An outbreak of parenterally transmitted hepatitis was probably first recorded in 1885 by Lurman who reported the occurrence of jaundice among personnel of a Bremen factory after revaccination against smallpox. Of 1289 individuals vaccinated in one day, 191 developed jaundice 2 to 8 months after administration of glycerinated human lymph preparations. The illness usually began with fatigue,anorexia and gastrointestinal complaints followed by jaundice and often pruritus; it generally lasted a total of 4 to 6 weeks.Personnel vaccinated on another day with another vaccine preparation as well as those who left the job before revaccination were not affected, Comparison of the water supply, domicile, alcohol abuse and vaccine exposure indicated the latter as the probable cause of the outbreak (1,2,3). In 1945 MacCallum postulated that, on the basis of differences in incubation period and mode of transmission, two different agents cause hepatitis: hepatitis A and hepatitis B. He was not able to isolate the infectious agents (4). In 1967 Krugman and Giles confirmed the existence of two types of hepatitis:one with a short and one with a long incubation period (5). In 1965 Blumberg had already discovered an antigen in the serum of an Australian aboriginal which he called 'Australia antigen' (6). In 1968 Prince identified an antigen in the serum of patients with post-transfusion hepatitis, an antigen which he called SH antigen (7). The antigens discovered by Blumberg and Prince were found to be identical and represent the hepatitis B surface antigen. Between 1968 and 1973 the other principal viral antigens <HBeAg,HBcAg) and their antibodies were identified (8,9). The electron microscopy features of the virus were described by Dane in 1970. In the blood of infected patients the large complete virus particle (diameter 42 nm), small 22 nm spherical surface antigen particles and tubular forms (length 100 nm,diameter 22 nm) were found (10). Infection with the hepatitis B virus is characterized not only by production of infectious complete virus particles (Dane particles) but also by an enhanced production of incomplete viral particles made up entirely of HBsAg without HBcAg, DNA-polymerase activity or HBV-DNA