1887

Abstract

Hepatitis B virus (HBV) infections can be prevented or controlled by the host humoral immune response (anti-HBs) directed against the major surface antigen (HBsAg), elicited either naturally or by vaccination. A chronic HBV carrier was found to have high levels of both virus and anti-HBs. Full-length HBV genomes were amplified from the patient's serum, sequenced and cloned. The genome was ‘wild-type’ HBV of genotype C and serotype . The sequence has remained stable, with no signs of emergence of an immune-escape mutant population. To study what was recognized by the patient's serum, viral particles were S-labelled and then immunoprecipitated by using the patient's serum or control sera. The patient's serum immunoprecipitated the HBsAg encoded by his HBV genome poorly, but efficiently recognized HBsAg of serotype . When his HBV genome was modified by a point mutation to express HBsAg of serotype , the patient's serum could recognize the antigen, as well as the control anti-HBs-positive serum. The patient appeared to have made a quasi-monoclonal humoral response to the epitope. By switching to the epitope, which requires only a point mutation, the virus could replicate, despite the high levels of anti-HBs. This study underlines the subtleties of virus–host interactions. Implications for HBV vaccination are discussed.

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2005-06-01
2024-04-25
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