CASE REPORT: Clinical and virological analyses of a patient positive for hepatitis C virus‐RNA by branched DNA assay but negative for anti‐hepatitis C virus antibodies

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Abstract
Infection with hepatitis C virus (HCV) is usually diagnosed by the presence of antibodies against fusion proteins or peptides derived from different regions of the HCV genome. However, a subgroup of patients with HCV viraemia are seronegative for antibody against hepatitis C virus (anti‐HCV) by conventional antibody assays. We analysed serum samples from a patient with liver cirrhosis who tested negative for anti‐HCV by a second‐generation assay, but positive for HCV‐RNA by reverse transcription‐polymerase chain reaction (RT‐PCR) and branched DNA signal amplification. To identify possible mutations that could explain the failure of detection of anti‐HCV by second‐generation assay, PCR‐amplified DNA fragments of the core region derived from the serum were cloned and sequenced. Nucleotide (nt) and amino acid (aa) sequence analyses (nt 1–486, aa 1–162) showed no mutations revealing stop codons, frame‐shifts, deletions or insertions, but the presence of two amino acid substitutions (aa 75 and 91) when compared with HCV‐J, a prototype strain of genotype 1b isolated from a Japanese patient. One of these two mutations (aa 75) was situated in the second hydrophilic domain of the core peptide, but analysis of the hydropathy profile showed only a little change. The two mutations were identical to those identified in other Japanese HCV isolates. The serum immunoglobulin level and T and B cell counts were normal in our patient. Our data suggest that the absence of anti‐HCV in this patient was not due to mutations of major epitopes of HCV. Low‐dose prednisolone administration just after transfusion may have induced immunological tolerance against HCV in this patient.

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