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Research Digest differentiated T-cells observed in HIV infection.T-cells go through various stages toward late differentiation, and it may be that the early-differentiated CD8 T-cells, which maintain the ability to proliferate, offer protective immunity. But highly differentiated cells, they propose, exhibit characteristics associated with “replicative senescence’’—they are in effect old, worn-out cells that can no longer proliferate.Though replicative senescence is a natural process for most cells, in the context of HIV—in which infected individuals also lose the ability to replenish T-cells—it creates an aging population of T-cells that are less effective at ?ghting infection. Synopses of Research Articles T-Cell Differentiation and Progression of HIV Infection of HIV-infected individuals collected at two distinct points in time: at the onset of acute infection—which is characterized Of the 300 or so viruses that cause disease in humans, HIV may have the greatest adaptive advantage. Like most persistent viruses—including the herpesviruses Epstein–Barr and cytomegalovirus (CMV)—HIV employs various strategies to counteract its host’s response to infection. But HIV possesses a unique ability to sustain a progressive attack on the immune system—infecting the very cells that coordinate the Papagno L, Spina CA, Marchant A, Salio M, Rufer N, et al. (2004) Immune activation immune response—leaving the body susceptible even to normally harmless microorganisms. It is these so-called opportunistic infections, rather than the human immunode?ciency virus itself, that makes HIV so deadly.The speci?c mechanisms that engineer this ongoing systemic attack have been the subject of intense research. HIV targets white blood cells with protein surface receptors called CD4. These CD4, or helper,T-cells normally orchestrate the body’s immune response by signaling killer T-cells (which are also called CD8 T-cells, after their CD8 surface receptors) and other immune cells to multiply an