Abstract: It would appear that a resident microglial population in the central nervous system might actually account for essential dynamics of an HIV-1 infection that transforms and amplifies various systemic forms of influence that bypass real participation by specific neurotropic mechanics. Indeed, one might perhaps view HIV-1 encephalitis as a true form of systemic infection that integrates a lymphocytic depletion with repetitive cyclic reinfection of neurons based on evolving dynamics of involved microglial cells. Indeed, as far as a conceptual rendering of HIV load quantification might in various ways influence such microglial participation in neuronal reinfections by HIV-1, one would in addition also recognize how viral antigen presentation is essentially inseparable from a whole series of integral immune reactivities that primarily evolve and transform as HIV-1 replicates and progressively spreads within the body. Indeed, one might recognize systemic processes as pathways that might predetermine various modes of involvement of the central nervous system. One would perhaps associate a concept of selective vulnerability of neuronal subsets in the central nervous system with essential attributes of systemic involvement that would predetermine how transformed immune reactivities influence even HIV-loading of brain microglia. One might perhaps even consider blood stream spread of the HIV-1 a simple series of inducing change that depletes not only T lymphocyte helper subset but especially induces a transforming role for microglia as a substitute cellular reservoir for the HIV- . Indeed, systemic determinants in establishment of HIV-1 encephalitis would in various ways perhaps amplify microglial participation in not simply exposing neurons to the virus but in rendering such neuronal infection a widespread phenomenon of cell loss. Effective participation of T lymphocyte helper subset depletion would in multiple ways constitute an active participation in the establishment of neuronal HIV-1 infection in specific modes of predetermined progression towards widespread cell loss of the ADIS dementia type as an abnormally transformed systemic immune reactivity.