Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 1, Pages 406-410Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01636-06
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Funding
- NCRR NIH HHS [RR15459-01, RR020141-01, C06 RR020141, C06 RR015459, P51 RR000167] Funding Source: Medline
- NIH HHS [P51 OD011106] Funding Source: Medline
- NATIONAL CENTER FOR RESEARCH RESOURCES [C06RR020141, P51RR000167, C06RR015459] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [P51OD011106] Funding Source: NIH RePORTER
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It is well established that host genetics, especially major histocompatibillity 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*17containing 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.
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