The amount of ISGs positively correlates with HIV viral load and inversely correlates with CD4+ T-cell counts.31 Further evidence of a role for increased IFN-α activity in causing HIV-induced immune dysfunction has been obtained from animal models; persistent upregulation of ISGs in CD4+ T cells and elevated levels of IFN-α are observed in SIV-infected rhesus macaques (which are not natural hosts and develop AIDS) but not in SIV-infected African green monkeys (which are natural hosts and do not progress to AIDS).33 This evidence concerns the gene IFNA1 and immune system disorder.