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Characteristics of hepatitis C virus (HCV), importance of its genotypes and mutant variants "quasi-species", as well as the mechanisms of disease chronicity and tissue injuries caused by HCV have been discussed. Both a presumed direct cytopathy of the virus and the host's immune response may play a role in the pathogenesis. HCV infects not only hepatocytes but lymphoid cells, thereby modulates immune functions. A molecular minicri--that is a cross-reaction between viral and host antigens--also contributes to autoimmune phenomena developed during chronic HCV infection, in addition a genetic predisposition for autoimmunity can be involved. Until now the only accepted therapy for HCV infection is interferon, that at a standard low dose regimen, results long-term benefit only in one-fourth of treated patients. In Hungary, between 1994-1996 601 chronic hepatitis C patients have been treated: biochemical remission (ALT normalization) was found in 38% of the patients and elimination of the HCV was achieved in 25%. Several questions are to be answered concerning the optimalization of the treatment, e.g. dosage, duration of treatment, re-treatment of relapse, problem of non-responders, the role of predictors of response in the individualized therapy, usefulness of combination treatment. The original end-points and goals of therapy are sustained HCV-RNA negativity, normalization of serum GPT/ALT, and inactivity in liver histology, yet the real end-points are incidence and prevention of cirrhosis and hepatocellular carcinoma, that is the better survival. Concerning these questions, newer therapeutic experiences are discussed, including results from Hungarian researchers.

High prevalence of hepatitis C antibodies (anti-HCV) have been found in the Middle- and Southern European countries in connection with chronic liver diseases. In a study of Finnish chronic liver disease patients no anti-HCV antibodies were found in 22 autoimmune chronic active hepatitis, in 5 chronic persistent hepatitis and in 38 alcoholic liver disease patients. 2/30 primary biliary cirrhosis patients were anti-HCV positive. As a comparison 3/9 patients with acute community acquired non-A non-B hepatitis and 28/48 i.v. drug addicts had anti-HCV antibodies. The results indicate that HCV infections in Finnish chronic hepatitis patients are rare.

In a study of 565 hepatitis B antigen (HBsAg) positive persons from the Auckland region, antibody to the hepatitis delta virus was detected in 38. The largest number were in Samoans (61%) although the infection was present in some other Pacific Islanders. Among HBsAg positive healthy blood donors, antenatal patients and acute hepatitis patients between 3.8 and 4.8% were anti-delta positive; while 28% of chronic hepatitis patients were positive suggesting an association between this disease and delta infection. Some positive results were also found in sera from intravenous drug addicts. By contrast, anti-delta was uncommon in New Zealand born Maoris or Europeans. Delta infection can be detected in some Pacific Islanders, some European immigrants as well as intravenous drug addicts and has the potential to spread in an epidemic form to HBsAg carriers in the general community. Widespread vaccination against hepatitis B is recommended to eventually reduce the number of HBsAg carriers in New Zealand.