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Determination of genotypes of hepatitis C virus in Venezuela by restriction fragment length polymorphism.委内瑞拉丙型肝炎病毒基因型的限制性片段长度多态性测定
J Clin Microbiol. 1997 Jul;35(7):1870-2. doi: 10.1128/jcm.35.7.1870-1872.1997.
2
Nucleotide sequences of the hepatitis C virus core region in patients without anti-core antibody.无抗核心抗体患者丙型肝炎病毒核心区域的核苷酸序列
J Med Virol. 1996 Jun;49(2):91-4. doi: 10.1002/(SICI)1096-9071(199606)49:2<91::AID-JMV4>3.0.CO;2-E.
3
Absence of extensive genetic heterogeneity of hepatitis C virus in antibody-negative chronic hepatitis C.抗体阴性的慢性丙型肝炎中丙型肝炎病毒不存在广泛的基因异质性。
J Med Virol. 1996 Jun;49(2):87-90. doi: 10.1002/(SICI)1096-9071(199606)49:2<87::AID-JMV3>3.0.CO;2-F.
4
Characterization of the antibody reactivity to synthetic peptides from different parts of the hepatitis C virus genome.针对丙型肝炎病毒基因组不同区域合成肽段的抗体反应性特征分析。
Viral Immunol. 1996;9(2):89-96. doi: 10.1089/vim.1996.9.89.
5
Analysis of hepatitis C virus isolates by serotyping and genotyping.通过血清分型和基因分型对丙型肝炎病毒分离株进行分析。
J Clin Microbiol. 1996 Jul;34(7):1784-7. doi: 10.1128/JCM.34.7.1784-1787.1996.
6
High incidence of hepatitis C virus infection in hemodialysis patients in units with high prevalence.在患病率高的单位中,血液透析患者丙型肝炎病毒感染的高发生率。
J Clin Microbiol. 1996 Jul;34(7):1633-6. doi: 10.1128/JCM.34.7.1633-1636.1996.
7
The long-term virologic and pathologic impact of renal transplantation on chronic hepatitis B virus infection.肾移植对慢性乙型肝炎病毒感染的长期病毒学和病理学影响。
Transplantation. 1996 Jul 27;62(2):297-9. doi: 10.1097/00007890-199607270-00025.
8
Immune response to epitopes of hepatitis C virus (HCV) structural proteins in HCV-infected humans and chimpanzees.
J Infect Dis. 1996 Apr;173(4):808-21. doi: 10.1093/infdis/173.4.808.
9
A comparative evaluation of the sensitivity of seven anti-hepatitis C virus screening tests.七种抗丙型肝炎病毒筛查试验敏感性的比较评估
Vox Sang. 1995;69(3):213-6. doi: 10.1111/j.1423-0410.1995.tb02597.x.
10
Epitope mapping of the NS4 and NS5 gene products of hepatitis C virus and the use of a chimeric NS4-NS5 synthetic peptide for serodiagnosis.丙型肝炎病毒NS4和NS5基因产物的表位作图以及嵌合NS4-NS5合成肽在血清学诊断中的应用。
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感染乙型肝炎病毒的血液透析患者对丙型肝炎病毒抗原的抗体反应性降低。

Reduced antibody reactivity to hepatitis C virus antigens in hemodialysis patients coinfected with hepatitis B virus.

作者信息

Devesa M, Khudyakov Y E, Capriles F, Blitz L, Fields H A, Liprandi F, Pujol F H

机构信息

Laboratorio de Biología de Virus, Centro de Microbiología y Biología Celular, IVIC, Caracas, Venezuela.

出版信息

Clin Diagn Lab Immunol. 1997 Nov;4(6):639-42. doi: 10.1128/cdli.4.6.639-642.1997.

DOI:10.1128/cdli.4.6.639-642.1997
PMID:9384281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC170632/
Abstract

Antibody reactivities to hepatitis C virus (HCV) antigens and to synthetic peptides derived from different parts of the HCV genome (core, NS4, and NS5) were evaluated in HCV-infected hemodialysis patients. In the RIBA 3 assay, NS5 was significantly less recognizable by sera of hemodialysis patients compared to other HCV-infected subjects. Among hemodialysis patients, those coinfected with hepatitis B virus (HBV) (positive for hepatitis B surface antigen [HBsAg+]) showed a reduction in reactivity to C33 and C100. Sera of only 23% of the hemodialysis patients (37 of 161) reacted with more than three of eight peptides tested, significantly fewer than the 60% (12 of 20) of the sera of other HCV-infected patients tested (P = 0.001). This immunosuppression was also manifested by a reduced frequency of recognition of additional peptides on follow-up. An even more reduced reactivity was observed among the HBV-coinfected patients (HBsAg+). The low-responder hemodialysis patients were not infected with any particular genotype of HCV, and the same HCV genotypes observed in the whole group of hemodialysis patients (1a, 1b, 2a, and 3a) were found circulating in the low-responder group. Even in this low-responder population, the good performance of two peptides (peptide 716, corresponding to a portion of the core, and peptide 59, corresponding to a portion of NS4) corroborates the immunodominance of the conserved epitopes within these peptides.

摘要

在丙型肝炎病毒(HCV)感染的血液透析患者中,评估了其对HCV抗原以及源自HCV基因组不同区域(核心区、NS4和NS5)的合成肽的抗体反应性。在重组免疫印迹分析(RIBA 3)中,与其他HCV感染受试者相比,血液透析患者血清对NS5的识别能力明显较低。在血液透析患者中,合并感染乙型肝炎病毒(HBV)(乙型肝炎表面抗原阳性[HBsAg+])的患者对C33和C100的反应性降低。在接受检测的血液透析患者中,只有23%(161例中的37例)的血清与所检测的8种肽中的3种以上发生反应,显著少于接受检测的其他HCV感染患者血清的60%(20例中的12例)(P = 0.001)。这种免疫抑制在随访中对其他肽的识别频率降低方面也有体现。在合并感染HBV(HBsAg+)的患者中观察到反应性更低的情况。低反应性的血液透析患者未感染任何特定基因型HCV,并且在血液透析患者全组中观察到的相同HCV基因型(1a、1b、2a和3a)也在低反应性组中循环。即使在这个低反应性人群中,两种肽(对应核心区一部分的肽716和对应NS4一部分的肽59)的良好表现证实了这些肽中保守表位的免疫显性。