Occurrence of identical hypervariable region 1 sequences of hepatitis C virus in transfusion recipients and their respective blood donors: divergence over time.
Occurrence of identical hypervariable region 1 sequences of hepatitis C virus in transfusion recipients and their respective blood donors: divergence over time.
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输血受者及其各自的献血者中相同的丙型肝炎病毒高变区 1 序列的出现：随着时间的推移而出现差异。
DOI：
10.1053/jhep.2001.26635
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Hollinger,FB
中科院分区：
文献类型：
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作者：
Lin,HJ;Seeff,LB;Barbosa,L;Hollinger,FB
对来自输血传播病毒研究 (TTVS) 的 30 名输血受者和 120 名献血者的总共 240 份储存的血清样本进行了评估，目的是确定特定献血者是否传播丙型肝炎病毒 (HCV)。对编码氨基酸329至410的基因组区域进行高变区1（HVR1）的系统发育分析和HCV基因分型。通过Kimura公式计算HVR1序列之间的氨基酸距离。 HVR1 序列的 Bootstrap 分析为将受体与特定供体联系起来提供了支持。线性回归分析显示，输血后 7.9 周供体和受体 HVR1 序列之间没有差异，但供体和受体序列此后出现分歧 (r = 0.690)。受感染受体中 HVR1 进化的最初滞后阶段归因于宿主针对病毒建立免疫防御所需的时间。 HVR1 的受者内差异是通过对丙氨酸转氨酶峰值后 2 周内、原始研究结束时（1974-1979 年）和后续研究（1987 年至今）收集的系列标本进行分析来确定的。在急性感染期间，HVR1 在 6.7 至 9.5 天的时间内保持不变（95% CI）。 HVR1 的患者内部差异在 11 至 15 年期间增加（r = 0.771），达到了未关联受试者之间观察到的差异程度。在输血涉及一种以上 HCV 亚型的情况下，只有一种 HCV 亚型在接受者体内引起感染。显示了 HVR1 的亚型特异性差异。
A total of 240 stored serum specimens from 30 transfusion recipients and 120 blood donors from the Transfusion–Transmitted Viruses Study (TTVS) were evaluated with the objective of establishing transmission of hepatitis C virus (HCV) by specific blood donors. Phylogenetic analysis of hypervariable region 1 (HVR1) and HCV genotyping were performed on the genomic region encoding amino acids 329 to 410. Amino acid distances between HVR1 sequences were calculated by the Kimura formula. Bootstrap analysis of HVR1 sequences provided support for linking recipients to specific donors. Linear regression analysis showed no differences between donor and recipient HVR1 sequences 7.9 weeks posttransfusion, but donor and recipient sequences diverged thereafter (r= 0.690). The initial lag phase in the evolution of HVR1 in the infected recipient was attributed to the time required to mount host immunologic defenses against the virus. Within–recipient divergence in HVR1 was determined from analyses of serial specimens collected within 2 weeks after the alanine transaminase peak, at the end of the original study (1974–1979), and in the follow–up study (1987–present). HVR1 remained invariant over a period of 6.7 to 9.5 days (95% CI) during acute infection. Within–patient divergence in HVR1 increased over a period of 11 to 15 years (r= 0.771), reaching the degree of divergence observed between unlinked subjects. In cases in which transfusion involved more than one HCV subtype, only one of the HCV subtypes established infection in the recipient. Subtype–specific differences in HVR1 were shown.