hepadnaviral P-gene encodes the terminal protein (genome-linked protein) believed to prime reverse transcription. EMBO J. 1988;7:4185–4192. - PMC - PubMed
    1. Feld J, Locarnini S. Antiviral therapy for hepatitis B virus infections: new targets and technical challenges. J Clin Virol. 2002;25:267–283. - PubMed