Host hindrance to HIV-1 replication in monocytes and macrophages

HIV-1 Latency in Monocytes/Macrophages

Human immunodeficiency virus type 1 (HIV-1) targets CD4+ T cells and cells of the monocyte/macrophage lineage. HIV pathogenesis is characterized by the depletion of T lymphocytes and by the presence of a population of cells in which latency has been established called the HIV-1 reservoir. Highly active antiretroviral therapy (HAART) has significantly improved the life of HIV-1 infected patients...

Plastic restriction of HIV-1 replication in human macrophages derived from M1/M2 polarized monocytes.

M1/M2 cytokine-dependent polarization of primary human MDMs has been shown to contain CCR5-dependent (R5) HIV-1 replication. In this study, a similar effect was achieved when monocytes were first polarized toward M1 or M2 and were infected 7 d after their differentiation into MDMs, regardless of whether the cytokines were removed 18 h after cell stimulation or were left in culture. Unlike polar...

HIV-1-specific CTLs effectively suppress replication of HIV-1 in HIV-1-infected macrophages.

Both CD4+ T cells and macrophages are major reservoirs of HIV-1. Previous study showed that HIV-1-specific cytolytic T lymphocytes (CTLs) hardly recognize HIV-1-infected CD4+ T cells because of Nef-mediated HLA class I down-regulation, suggesting that HIV-1 escapes from HIV-1-specific CTLs and continues to replicate in HIV-1-infected donors. On the other hand, the CTL recognition of HIV-1-infec...

Cutting Edge: Dichotomous Effects of b-Chemokines on HIV Replication in Monocytes and Monocyte-Derived Macrophages

Hepcidin Induces M1 Macrophage Polarization in Monocytes or THP-1 Derived Macrophages

Background: Macrophage polarization plays a critical role in determining the inflammatory states. Hepcidin is a key negative regulator of iron homeostasis and functions. Although hepcidin has been shown to affect ferroportin expression in macrophages, whether it affects macrophage polarization is still largely unknown. Objective: To address whether hepcidin ind...