Differences in early events during entry and integration of HIV-1 into peripheral blood mononuclear cells (PBMC) might contribute to the absence of AIDS-like disease in chimpanzees as compared to humans. To address this question, we first tested the in vitro susceptibility of human and chimpanzee PBMC for infection with the two HIV-1 isolates III B and RF. The results of these studies revealed that chimpanzee PBMC had a slightly lower capability to support the growth of HIV-1 as compared to human PBMC. This was accompanied by a delayed accumulation of proviral HIV-1 DNA in cultures of HIV-1-infected chimpanzee PBMC. However, no differences between cells of the two species were observed when very early events of HIV-1 infection were studied. Shortly (20 h) after infection chimpanzee and human cells harbored similar amounts of proviral HIV-1 DNA and PBMC of both species behaved comparably with respect to pre-integration latency (i.e. the ability to activate extrachromosomal HIV-1 intermediates in HIV-1 infected quiescent cells at various times after infection). These results strongly suggest that the absence of AIDS-like disease in chimpanzees cannot be correlated with defects in early events of the HIV-1 replicative cycle.