Antiviral combination therapy in chronic hepatitis B
1987
textabstractAn 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 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
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