Is repetitive opportunistic infection in AIDS patients the effective mechanism for neurodegeneration in terms of endlessly amplifying cytokine/chemokine effect?

With strict reference to how AIDS dementia somehow evolves from HIV infection through stages of initial monocyte-macrophage stimulation via a series of transendothelial and infiltrative events, it is perhaps significant to consider systemic body involvement by the HIV-associated processes to culminate in a concerted series of effects involving cascades and amplifications of action of cytokines and chemokines. Indeed, in terms that would implicate neurons only secondarily in AIDS dementia, one might perhaps consider HIV-1-dementia as an effective result of ongoing inflammation in the brain dependent not only on macrophage-microglial activation and replication, but also on glial participation in an overall process particularly conducive to increasing the brain HIV-1 load. In effect, perhaps, HIV encephalitis would constitute a system of mutually self-enhancing series of events ranging from macrophage-monocyte activation and replication on the one hand, and also HIV-1-induced cellular effects on the other that would result in progressively amplifying neuronal injury induced by cytokines and chemokines in AIDS patients suffering from repetitive opportunistic infections.