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Sozial- und Präventivmedizin

, Volume 43, Supplement 1, pp S79–S83 | Cite as

Virus et pathogénie de l'hépatite B

  • Peter J. Grob
  • Philippe C. Frei
Article
  • 36 Downloads

Résumé

  • ⋅ Le virus de l'hépatite B (VHB) est un virus à ADN.

  • ⋅ Le génome viral peut s'intégrer dans le génome de la cellule-hôte (implication dans carcinogenèse).

  • ⋅ Le VHB n'est pas cytopathogène en soi; la pathogénie est induite par la réponse immune de l'hôte infecté.

  • ⋅ La présentation clinique est essentiellement déterminée par le type et l'intensité de la réponse immunitaire.

  • ⋅ L'antigène de surface, du virus (AgHBs) induit la production d'anticorps anti-HBs qui sont protecteurs.

  • ⋅ Les 6 génotypes du VHB ont un épitope commun de l'AgHBs. Les anticorps anti-HBs sont donc protecteurs contre tous les génotypes et ces derniers sont tous détectés par les tests actuels.

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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Copyright information

© Birkhäuser Verlag 1998

Authors and Affiliations

  • Peter J. Grob
    • 1
  • Philippe C. Frei
    • 2
  1. 1.Abteilung für klinische Immunologie, UniversitätsspitalZürich
  2. 2.Division d'immunologie et d'allergieLausanne

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