Abstract
Background Monocyte/macrophages are reservoirs capable of producing replication-competent HIV virions for many years despite suppressive HAART. APOBEC3 proteins represent critical determinants of monocyte resistance to HIV-1 infection, and their decreased expression during macrophage differentiation results in a permissive target cell population. Chemokines and their receptors are deeply involved in HIV-1 infection control. Monocytes/ macrophages are the major source of CCL2 in vitro and in vivo. Growing evidences suggest that CCL2 plays important roles in AIDS pathogenesis. We previously reported that CCL2 expression is up-regulated during monocyte differentiation to macrophages and is further increased in HIV-1 infected cells, where it acts as an autocrine factor promoting HIV-1 replication. The aim of this study was to investigate the mechanisms by which CCL2 affects HIV-1 replication in macrophages.
Highlights
Monocyte/macrophages are reservoirs capable of producing replication-competent HIV virions for many years despite suppressive HAART
We previously reported that CCL2 expression is up-regulated during monocyte differentiation to macrophages and is further increased in HIV-1 infected cells, where it acts as an autocrine factor promoting HIV-1 replication
We found that CCL2 neutralization induces a strong reduction of HIV-1 DNA level 4 and 7 days postinfection
Summary
Monocyte/macrophages are reservoirs capable of producing replication-competent HIV virions for many years despite suppressive HAART. APOBEC3 proteins represent critical determinants of monocyte resistance to HIV-1 infection, and their decreased expression during macrophage differentiation results in a permissive target cell population. Chemokines and their receptors are deeply involved in HIV-1 infection control. Monocytes/ macrophages are the major source of CCL2 in vitro and in vivo. We previously reported that CCL2 expression is up-regulated during monocyte differentiation to macrophages and is further increased in HIV-1 infected cells, where it acts as an autocrine factor promoting HIV-1 replication. The aim of this study was to investigate the mechanisms by which CCL2 affects HIV-1 replication in macrophages
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