Macrophage infection via selective capture of HIV-1-infected CD4+ T cells.

Journal article

Macrophages contribute to HIV-1 pathogenesis by forming a viral reservoir and mediating neurological disorders. Cell-free HIV-1 infection of macrophages is inefficient, in part due to low plasma membrane expression of viral entry receptors. We find that macrophages selectively capture and engulf HIV-1-infected CD4+ T cells leading to efficient macrophage infection. Infected T cells, both healthy and dead or dying, were taken up through viral envelope glycoprotein-receptor-independent interactions, implying a mechanism distinct from conventional virological synapse formation. Macrophages infected by this cell-to-cell route were highly permissive for both CCR5-using macrophage-tropic and otherwise weakly macrophage-tropic transmitted/founder viruses but restrictive for nonmacrophage-tropic CXCR4-using virus. These results have implications for establishment of the macrophage reservoir and HIV-1 dissemination in vivo.

Authors: Baxter, A; Russell, R; Duncan, C; Moore, R; Willberg, C

• Publication status: Published
• Peer review status: Peer reviewed
• Publisher: Elsevier
• Journal: Cell host and microbe
• Volume: 16
• Issue: 6
• Pages: 711-721
• Publication date: 2014-11-20
• Acceptance date: 2014-10-14
• DOI: 10.1016/j.chom.2014.10.010
• EISSN: 1934-6069
• ISSN: 1931-3128
• Language: English
• Keywords: receptors, HIV; humans; CD4-Positive T-Lymphocytes; HIV infections; macrophages; viral tropism; HIV-1; cell line; viral envelope proteins; SBTMR