HIV-1 Primarily Targets the Innate Immune System and Only Secondarily Modulates Adaptive Immune Cell Depletion

Persistence of HIV-1 infection allows for permissive microenvironmental conditioning in terms of contextual innate immune participation. The progression of host cell injury constitutes an additional parametric formulation in self-amplifying modulation of the adaptive immune response in a manner that inclusively promotes the emergence of a final stage of AIDS that is both depletive and permissive for opportunistic infections and various forms of neoplasia. It is within contextual indices of promotion of depleted T-helper lymphocytes and of augmented viremic loads that manifestations of classic lesions emerge as the AIDS phenomenon. It is further to be realized that an apoptotic response of multiple cell subtypes including T-lymphocytes includes host-cell participation within formulated settings of further persistence of the retroviral infection. An all-inclusive phenomenon of dendritic cell-lymphocyte synapse formulation corresponds to the establishment of HIV-1 infection that specifically conditions all subsequent stages in depletion of the injured host cells regardless of the dynamics or kinetics of the retroviral replicative infectious process itself.