Hepaciviruses Hepatitis C and G

Pathogen. A series of hepatitis infections following blood transfusions was observed that could not be identified as either hepatitis A (p. 437) or hepatitis B (p. 429), and were therefore designated as "non-A-non-B (NANB) hepatitis." The discovery of the hepatitis C virus (HCV) by molecular biological means in 1988 was an elegant piece of work: RNA was extracted from the plasma of an infected chimpanzee, from which cDNA was produced using reverse transcriptase. The cDNA was then cloned and the corresponding proteins expressed. About one million clones were tested for reactivity with sera from patients suffering from chronic NANB hepatitis. A protein was found by this method that reacted with antibodies to NANB, whereupon the corresponding cloned DNA was used as a probe to identify further overlapping gene segments. They belong to a flavivirus with approximately 10 kb sense RNA and several genotypes. A similar strategy led to identification of a further flavivirus that also causes hepatitis, now known as the hepatitis G virus (HGV).

Pathogenesis and clinical picture. Hepatitis C resembles hepatitis B in many respects. One major difference is that it much more frequently produces a persistent infection (85%) and, in 70% of cases, develops into a chronic hepatitis, resulting in cirrhosis of the liver within 20 years and a hepatocellular 8 carcinoma (HCC) in a further 10 years. The reason for the high level of viral persistence is thought to be a pronounced mutability facilitating evasion of the immune defenses (quasispecies of RNA viruses, p. 391).

Diagnosis of hepatitis C is done with antibody EIA using genetically engineered viral proteins. Western blot can be used to confirm the result. The RNA can be detected by means of RT-PCR and the course of therapy can be monitored with quantitative PCR.

Epidemiology and prevention. The incidence of HCV in Europe is about 0.3%, with a decreasing tendency in the younger segment of the population. About 50% of acute hepatitis cases are HCV infections. Transmission is by blood and blood products. High-risk persons include dialysis patients, healthcare staff, and needle-sharing drug consumers. Perinatal transmission is possible, but sexual contact does not appear to be a risk factor. The transmission route is not apparent in many cases, giving rise to the expression "community-acquired infection." Feasible protective measures are the same as in hep atitis B; no immunization by vaccine is available. Especially in combination with ribavirin (Table 7.5), therapeutic use of interferon can lead to elimination of the virus in persistent infections and thus to prevention of cirrhosis of the liver and HCC.

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