从CD8 + T细胞免疫中发生的突变逃逸：丙型肝炎病毒从黑猩猩到人类的进化。
Mutational escape from CD8+ T cell immunity: HCV evolution, from chimpanzees to man.
作者信息
Bowen David G, Walker Christopher M
机构信息
Center for Vaccines and Immunity, Columbus Children's Research Institute, Columbus, OH 43205, USA.
出版信息
J Exp Med. 2005 Jun 6;201(11):1709-14. doi: 10.1084/jem.20050808.
The mechanisms by which the hepatitis C virus (HCV) establishes persistence are not yet fully understood. Previous chimpanzee and now human studies suggest that mutations within MHC class I-restricted HCV epitopes might contribute to viral escape from cytotoxic T lymphocyte (CTL) responses. However, there are several outstanding questions regarding the role of escape mutations in viral persistence and their fate in the absence of immune selection pressure.
丙型肝炎病毒（HCV）建立持续感染的机制尚未完全明确。先前针对黑猩猩以及现在针对人类的研究表明，MHC I类限制性HCV表位内的突变可能有助于病毒逃避细胞毒性T淋巴细胞（CTL）反应。然而，关于逃逸突变在病毒持续感染中的作用以及在缺乏免疫选择压力时它们的转归，仍存在几个悬而未决的问题。
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