Mutational escape from CD8+ T cell immunity : HCV evolution, from chimpanzees to man (original) (raw)
Commentary| June 06 2005
aD.G.B. and C.M.W. are at Center for Vaccines and Immunity, Columbus Children's Research Institute, Columbus, OH 43205.
bC.M.W. is at College of Medicine and Public Health, Ohio State University, Columbus, OH 43210.
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aD.G.B. and C.M.W. are at Center for Vaccines and Immunity, Columbus Children's Research Institute, Columbus, OH 43205.
bC.M.W. is at College of Medicine and Public Health, Ohio State University, Columbus, OH 43210.
Search for other works by this author on:
David G. Bowen, Christopher M. Walker
aD.G.B. and C.M.W. are at Center for Vaccines and Immunity, Columbus Children's Research Institute, Columbus, OH 43205.
bC.M.W. is at College of Medicine and Public Health, Ohio State University, Columbus, OH 43210.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
The Rockefeller University Press
2005
J Exp Med (2005) 201 (11): 1709–1714.
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.
The Rockefeller University Press
2005
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