[Chronic hepatitis C: virologic and immunologic aspects and questions of therapy].
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.
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Pécsi Orvostudományi Egyetem I. Belgyógyászati Klinika.
D000349:Africa / Q000453:epidemiology; D000998:Antiviral Agents / Q000627:therapeutic use; D001208:Asia / Q000453:epidemiology; D005060:Europe / Q000453:epidemiology; D005838:Genotype; D005938:Glucocorticoids / Q000627:therapeutic use; D016174:Hepacivirus / Q000276:immunology* / Q000472:pathogenicity; D006514:Hepatitis B Surface Antigens / Q000276:immunology; D006526:Hepatitis C / Q000453:epidemiology / Q000235:genetics / Q000276:immunology* / Q000628:therapy; D006521:Hepatitis, Chronic / Q000276:immunology / Q000628:therapy / Q000821:virology*; D006801:Humans; D007376:Interleukin-2 / Q000627:therapeutic use; D011239:Prednisolone / Q000627:therapeutic use; D014481:United States / Q000453:epidemiology
D000998:Antiviral Agents; D005938:Glucocorticoids; D006514:Hepatitis B Surface Antigens; D007376:Interleukin-2; D011239:Prednisolone