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Journal of Virology, January 2007, p. 406-410, Vol. 81, No. 1
0022-538X/07/$08.00+0     doi:10.1128/JVI.01636-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Control of Simian Immunodeficiency Virus SIVmac239 Is Not Predicted by Inheritance of Mamu-B*17-Containing Haplotypes{triangledown}

Jason A. Wojcechowskyj,1 Levi J. Yant,1,2 Roger W. Wiseman,1 Shelby L. O'Connor,2 and David H. O'Connor1,2*

Wisconsin National Primate Research Center, University of Wisconsin—Madison, Madison, Wisconsin 53715,1 Department of Pathology and Laboratory Medicine, University of Wisconsin—Madison, Madison, Wisconsin 537152

Received 31 July 2006/ Accepted 28 September 2006

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.

* Corresponding author. Mailing address: University of Wisconsin—Madison, 555 Science Dr., Madison, WI 53711. Phone: (608) 890-0845. Fax: (608) 265-8084. E-mail: doconnor{at}primate.wisc.edu.

{triangledown} Published ahead of print on 1 November 2006.

Journal of Virology, January 2007, p. 406-410, Vol. 81, No. 1
0022-538X/07/$08.00+0     doi:10.1128/JVI.01636-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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