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The 18th United States-Japan Joint Hepatitis Panel reporter protein expressed when plasmids containing various 5NTR sequences were analyzed.These data suggest that Meeting was held November 16-18, 1996, near Nagasaki, Japan.As in other meetings held in recent years, most presenta-HCV RNAs might vary in terms of their intrinsic translational activity, and that this must be considered as a possible tions focused on hepatitis C virus (HCV) infections.However, a considerable amount of new information concerning the determinant of viral pathogenicity.Dr. Kunitada Shimotohno (Kyoto University) described the novel human GB virus C (GBV-C)/HGV flavivirus (''hepatitis G virus'') was also presented.Dr. Kusuya Nishioka (Viral replication of HCV in the human T-cell leukemia virus type I (HTLV-1)-infected, MT-2C human T lymphocyte cell line.Hepatitis Research Foundation of Japan), Chairman of the Japanese delegation, opened the meeting with a brief discus-These cells were shown to be permissive for replication of a genotype 1b inoculum over four cell-free viral passages.By sion of the role of hepatitis viruses as agents of emerging and re-emerging infectious diseases.He noted the existence of a 12 days' postinfection, the degree of genetic diversity of the primary inoculum had been reduced with a lesser number of small fraction of cases of viral hepatitis for which no viral etiology could yet be found.This implies the existence of at viral quasispecies present.The ''3X tail'' sequence identified previously by Dr. Shimotohno's group and by Dr. Rice's labo-least one, yet-to-be-discovered hepatitis virus.Dr. Nishioka also noted the increasing recognition of the role played by ratory at the 3 terminus of the viral RNA was present in the virus recovered from these cells.HCV in the causation of liver-specific morbidity and mortality, both in Asia and in the United States.His remarks were Dr. Joe Kim (Vertex Pharmaceuticals) described the recently solved x-ray structure of the complex formed by the followed by eight scientific sessions.NS3 protease domain of HCV and its NS4A cofactor.The
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Lemon et al. (1997) studied this question.
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