The role of CD32 during HIV-1 infection
Persistence of latent HIV-1 in long-lived resting memory CD4+ T cells is a major barrier to curing HIV-1 infection, and thus a biomarker for latently infected cells would be of great scientific and clinical importance. 1 , 2 , 3 , 4 , 5 Through an elegant discovery-based approach, Descours et al . r...
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| Veröffentlicht in: | Nature (London) 2018-09, Vol.561 (7723), p.E17-E19 |
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| creator | Bertagnolli, Lynn N. White, Jennifer A. Simonetti, Francesco R. Beg, Subul A. Lai, Jun Tomescu, Costin Murray, Alexandra J. Antar, Annukka A. R. Zhang, Hao Margolick, Joseph B. Hoh, Rebecca Deeks, Stephen G. Tebas, Pablo Montaner, Luis J. Siliciano, Robert F. Laird, Gregory M. Siliciano, Janet D. |
| description | Persistence of latent HIV-1 in long-lived resting memory CD4+ T cells is a major barrier to curing HIV-1 infection, and thus a biomarker for latently infected cells would be of great scientific and clinical importance.
1
,
2
,
3
,
4
,
5
Through an elegant discovery-based approach, Descours
et al
. reported that CD32a, an Fcγ receptor not normally expressed on T cells, is a potential biomarker for latently infected cells.
6
Using the quantitative viral outgrowth assay, we show that CD32+ CD4+ T cells do not harbor the majority of intact proviruses in the latent reservoir and that the enrichment found by Descours
et al
. may in part reflect the use of an ultrasensitive ELISA for HIV-1 p24 antigen that does not predict exponential viral outgrowth. Our studies show that CD32 is not a biomarker for the major population of latently infected CD4+ T cells. |
| doi_str_mv | 10.1038/s41586-018-0494-3 |
| format | Article |
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1
,
2
,
3
,
4
,
5
Through an elegant discovery-based approach, Descours
et al
. reported that CD32a, an Fcγ receptor not normally expressed on T cells, is a potential biomarker for latently infected cells.
6
Using the quantitative viral outgrowth assay, we show that CD32+ CD4+ T cells do not harbor the majority of intact proviruses in the latent reservoir and that the enrichment found by Descours
et al
. may in part reflect the use of an ultrasensitive ELISA for HIV-1 p24 antigen that does not predict exponential viral outgrowth. Our studies show that CD32 is not a biomarker for the major population of latently infected CD4+ T cells.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/s41586-018-0494-3</identifier><identifier>PMID: 30232425</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/106 ; 13/31 ; 631/326/2521 ; 631/326/596/1787 ; Biological markers ; Brief Communications Arising ; Fc receptors ; HIV ; HIV infections ; Humanities and Social Sciences ; Medical schools ; multidisciplinary ; Science ; Science (multidisciplinary) ; T cells ; Universities and colleges</subject><ispartof>Nature (London), 2018-09, Vol.561 (7723), p.E17-E19</ispartof><rights>Springer Nature Limited 2018</rights><rights>COPYRIGHT 2018 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c644t-25efc15ec64b3ddae3ca670a0fe7d1b076a8abcd5d65af12140b7afa097a26423</citedby><cites>FETCH-LOGICAL-c644t-25efc15ec64b3ddae3ca670a0fe7d1b076a8abcd5d65af12140b7afa097a26423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30232425$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bertagnolli, Lynn N.</creatorcontrib><creatorcontrib>White, Jennifer A.</creatorcontrib><creatorcontrib>Simonetti, Francesco R.</creatorcontrib><creatorcontrib>Beg, Subul A.</creatorcontrib><creatorcontrib>Lai, Jun</creatorcontrib><creatorcontrib>Tomescu, Costin</creatorcontrib><creatorcontrib>Murray, Alexandra J.</creatorcontrib><creatorcontrib>Antar, Annukka A. R.</creatorcontrib><creatorcontrib>Zhang, Hao</creatorcontrib><creatorcontrib>Margolick, Joseph B.</creatorcontrib><creatorcontrib>Hoh, Rebecca</creatorcontrib><creatorcontrib>Deeks, Stephen G.</creatorcontrib><creatorcontrib>Tebas, Pablo</creatorcontrib><creatorcontrib>Montaner, Luis J.</creatorcontrib><creatorcontrib>Siliciano, Robert F.</creatorcontrib><creatorcontrib>Laird, Gregory M.</creatorcontrib><creatorcontrib>Siliciano, Janet D.</creatorcontrib><title>The role of CD32 during HIV-1 infection</title><title>Nature (London)</title><addtitle>Nature</addtitle><addtitle>Nature</addtitle><description>Persistence of latent HIV-1 in long-lived resting memory CD4+ T cells is a major barrier to curing HIV-1 infection, and thus a biomarker for latently infected cells would be of great scientific and clinical importance.
