Control of simian immunodeficiency virus SIVmac239 is not predicted by inheritance of Mamu-B*17-containing haplotypes.
It is well established that host genetics, especially major histocompatibility complex (MHC) genes, are important determinants of human immunodeficiency virus disease progression. Studies with simian immunodeficiency virus (SIV)-infected Indian rhesus macaques have associated Mamu-B*17 with control of virus replication. Using microsatellite haplotyping of the 5-Mb MHC region, we compared disease progression among SIVmac239-infected Indian rhesus macaques that possess Mamu-B*17-containing MHC haplotypes that are identical by descent. We discovered that SIV-infected animals possessing identical Mamu-B*17-containing haplotypes had widely divergent disease courses. Our results demonstrate that the inheritance of a particular Mamu-B*17-containing haplotype is not sufficient to predict SIV disease outcome.
Wojcechowskyj
Jason A
JA
Wisconsin National Primate Research Center, University of Wisconsin-Madison, 555 Science Dr., Madison, WI 53711, USA.
Yant
Levi J
LJ
Wiseman
Roger W
RW
O'Connor
Shelby L
SL
O'Connor
David H
DH
D000818:Animals; D018450:Disease Progression; D006239:Haplotypes; D015395:Histocompatibility Antigens Class I / Q000235:genetics*; D008253:Macaca mulatta; D018895:Microsatellite Repeats; D016097:Simian Acquired Immunodeficiency Syndrome / Q000235:genetics* / Q000517:prevention & control; D015302:Simian Immunodeficiency Virus / Q000502:physiology*; D014779:Virus Replication
D015395:Histocompatibility Antigens Class I