Host hindrance to HIV-1 replication in monocytes and macrophages

Abstract

Monocytes and macrophages are targets of HIV-1 infection and play critical roles in multiple aspects of viral pathogenesis. HIV-1 can replicate in blood monocytes, although only a minor proportion of circulating monocytes harbor viral DNA. Resident macrophages in tissues can be infected and function as viral reservoirs. However, their susceptibility to infection, and their capacity to actively replicate the virus, varies greatly depending on the tissue localization and cytokine environment. The susceptibility of monocytes to HIV-1 infection in vitro depends on their differentiation status. Monocytes are refractory to infection and become permissive upon differentiation into macrophages. In addition, the capacity of monocyte-derived macrophages to sustain viral replication varies between individuals. Host determinants regulate HIV-1 replication in monocytes and macrophages, limiting several steps of the viral life-cycle, from viral entry to virus release. Some host factors responsible for HIV-1 restriction are shared with T lymphocytes, but several anti-viral mechanisms are specific to either monocytes or macrophages. Whilst a number of these mechanisms have been identified in monocytes or in monocyte-derived macrophages in vitro, some of them have also been implicated in the regulation of HIV-1 infection in vivo, in particular in the brain and the lung where macrophages are the main cell type infected by HIV-1. This review focuses on cellular factors that have been reported to interfere with HIV-1 infection in monocytes and macrophages, and examines the evidences supporting their role in vivo, highlighting unique aspects of HIV-1 restriction in these two cell types.

HIV-1–Mediated BAFF Secretion in Macrophages Does Not Require Endosomal TLRs, Type-I IFN, and Nef, but Depends on the Cellular Phenotype Status

“…These results motivated us to investigate whether HIV-1 could also modulate BAFF production in macrophages, because they represent another important cellular source of BAFF (35,36,(44)(45)(46)(47) and are, contrary to monocytes, permissive to productive HIV-1 infection (48). As shown in Fig.…”

Equine herpesvirus type 1 replication is delayed in CD172a+ monocytic cells and controlled by histone deacetylases

“…An early block in the replication cycle of EHV-1 may protect infected leukocytes from efficient recognition by the immune system and hence allow these carrier cells to reach target organs. Interestingly, retroviruses such as human immunodeficiency virus (HIV) and maedi-visna virus, and other herpesviruses, such as pseudorabies virus and human cytomegalovirus (HCMV), are known to influence early response systems by blocking several steps of their replication cycle in their target cells in order to evade immune responses and promote viral pathogenesis (Rice et al, 1984;Nauwynck & Pensaert, 1994;Thormar, 2005;Bergamaschi & Pancino, 2010). However, until now, the mechanism of how EHV-1 uses CD172a…”

p21-mediated RNR2 repression restricts HIV-1 replication in macrophages by inhibiting dNTP biosynthesis pathway

“…Environmental stimuli such as cytokines, bacterial products, and immune complexes also influence macrophage permissiveness to HIV-1 infection (8). HIV-1 replication in macrophages is regulated by cellular factors that can either enhance or inhibit various steps of the viral replicative cycle (9). In particular, HIV-1 reverse transcription is much slower in monocyte-derived macrophages (MDMs) than in activated T cells.…”