Human and simian immunodeficiency virus-infected chimpanzees do not have increased intracellular levels of beta-chemokines in contrast to infected humans.

This study was undertaken to explain why chimpanzees infected with HIV-1 (human immunodeficiency virus type 1) or SIV(cpz) (simian immunodeficiency virus of chimpanzee) are relatively resistant to AIDS (acquired immunodeficiency syndrome). The numbers of beta-chemokine-positive cells were compared between uninfected and infected humans and chimpanzees using three-color cytofluorometry. In humans, the percentage of beta-chemokine-positive cells was significantly higher in CD8(+) T and natural killer (NK) cells than in CD4(+) T cells in both uninfected and HIV-1-infected individuals. In the presence of HIV-1 infection, however, both CD8(+) and CD4(+) T cell subsets contained significantly more beta-chemokine-positive cells than in the absence of infection. Interestingly, in chimpanzees two important differences were noted. First, their percentage of beta-chemokine-positive CD8(+) T and NK cells was significantly higher than in uninfected humans. Second, in contrast to humans, infection with either HIV-1 or with SIV(cpz) was not associated with increased numbers of beta-chemokine-positive cells. These results indicate that: constitutive high levels of intracellular beta-chemokines in chimpanzees' CD8 lymphocytes and NK cells do not necessarily correspond to lower levels of virus replication during the chronic phase of infection; and increased percentages of beta-chemokine-positive cells in HIV-infection are not a correlate of disease resistance. The data suggest that neither pre-nor post-exposure levels of intracellular beta-chemokines are correlated with the subsequent control of disease progression.