The identification of various genes involved in ability of some chimpanzees to control the pathogenicity of simian immunodeficiency virus (SIV), which parallels human immunodeficiency virus (HIV), is reported in PLOS Genetics this week. The findings offer insights into how the animals prevent infection from progressing to acquired immunodeficiency syndrome (AIDS). SIV — which jumped to humans as HIV-1 in the early 20th century — is largely endemic in chimpanzees and, in some groups, does not cause symptoms. To better understand these control mechanisms, a team led by scientists from the University of Pennsylvania used population genomics to uncover specific genes and molecular pathways involved in central and eastern chimpanzees' adaptation to SIV, including ones involved in the immune response to SIV and those encoding for host genes that physically interact with SIV/HIV. The researchers also provide evidence of SIV as a strong and recurrent selective pressure in the primates. "Our results confirm the importance of SIV as a selective factor, identify specific genetic changes that may have allowed our closest living relatives to reduce SIV's pathogenicity, and demonstrate the potential of population genomics to reveal the evolutionary mechanisms used by naïve hosts to reduce the pathogenicity of zoonotic pathogens," they write.