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Variation in genes underlying host immunity can lead to marked differences in susceptibility to HIV infection among humans. Despite heavy reliance on non-human primates as models for HIV/AIDS, little is known about which host factors are shared and which are unique to a given primate lineage. Here, we investigate whether copy number variation (CNV) at  CCL3 -like genes ( CCL3L ), a key genetic host factor for HIV/AIDS susceptibility and cell-mediated immune response in humans, is also a determinant of time until onset of simian-AIDS in rhesus macaques. Using a retrospective study of 57 rhesus macaques experimentally infected with SIVmac, we find that  CCL3L  CNV explains approximately 18% of the variance in time to simian-AIDS ( p <0.001) with lower  CCL3L  copy number associating with more rapid disease course. We also find that  CCL3L  copy number varies significantly ( p <10 −6 ) among rhesus subpopulations, with Indian-origin macaques having, on average, half as many  CCL3L  gene copies as Chinese-origin macaques. Lastly, we confirm that  CCL3L  shows variable copy number in humans and chimpanzees and report on  CCL3L  CNV within and among three additional primate species. On the basis of our findings we suggest that (1) the difference in population level copy number may explain previously reported observations of longer post-infection survivorship of Chinese-origin rhesus macaques, (2) stratification by  CCL3L  copy number in rhesus SIV vaccine trials will increase power and reduce noise due to non-vaccine-related differences in survival, and (3)  CCL3L  CNV is an ancestral component of the primate immune response and, therefore, copy number variation has not been driven by HIV or SIV per se.

Copy Number Variation of CCL3-like Genes Affects Rate of Progression to Simian-AIDS in Rhesus Macaques (Macaca mulatta)