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999			_c16396 _d16396
003			PC16396
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008			210513b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_91010 _aPablos Álvarez, José Luis _eReumatología
245	0	0	_aMacrophage infection via selective capture of HIV-1-infected CD4+ T cells. _h[artículo]
260			_bCell host & microbe, _c2014
300			_a16(6):711-21.
500			_aFormato 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.
501			_aPMID: 25467409 PMC4271767
504			_aContiene 35 referencias
520			_aMacrophages 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.
710			_9123 _aServicio de Reumatología
710			_9625 _aInstituto de Investigación imas12
856			_uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271767/ _yAcceso libre
942			_2ddc _cART _n0