Pablos Álvarez, José Luis
Macrophage infection via selective capture of HIV-1-infected CD4+ T cells. [artículo] - Cell host & microbe, 2014 - 16(6):711-21.
Formato Vancouver:
Baxter AE, Russell RA, Duncan CJ, Moore MD, Willberg CB, Pablos JL et al. Macrophage infection via selective capture of HIV-1-infected CD4+ T cells. Cell Host Microbe. 2014 Dec 10;16(6):711-21.
PMID: 25467409
PMC4271767
Contiene 35 referencias
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.
Macrophage infection via selective capture of HIV-1-infected CD4+ T cells. [artículo] - Cell host & microbe, 2014 - 16(6):711-21.
Formato Vancouver:
Baxter AE, Russell RA, Duncan CJ, Moore MD, Willberg CB, Pablos JL et al. Macrophage infection via selective capture of HIV-1-infected CD4+ T cells. Cell Host Microbe. 2014 Dec 10;16(6):711-21.
PMID: 25467409
PMC4271767
Contiene 35 referencias
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.