1
,
2
,
3
,
4
,
5
Through an elegant discovery-based approach, Descours
et al
. reported that CD32a, an Fcγ receptor not normally expressed on T cells, is a potential biomarker for latently infected cells.
6
Using the quantitative viral outgrowth assay, we show that CD32+ CD4+ T cells do not harbor the majority of intact proviruses in the latent reservoir and that the enrichment found by Descours
et al
. may in part reflect the use of an ultrasensitive ELISA for HIV-1 p24 antigen that does not predict exponential viral outgrowth. Our studies show that CD32 is not a biomarker for the major population of latently infected CD4+ T cells.</description><subject>13/106</subject><subject>13/31</subject><subject>631/326/2521</subject><subject>631/326/596/1787</subject><subject>Biological markers</subject><subject>Brief Communications Arising</subject><subject>Fc receptors</subject><subject>HIV</subject><subject>HIV infections</subject><subject>Humanities and Social Sciences</subject><subject>Medical schools</subject><subject>multidisciplinary</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>T cells</subject><subject>Universities and colleges</subject><issn>0028-0836</issn><issn>1476-4687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp90l1r1EAUBuBBFLtWf4A3EuyFiqTO92RvhGX96EJR0FUvh8nkJJ2SzWxnEmn_vRNSSwOr5CJk5jnvkORF6DnBpwSz4l3kRBQyx6TIMV_ynD1AC8KVzLks1EO0wJimnYLJI_QkxkuMsSCKP0ZHDFNGORUL9Gp7AVnwLWS-ztYfGM2qIbiuyc42P3OSua4G2zvfPUWPatNGeHZ7P0Y_Pn3crs_y86-fN-vVeW4l531OBdSWCEhPJasqA8waqbDBNaiKlFhJU5jSVqKSwtSEEo5LZWqDl8pQySk7Ru-n3P1Q7qCy0PXBtHof3M6EG-2N0_Odzl3oxv_W6Xiq6Bjw-jYg-KsBYq93LlpoW9OBH6KmhEhCpVAy0ZOJNqYFnV7Vp0Q7cr0Sii6FXAqVVH5ANdBBOt53ULu0PPMvD3i7d1f6Pjo9gNJVwc7Zg6lvZgPJ9HDdN2aIUW--f5vbt_-2q-2v9Ze5JpO2wccYoL772ATrsWZ6qplONdNjzTRLMy_u_6W7ib-9SoBOIO7HNkHQl34IXWrOf1L_AOTt10M</recordid><startdate>20180901</startdate><enddate>20180901</enddate><creator>Bertagnolli, Lynn N.</creator><creator>White, Jennifer A.</creator><creator>Simonetti, Francesco R.</creator><creator>Beg, Subul A.</creator><creator>Lai, Jun</creator><creator>Tomescu, Costin</creator><creator>Murray, Alexandra J.</creator><creator>Antar, Annukka A. R.</creator><creator>Zhang, Hao</creator><creator>Margolick, Joseph B.</creator><creator>Hoh, Rebecca</creator><creator>Deeks, Stephen G.</creator><creator>Tebas, Pablo</creator><creator>Montaner, Luis J.</creator><creator>Siliciano, Robert F.</creator><creator>Laird, Gregory M.</creator><creator>Siliciano, Janet D.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ATWCN</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180901</creationdate><title>The role of CD32 during HIV-1 infection</title><author>Bertagnolli, Lynn N. ; White, Jennifer A. ; Simonetti, Francesco R. ; Beg, Subul A. ; Lai, Jun ; Tomescu, Costin ; Murray, Alexandra J. ; Antar, Annukka A. R. ; Zhang, Hao ; Margolick, Joseph B. ; Hoh, Rebecca ; Deeks, Stephen G. ; Tebas, Pablo ; Montaner, Luis J. ; Siliciano, Robert F. ; Laird, Gregory M. ; Siliciano, Janet