Macrophage sequestration of HIV-1 enhances homeostatic-related systems in promoting viral spread and replication

Abstract

Decisive modulatory systems of compromise and systems of dynamic turnover in lymphoid cells and macrophages are activated by repeated bursts of viremia and as promotional schemes of representation of subsequent spread and replication of HIV-1. In such operative systems of micro-environmental conditioning and reconditioning, a significant mechanism towards the turnover of specific cell-types occurs within context of sequestration within macrophages and circulating monocytes. Dendritic cells in germinal follicles and within specific organs such as the Langerhans cells of the skin are allied to dysfunctionality of such cellular subtypes as exemplified by the resident microglia of the central nervous system. Decisive perturbation in cell-type number and in dysfunctional activation indicate an exquisite modulatory role for HIV-1 in promoting homeostatic-related mechanisms within organs and tissues towards utilization in terms of viral dynamics and cytokine operability. In such manner, HIV-1 replication is itself a system of promotion in spread of viruses across cell-type and host cell specificities that tend to characterize and recharacterize systems of cytokine network operability in particular.