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Nucleotide sequences of the hepatitis C virus core region in patients without anti‐core antibody
Author(s) -
Nagasaka Atsushi,
Hige Shuhei,
Kurosawa Mitsutoshi,
Yoshida Junichi,
Karino Yoshiyasu,
Toyota Jyoji,
Matsushima Takashi,
Asaka Masahiro
Publication year - 1996
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199606)49:2<91::aid-jmv4>3.0.co;2-e
Subject(s) - antibody , virology , epitope , biology , hepatitis c virus , reverse transcriptase , virus , rna , amino acid , ns3 , microbiology and biotechnology , gene , genetics
Abstract Second‐generation assays for detection of hepatitis C virus (HCV) infection that include reactivity of antibodies to core, NS3, NS4 are used because of their high sensitivity. Among these antibodies, anti‐core antibody seems to be the most sensitive. However, there are some patients without anti‐core antibodies, although HCV RNA is detectable by reverse transcription‐polymerase chain reaction and branched DNA assay. The mechanism for the absence of anti‐core antibody on its own is unclear. We therefore determined the nucleotide and deduced amino acid sequences of the core region obtained from two anti‐core antibody‐negative patients with HCV RNA (genotype 1b) and compared them with those of four anti‐core antibody‐positive patients and a previously reported sequence. Amino acids spanning 1–47, which seemed to exist in major B cell epitopes, were found to be completely conserved among these patients. Furthermore, the predictive binding motif to HLA DR4 (a.a 81–90) was completely conserved in both of the anti‐core antibody‐negative patients. There were various mutations in the residual amino acids spanning 49–108, but specific mutations could not be found in anti‐core antibody‐negative patients. These data indicate that the absence of anti‐core antibody in two patients is not due to the presence of some formerly unknown viral variants, but due to a possible defect in the host's immune system. © 1996 Wiley‐Liss, Inc.