VIRAL-HEPATITIS - PARENTERAL AND NONPARENTERAL NON-A, NON-B, AND HEPATITIS-B

The cloning and part-sequencing of the hepatitis C virus has allowed the rapid development of an assay for detecting a serologic marker, anti-C100-3 antibody (anti-hepatitis C virus antibody), to nonstructural regions of the virus. The significance of the finding of a high prevalence of this antibody in a variety of liver diseases remains unclear. The antibody is nonneutralizing; there is no independent confirmatory test, and several steps in the current C100-3 assays lend themselves to false positivity. Evidence continues to accumulate in favor of there being more than one agent to explain parenteral, sporadic, and even enteral forms of non-A, non-B hepatitis, but their interrelations remain unclear. Point mutations in the genomic sequences of certain viruses, including hepatitis B virus, can influence immunogenicity, virulence, and, hence, pathogenicity.