sialoadhesin expressed on ifn-induced monocytes binds hiv-1 and enhances infectivitysialoadhesin ifn-induced单核细胞结合hiv - 1表达,提高传染性.pdfVIP

sialoadhesin expressed on ifn-induced monocytes binds hiv-1 and enhances infectivitysialoadhesin ifn-induced单核细胞结合hiv - 1表达,提高传染性.pdf

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sialoadhesin expressed on ifn-induced monocytes binds hiv-1 and enhances infectivitysialoadhesin ifn-induced单核细胞结合hiv - 1表达,提高传染性

Sialoadhesin Expressed on IFN-Induced Monocytes Binds HIV-1 and Enhances Infectivity 1 1 1 1,2 Hans Rempel , Cyrus Calosing , Bing Sun , Lynn Pulliam * 1 Department of Laboratory Medicine at the Veterans Affairs Medical Center, San Francisco, California, United States of America, 2 University of California San Francisco, San Francisco, California, United States of America Abstract Background: HIV-1 infection dysregulates the immune system and alters gene expression in circulating monocytes. Differential gene expression analysis of CD14+ monocytes from subjects infected with HIV-1 revealed increased expression of sialoadhesin (Sn, CD169, Siglec 1), a cell adhesion molecule first described in a subset of macrophages activated in chronic inflammatory diseases. Methodology/Principal Findings: We analyzed sialoadhesin expression on CD14+ monocytes by flow cytometry and found significantly higher expression in subjects with elevated viral loads compared to subjects with undetectable viral loads. In cultured CD14+ monocytes isolated from healthy individuals, sialoadhesin expression was induced by interferon-a and interferon-c but not tumor necrosis factor-a. Using a stringent binding assay, sialoadhesin-expressing monocytes adsorbed HIV-1 through interaction with the sialic acid residues on the viral envelope glycoprotein gp120. Furthermore, monocytes expressing sialoadhesin facilitated HIV-1 trans infection of permissive cells, which occurred in the absence of monocyte self- infection. Conclusions/Significance: Increased sialoadhesin expression on CD14+ monocytes occurred in response to HIV-1 infection with maximum expression associated with high viral load. We show that interferons induce

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