Emma L. Turnbull

TL;DR: Kinetic analysis and mathematical modeling of virus immune escape showed that the contribution of CD8 T cell–mediated killing of productively infected cells was earlier and much greater than previously recognized and that it contributed to the initial decline of plasma virus in acute infection.

TL;DR: Observations document the preferential expansion of CD8+ T cells recognizing a subset of epitopes during the viral burst in acute HIV-1 infection and suggest that the nature of the initial, very rapidly expanded T cell response may influence the efficiency with which viral replication is contained in acute/early HIV infection.

TL;DR: Interestingly, only the magnitude of the total and not of the poly-functional T-cell responses was significantly associated with the selection of escape mutants, but the high contribution of MIP-1β-producing CD8+ T-cells to the total response suggests that mechanisms not limited to cytotoxicity could be exerting immune pressure during acute infection.

TL;DR: The model the team has developed in the rat permits analysis of DC in a near‐physiological setting, and provides a description of DC biology that other systems must take into account, to provide an overall picture of what is known regarding the nature of this complex cell type in the rats.

TL;DR: It is shown that during human chronic HIV‐1 infection, a CD8+ T‐cell positive costimulatory pathway mediated by DNAX‐activating molecule‐1 is also disrupted and aggravates the impairment of CTL effector function in chronic HIV-1 infection.