| Literature DB >> 9766848 |
D A Price1, U C Meier, P Klenerman, M A Purbhoo, R E Phillips, A K Sewell.
Abstract
The propensity of HIV-1 for genetic variation, a consequence of error-prone reverse transcription combined with high rates of replication, is thought to contribute to the establishment of persistent infection in the host despite the presence of a vigorous antiviral immune response. Protective immunity to viruses is mediated primarily by cytotoxic T lymphocytes, which recognize viral peptides of 8-11 amino acids bound to major histocompatibility complex class I molecules on the surface of infected cells. In this review we examine the mechanisms by which mutation within peptide antigen-encoding regions of the viral genome enables HIV-1 to evade recognition by virus-specific cytotoxic T lymphocytes. The discussion is relevant to other genetically unstable viruses and more generally to intracellular pathogens of variable antigenicity.Entities:
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Year: 1998 PMID: 9766848 DOI: 10.1007/s001090050270
Source DB: PubMed Journal: J Mol Med (Berl) ISSN: 0946-2716 Impact factor: 4.599