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.