<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Soto, PC</style></author><author><style face="normal" font="default" size="100%">Karris, MY</style></author><author><style face="normal" font="default" size="100%">Spina, CA</style></author><author><style face="normal" font="default" size="100%">Richman, DD</style></author><author><style face="normal" font="default" size="100%">Ajit Varki</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cell-intrinsic mechanism involving Siglec-5 associated with divergent outcomes of HIV-1 infection in human and chimpanzee CD4 T cells</style></title><secondary-title><style face="normal" font="default" size="100%">J Mol Med (Berl)</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Feb</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22945238</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">2</style></number><edition><style face="normal" font="default" size="100%">2012/09/05</style></edition><volume><style face="normal" font="default" size="100%">91</style></volume><pages><style face="normal" font="default" size="100%">261-70</style></pages><isbn><style face="normal" font="default" size="100%">1432-1440 (Electronic)09</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Human and chimpanzee CD4+ T cells differ markedly in expression of the inhibitory receptor Siglec-5, which contributes towards differential responses to activating stimuli. While CD4+ T cells from both species are equally susceptible to HIV-1 infection, chimpanzee cells survive better, suggesting a cell-intrinsic difference. We hypothesized that Siglec-5 expression protects T cells from activation-induced and HIV-1-induced cell death. Transduction of human CEM T cells with Siglec-5 decreased cell responses to stimulation. Following HIV-1 infection, a higher percentage of Siglec-5-positive cells survived, suggesting relative resistance to virus-induced cell death. Consistent with this, we observed an increase in percentage of Siglec-5-positive cells surviving in mixed infected cultures. Siglec-5-transduced cells also showed decreased expression of apoptosis-related proteins following infection and reduced susceptibility to Fas-mediated cell death. Similar Siglec-5-dependent differences were seen when comparing infection outcomes in primary CD4+ T cells from humans and chimpanzees. A protective effect of Siglec-5 was further supported by observing greater proportions of circulating CD4+ T cells expressing Siglec-5 in acutely infected HIV-1 patients, compared to controls. Taken together, our results suggest that Siglec-5 expression protects T cells from HIV-1- and apoptosis-induced cell death and contributes to the different outcomes of HIV-1 infection in humans and chimpanzees.&lt;/p&gt;</style></abstract><work-type><style face="normal" font="default" size="100%">Research Support, American Recovery and Reinvestment ActResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov&#039;tResearch Support, U.S. Gov&#039;t, Non-P.H.S.</style></work-type><accession-num><style face="normal" font="default" size="100%">22945238</style></accession-num><notes><style face="normal" font="default" size="100%">&lt;p&gt;&lt;span role=&quot;menubar&quot;&gt;J Mol Med (Berl).&lt;/span&gt;&amp;nbsp;2013 Feb;91(2):261-70. doi: 10.1007/s00109-012-0951-7. Epub 2012 Sep 4.&lt;/p&gt;</style></notes><custom2><style face="normal" font="default" size="100%">3558668</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Pathology, University of California, San Diego and Veterans Affairs San Diego Healthcare System, La Jolla, CA, USA.</style></auth-address></record></records></xml>