Zusammenfassung
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• Das Hepatitis-B-Virus (HBV) ist ein DNS-Virus.
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• Das virale Genom kann in die Wirtszelle eingebaut werden (spielt eine Rolle bei der Karzinogenese).
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• Das Hepatitis-B-Virus ist als solches nicht zytopathogen; die Pathogenität wird durch die Immunantwort der infizierten Person bestimmt.
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• Das klinische Bild hängt wesentlich von der Art und Intensität der Immunantwort ab.
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• Das Oberflächenantigen des Virus (HBsAg) induziert die Produktion von schützenden HBs-Antikörpern.
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• Alle sechs HBV-Genotypen besitzen ein gemeinsames HBs-Ag Epitop; die HBs-Antikörper schützen daher vor allen Genotypen. Diese werden durch die heutigen Tests alle erfasst.
Summary
The hepatitis B virus belongs to the hepadna viruses family. Its genome consists of an incompletely double stranded DNA. The preS/S domain encodes proteins which make up the outer viral coat containing the HBs surface antigen (HBsAg). Other viral genes programme for structures inside the virus and for various regulatory enzymes. HBV mainly infects hepatocytes. The virus replicates in the cytoplasm and is primarily noncytopathogenic. HBV can also integrate into the host cell. Various stable genotypes and subtypes are known, which have a characteristic geographic distribution. They all share a common HBsAg epitop, which has allowed the development of a vaccine which is efficient world-wide. The protective principle consists of inducing protective anti-HBs. The infected cell has to be destroyed to eliminate the virus. Cellular immune defence mechanisms are mainly relevant, the principle effectors being cytotoxic T lymphocytes, activated monocytes/macrophages and cytokines such as interferon-gamma. The natural course of infection is highly variable, comprising viral elimination with or without acute hepatitis and chronic infection which might lead to chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. This is due to the balance respectively to the inbalance between the viral replication capacity and the immune defence mechanisms.
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