The hepatic flaviviridae: summary

Hepatitis C envelope proteins (E1, E2) induce protective neutralizing antibodies. The extent of sequence diversity reflects the host's ability to control viral populations and the response to antiviral therapy. Attempts to prepare effective vaccines against HCV are foiled by lack of prolonged protective immunity. Plasmid vaccines and the use of uninfectious virus‐like particles are being developed. HCV induces a cellular humoral immune response, but this is inadequate to clear the virus and the disease becomes chronic. In any patient, the natural history of HCV infection depends on the age when infected, and the presence of other diseases. The transfusion‐related disease has a worse prognosis than that transmitted by syringes and needles. The outlook in ‘healthy blood donors’ is uncertain. Interferon therapy for 3 or preferably 6 months results in a sustained response in about 30% of patients. Negative serum HCV RNA and normal AST values after 3 months of therapy indicates that there may be a sustained response. Whether or not to stop treatment at that time if HCV is still positive remains a matter of debate. The role of interferon treatment in preventing progression to cirrhosis and hepatocellular cancer is still uncertain. Ribavirin therapy alone reduces transaminases and hepatic histology improves. Improved results follow the combination of ribavirin with interferon. Ribavirin may have immuno‐modularity and anti‐inflammatory actions. Hepatitis G virus (HGV) is unlikely to play a significant role in liver disease in man.