[Physiopathology of hepatitis B virus infection]

Hepatitis B associated antigen (HB-Ag) may be observed in the serum in subjects either apparently healthy or exhibiting a number of disease symptoms. Its incidence among the Geneva voluntary blood donors is 0.48% with 54% exhibiting the surface antigen ad and 34% ay. While the HB-Ag positive blood donors appeared clinically healthy, minor pathology was found in the majority of them (thrombocytopenia, histological evidence of inflammatory foci, of persistent hepatitis and of chronic aggressive hepatitis). In 82 patients suffering from hepatitis B the same ad-ay type distribution of the HB-Ag has been found. In 11 out of 31 patients increased Clq binding suggests the presence of circulating complexes. Diminutions in the level of complement components also indicates participation of complement in the formation of immunocomplexes. In 2 out of 3 patients with Hb-Ag positive polyarteritis nodosa, the Clq binding test was also positive. The pathophysiologic implications of hepatitis B infection are discussed in connection with the authors and other findings. It appears that the main defense mechanism leading to elimination of the viruses within the hepatocytes lies in cell mediated immunity. Hepatitis would then represent the side reaction of this defense mechanism. Antibodies are probably useful in preventing the virus from entering the cell, but also in the course of the cell mediated defense mechanism (elimination of viral material liberated during the T-cell hepatocellular interaction). Immune complexes may be operative in certain extrahepatic manifestations such as arthralgia. Polyarteritis nodosa may result from local antibody interaction with antigen fixed within arterial walls.