HEPATITIS-B VIRUS AND PATHOGENESES

Authors
Citation
Pj. Grob et Pc. Frei, HEPATITIS-B VIRUS AND PATHOGENESES, Sozial- und Praventivmedizin, 43, 1998, pp. 5-9
Citations number
9
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
03038408
Volume
43
Year of publication
1998
Supplement
1
Pages
5 - 9
Database
ISI
SICI code
0303-8408(1998)43:<5:HVAP>2.0.ZU;2-E
Abstract
The hepatitis B virus belongs to the hepadna viruses family. Ifs genom e consists of an incompletely double stranded DNA. The preS/S domain e ncodes proteins which make up the outer viral coat containing the HBs surface antigen (HBsAg). Other viral genes programme for structures in side the virus and for various regulatory enzymes. HBV mainly infects hepatocytes. The virus replicates in the cytoplasm and is primarily no ncytopathogenic. HBV can also integrate into the host cell. Various st able genotypes and subtypes are known, which have a characteristic geo graphic distribution. They all share a common HBsAg epitop, which has allowed the development of a vaccine which is efficient world-wide. Th e protective principle consists of inducing protective anti-HBs. The i nfected cell has to be destroyed to eliminate the virus. Cellular immu ne defence mechanisms are mainly relevant the principle effectors bein g cytotoxic T lymphocytes, activated monocytes/macrophages and cytokin es such as interferon-gamma. The natural course of infection is highly variable, comprising viral elimination with or without acute hepatiti s a,and chronic infection which might lead to chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. This is due to the balance re spectively to the inbalance between the viral replication capacity and the immune defence mechanisms.