Recent advances in basic science
Hepatitis C virus entry: possible targets for therapy
Institute for Biomedical Research, University of Birmingham, Birmingham, UK
Correspondence to:
Professor J A McKeating, Institute for Biomedical Research, The Medical School, Vincent Drive, Birmingham B15 2TT, UK; j.a.mckeating@bham.ac.uk
| The first 150 words of the full text of this article appear below. |
Hepatitis C virus (HCV), a major cause of liver disease, has been a challenging opponent for researchers and clinicians for more than 35 years. The introduction of diagnostic tests in the mid-1970s revealed that the causative agent of most cases of post-transfusion hepatitis was neither hepatitis A virus (HAV) nor B (HBV). Bearing the moniker non-A non-B hepatitis (NANB), the virus eluded identification for nearly 15 years. Attempts to isolate the virus by standard immunological techniques were unsuccessful, so, in 1989, Choo and colleagues used viral antigen to screen for reactivity with patient-derived antibodies.1 Expression of a cDNA library of genetic material cloned from the plasma of an infected chimpanzee identified clones that were reactive with NANB-positive patient sera. The genome was identified as a single-stranded RNA of approximately 10 000 nucleotides and the virus named hepatitis C. At the time of its discovery HCV imposed a significant healthcare burden,
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Schwarz, A. K., Grove, J., Hu, K., Mee, C. J., Balfe, P., McKeating, J. A.
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