期刊
CELL HOST & MICROBE
卷 16, 期 6, 页码 711-721出版社
CELL PRESS
DOI: 10.1016/j.chom.2014.10.010
关键词
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资金
- MRC UK [G0901732]
- Fondation Dormeur, Vaduz
- American Foundation for AIDS Research (amfAR) [107404-45-RFRL]
- Wellcome Trust [089577/Z/09/Z, 094449/Z/10/Z]
- NIH Center for HIV/AIDS Vaccine Immunology (CHAVI) [UO1-AI067854]
- Bill & Melinda Gates Foundation's Collaboration for AIDS Vaccine Discovery (CAVD)/CA-VIMC [38619]
- National Heart Lung and Blood Institute of the National Institutes of Health [RO1 HL-092565]
- Research Scholar Career Award from the Quebec Health Research Fund (FRQS)
- Medical Research Council [G0901732, G0400453] Funding Source: researchfish
- MRC [G0901732, G0400453] Funding Source: UKRI
- Wellcome Trust [094449/Z/10/Z, 089577/Z/09/Z] Funding Source: Wellcome Trust
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.
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