Wojcechowskyj Jason A, Yant Levi J, Wiseman Roger W, O'Connor Shelby L, O'Connor David H
Wisconsin National Primate Research Center, University of Wisconsin-Madison, 555 Science Dr., Madison, WI 53711, USA.
J Virol. 2007 Jan;81(1):406-10. doi: 10.1128/JVI.01636-06. Epub 2006 Nov 1.
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-B17 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-B17-containing MHC haplotypes that are identical by descent. We discovered that SIV-infected animals possessing identical Mamu-B17-containing haplotypes had widely divergent disease courses. Our results demonstrate that the inheritance of a particular Mamu-B17-containing haplotype is not sufficient to predict SIV disease outcome.
众所周知,宿主遗传学,尤其是主要组织相容性复合体(MHC)基因,是人类免疫缺陷病毒疾病进展的重要决定因素。对感染猿猴免疫缺陷病毒(SIV)的印度恒河猴的研究表明,Mamu - B17与病毒复制的控制有关。我们利用5兆碱基MHC区域的微卫星单倍型分析,比较了感染SIVmac239的印度恒河猴中疾病进展情况,这些猴子拥有通过血统相同的含Mamu - B17的MHC单倍型。我们发现,感染SIV且拥有相同含Mamu - B17单倍型的动物疾病进程差异很大。我们的结果表明,继承特定的含Mamu - B17单倍型不足以预测SIV疾病结果。