Important note: Information in this article was accurate in February 1999. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, February 22, 1999
Daniel J. DeNoon, Senior Editor
The suggestion comes from a study of a single family of macaque monkeys experimentally infected with SIVmac251, a pathogenic strain of simian immunodeficiency virus (SIV).
Two of the animals rapidly progressed to disease, both had identical major histocompatibility complex (MHC) class 1 alleles. They differed from two slow progressors only by a single MHC class 1 haplotype.
"Remarkably, this haplotype was shared by both slow progressors, and encoded two molecules used to present three different CTL [cytotoxic lymphocyte] epitopes derived from the SIV Env and Nef proteins," Harvard University reported D. Evans."
Evans described the studies in a presentation to the 6th Conference on Retroviruses and Opportunistic Infections, held January 31-February 4, 1999, in Chicago, Illinois.
Analysis of this haplotype in another animal with intermediate disease progression revealed two MHC class 1 molecules that recognized two additional Env and Nef CTL epitopes.
Evans and colleagues sequenced env and nef sequences of SIV isolated from the animals at various time points after infection. Just before disease progression, they found CTL escape mutants with amino-acid changes in all five identified CTL epitopes.
"These data provide compelling evidence that allelic differences ... may be responsible for the differences in survival," Evans said. "Family members that made CTL responses to multiple CTL epitopes exhibited a slower course of disease."
Evans said that the most effective CTL epitopes appear to be those from the SIV Nef protein.
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