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Hepatitis C infection: a review.

Hepatitis C, transmitted through body fluid exchange, affects approximately 1.8% of the U.S. population, roughly 3.9 million persons. Transfusion of blood and blood products was once an important source of hepatitis C transmission. Since the initiation of the hepatitis C screening program in 1985, however, injection drug use has become a major route. Hepatitis C is a leading cause of chronic liver disease. In 80% to 85% of those infected with the virus, chronic hepatitis C eventually develops, which can lead to cirrhosis and hepatocellular carcinoma, with alcohol abuse and coinfection with hepatitis B as additional risk factors. Screening for hepatitis C can be achieved with serologic assays. Molecular assays are helpful in confirming the diagnosis, assessing viral load, and characterizing the genetic nature of the viruses. Interferon alpha (IFN-alpha) and a combination of IFN-alpha 2B and ribavirin are therapies available in treatment of hepatitis C, but sustained response to the treatment has been unsatisfactory. Further studies are indicated to obtain more effective therapies for eradication of the disease. Hepatitis C is preventable, and clinicians should use every opportunity possible in their practice to assess those at risk and actively engage them in risk factor reductions.

Antiviral Agents↗

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p21ras independent down-regulation of ras-induced increases in natural antibody binding during tumor progression.

Selective outgrowth of v-H-ras-infected 10T1/2 cells based on the cointroduction of a gene for resistance to geneticin (G418), yielded cells which exhibited an increased capacity to bind polyclonal serum natural antibody (NAb). This demonstrated an NAb-susceptible phase of tumor development which would be a basic requirement for NAb-mediated surveillance of tumors. The ras-oncogene dependence of the high-NAb-binding phenotype provided a model for assessing NAb resistance against ras transformants in vivo and for a comparative analysis of phenotypic and genetic alterations contributing to the progression of ras transformants. Variants were developed through in vitro and in vivo models of tumor progression. T24-H-ras and v-H-ras transformants were isolated in vitro through more rigorous growth conditions, focus formation in the presence of untransformed cells with no selecting drug. These clones expressed p21ras but exhibited little or no increase in NAb binding. Variants recovered following growth from intravenous or threshold subcutaneous (s.c.) inocula of high-NAb-binding ras transformants in syngeneic C3H/HeN mice exhibited decreases in NAb binding but no uniform change in p21ras. Concurring inverse correlations between NAb binding and s.c. tumorigenicity were exhibited by the T24-H-ras transformant clones, the ras transformants grown in vivo, and the v-H-ras-transformed clones isolated in the presence versus the absence of untransformed cells. This consistent inverse correlation, together with the reduced NAb binding of the ras transformants grown in vivo, provides strong evidence that NAb participates in the defense against ras-transformed cells in vivo. The lack of any direct correlation between p21ras expression and the reduction in NAb binding or the increase in tumorigenicity of cells generated through progression in vivo suggested the regulatory action of additional genes. Hybridization studies between high- and low-NAb-binding clones implicated the activation of an additional oncogene and inactivation of an antioncogene in the down-regulation of the ras-induced increases in NAb binding associated with tumor progression.

Animals↗