This study was designed to find correlations between the various courses of disease after hepatitis B virus (HBV) infection and factors that could conceivably have influenced the course of disease. The aim of the study was to find correlations between parameters of viral replication and liver cell damage, factors related to the viral subtypes and the immunological response and the various well defined courses of disease after hepatitis B virus infection, in order to gain insight into the timing and the mechanism of the development of chronic hepatitis B. The course of disease after hepatitis B virus infection is heterogeneous (see fig. 2.3). Acute hepatitis B may cause hepatitis with jaundice, hepatitis without jaundice or no hepatitis at all. In any of these instances, the HBV may be cleared, leading to recovery, or may persist, resulting in chronic HBV carriership. Chronic HBV carriers may have varying degrees of chronic hepatitis, or no hepatitis at all. Viral clearance seems to run independently from hepatitis activity, in acute as well as in chronic hepatitis B. However, a close relationship between viral replication activity, partial viral clearance and hepatitis activity has been described (l-6) in a group of patients who have developed chronic active hepatitis, suggesting a causal role of active viral replication in the pathogenesis of persisting liver cell degradation. In this patient group, serological tests for hepatitis Be antigen (HBeAg) become negative during the natural history, which is considered to be a sign of partial viral clearance (4). Liver cell damage is often increased during some weeks preceding the seroconversion. After HBeAg seroconversion the virus is usually not completely cleared, but incorporated into the host's liver cell genome (7,8).1n the other courses of disease such a correlation between viral clearance and liver cell damage has not become apparent. In particular, it is not clear whether in early acute hepatitis B liver cell damage plays a causal role in viral elimination, or is merely the result of the viral infection of liver cells.

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J.H.P. Wilson (Paul) , G.C. de Gast
Erasmus University Rotterdam
Erasmus MC: University Medical Center Rotterdam

van Hattum, J. (1986, November 26). Hepatitus B virus infection : factors influencing the outcome. Retrieved from