Higher immune activation and proliferation after SIV infection is purportedly associated with higher levels of T cell apoptosis, and central memory CD4+ T-cells are considered preferential targets for ‘‘bystander’’ activation. However, the level of central memory CD4+ T cell destruction was essentially identical in early infection, indicating that target cell availability of ability to infect/ destroy these cells was not likely a factor in early infection or the outcome. Importantly, the early cytokine responses were largely dominated by the induction of proinflammatory cytokines, which may amplify the immunopathology during early HIV infection. In pathogenic SIVmac251 infection, marked increases in essentially all cytokines/chemokines tested were detected in plasma through 56 days postinfection,Tiliroside and significantly elevated levels of IL-1b, IL-6, IL-10 and TNF-a, were detected at day 21 infection in SIVmac251-infected macaques compared with SHIV162P3 infected macaques. Elevated levels of several cytokines/chemokines in plasma are consistent with marked immune activation which could result in increased viral infection and amplification in multiple cells and tissue sites. Further, this elevated cytokine milieu could favor continued or sustained immune cell activation, resulting in continued cell turnover, and destruction of viral target cells in SIV infection. Thus, early, constrained immune activation and proliferation might contribute to reduced lymphocyte destruction, preservation of memory T cells, and lower viral amplification in tissues, at least until effective immune responses can be mounted against potentially pathogenic infections. In summary, marked differences in early host responses including T-cell activation and proliferation,Berbamine and cytokine/ chemokine responses were detected between macaques intravaginally infected with the minimally pathogenic SHIVsf162P3 and highly pathogenic SIVmac251, suggesting that early immune activation and proliferation are key factors in AIDS pathogenesis, and associated with disease outcome. Classically, investigators have sought enhanced immune responses for correlates of protection, and vaccine candidates are usually selected and advanced based on their ability to induce more potent immune responses to viral antigens. In contrast, in non-progressing host species, it has been proposed that suppressed immune response are associated with viral control. However, here we show that even within the same species of susceptible macaques, dampened immune responses to a virus that initially proliferates well within the host, may be associated with long term control and potential clearance of the virus. If so, perhaps vaccine strategies aimed at inducing temporary ‘‘tolerance’’, rather than ‘‘stimulatory’’ responses, may preserve key immunoregulatory cells and give the host time to mount effective immune responses. Cytokinesis is the final step of cell division that mechanically separates a mother cell into two daughter cells. Cytokinesis is accomplished via constriction of a cortical contractile ring. Although the constriction force generated by the actomyosinbased contractile ring is typically considered to be the principal mechanical component for cleavage furrow ingression, the mechanical properties of the cell surface also contribute to cleavage furrow ingression. One example that illustrates the importance of cortical mechanics is the fact that furrow ingression is completely inhibited by the disruption of cell surface actin filaments around the polar regions. The relative importance of contractile stress in the ring and modulation of cortical mechanics has not been well characterized. Some gene products required for cytokinesis are involved in cell surface stiffness, e.g., the actin regulator racE of Dictyostelium discoideum.