D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c644t-25efc15ec64b3ddae3ca670a0fe7d1b076a8abcd5d65af12140b7afa097a26423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13/106</topic><topic>13/31</topic><topic>631/326/2521</topic><topic>631/326/596/1787</topic><topic>Biological markers</topic><topic>Brief Communications Arising</topic><topic>Fc receptors</topic><topic>HIV</topic><topic>HIV infections</topic><topic>Humanities and Social Sciences</topic><topic>Medical schools</topic><topic>multidisciplinary</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>T cells</topic><topic>Universities and colleges</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bertagnolli, Lynn N.</creatorcontrib><creatorcontrib>White, Jennifer A.</creatorcontrib><creatorcontrib>Simonetti, Francesco R.</creatorcontrib><creatorcontrib>Beg, Subul A.</creatorcontrib><creatorcontrib>Lai, Jun</creatorcontrib><creatorcontrib>Tomescu, Costin</creatorcontrib><creatorcontrib>Murray, Alexandra J.</creatorcontrib><creatorcontrib>Antar, Annukka A. 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R.</au><au>Zhang, Hao</au><au>Margolick, Joseph B.</au><au>Hoh, Rebecca</au><au>Deeks, Stephen G.</au><au>Tebas, Pablo</au><au>Montaner, Luis J.</au><au>Siliciano, Robert F.</au><au>Laird, Gregory M.</au><au>Siliciano, Janet D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of CD32 during HIV-1 infection</atitle><jtitle>Nature (London)</jtitle><stitle>Nature</stitle><addtitle>Nature</addtitle><date>2018-09-01</date><risdate>2018</risdate><volume>561</volume><issue>7723</issue><spage>E17</spage><epage>E19</epage><pages>E17-E19</pages><issn>0028-0836</issn><eissn>1476-4687</eissn><abstract>Persistence of latent HIV-1 in long-lived resting memory CD4+ T cells is a major barrier to curing HIV-1 infection, and thus a biomarker for latently infected cells would be of great scientific and clinical importance.
1
,
2
,
3
,
4
,
5
Through an elegant discovery-based approach, Descours
et al
. reported that CD32a, an Fcγ receptor not normally expressed on T cells, is a potential biomarker for latently infected cells.
6
Using the quantitative viral outgrowth assay, we show that CD32+ CD4+ T cells do not harbor the majority of intact proviruses in the latent reservoir and that the enrichment found by Descours
et al
. may in part reflect the use of an ultrasensitive ELISA for HIV-1 p24 antigen that does not predict exponential viral outgrowth. Our studies show that CD32 is not a biomarker for the major population of latently infected CD4+ T cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30232425</pmid><doi>10.1038/s41586-018-0494-3</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| source | Nature; Alma/SFX Local Collection |
| subjects | 13/106 13/31 631/326/2521 631/326/596/1787 Biological markers Brief Communications Arising Fc receptors HIV HIV infections Humanities and Social Sciences Medical schools multidisciplinary Science Science (multidisciplinary) T cells Universities and colleges |
| title | The role of CD32 during HIV-1 infection |
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