To investigate whether nosocomial infection with hepatitis Cvirus (HCV) in chronic hemodialysis patients is related primarily to hemodialysis procedures, a multicenter analysis was carried out on 2,132 chronic hernodialysis patients (male: 1,274, female: 858) from 23 dialysis units using a second-ge
Nucleotide sequences of the hepatitis C virus core region in patients without anti-core antibody
β Scribed by Nagasaka, Atsushi; Hige, Shuhei; Kurosawa, Mitsutoshi; Yoshida, Junichi; Karino, Yoshiyasu; Toyota, Jyoji; Matsushima, Takashi; Asaka, Masahiro
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 444 KB
- Volume
- 49
- Category
- Article
- ISSN
- 0146-6615
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β¦ Synopsis
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 I b ) and compared them with those of four anti-core antibody-positive patients and a previously reported sequence. Amino acids spanning 1-47, which seemed t o exist in major B cell epitopes, were found t o 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 anticore 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 anticore 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. o 1996 Wiiey-Liss, Inc.
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