<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ortiz AM</submitter><funding>CCR NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NCI NIH HHS</funding><funding>PHS HHS</funding><pagination>4433-45</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3204830</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>121(11)</volume><pubmed_abstract>CD4+ T cells play a central role in the immunopathogenesis of HIV/AIDS, and their depletion during chronic HIV infection is a hallmark of disease progression. However, the relative contribution of CD4+ T cells as mediators of antiviral immune responses and targets for virus replication is still unclear. Here, we have generated data in SIV-infected rhesus macaques (RMs) that suggest that CD4+ T cells are essential in establishing control of virus replication during acute infection. To directly assess the role of CD4+ T cells during primary SIV infection, we in vivo depleted these cells from RMs prior to infecting the primates with a pathogenic strain of SIV. Compared with undepleted animals, CD4+ lymphocyte-depleted RMs showed a similar peak of viremia, but did not manifest any post-peak de</pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Depletion of CD4⁺ T cells abrogates post-peak decline of viremia in SIV-infected rhesus macaques.</pubmed_title><pmcid>PMC3204830</pmcid><funding_grant_id>R37 AI066998</funding_grant_id><funding_grant_id>HHSN261200800001E</funding_grant_id><funding_grant_id>HHSN261200800001C</funding_grant_id><funding_grant_id>P30 AI045008</funding_grant_id><funding_grant_id>RR-00165</funding_grant_id><funding_grant_id>P51 RR000165</funding_grant_id><funding_grant_id>261200800001E</funding_grant_id><funding_grant_id>AI-66998</funding_grant_id><funding_grant_id>R01 AI066998</funding_grant_id><pubmed_authors>Little DM</pubmed_authors><pubmed_authors>Yi Y</pubmed_authors><pubmed_authors>Paiardini M</pubmed_authors><pubmed_authors>Hao XP</pubmed_authors><pubmed_authors>Ansari AA</pubmed_authors><pubmed_authors>Collman RG</pubmed_authors><pubmed_authors>Cramer EM</pubmed_authors><pubmed_authors>Klatt NR</pubmed_authors><pubmed_authors>Tabb B</pubmed_authors><pubmed_authors>Gonzalez-Scarano F</pubmed_authors><pubmed_authors>Brenchley JM</pubmed_authors><pubmed_authors>Estes JD</pubmed_authors><pubmed_authors>Ryzhova E</pubmed_authors><pubmed_authors>Else JG</pubmed_authors><pubmed_authors>Li B</pubmed_authors><pubmed_authors>Sternberg L</pubmed_authors><pubmed_authors>Ratcliffe S</pubmed_authors><pubmed_authors>Derdeyn CA</pubmed_authors><pubmed_authors>Lawson B</pubmed_authors><pubmed_authors>Carnathan PM</pubmed_authors><pubmed_authors>Silvestri G</pubmed_authors><pubmed_authors>Ortiz AM</pubmed_authors><pubmed_authors>Engram JC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Depletion of CD4⁺ T cells abrogates post-peak decline of viremia in SIV-infected rhesus macaques.</name><description>CD4+ T cells play a central role in the immunopathogenesis of HIV/AIDS, and their depletion during chronic HIV infection is a hallmark of disease progression. However, the relative contribution of CD4+ T cells as mediators of antiviral immune responses and targets for virus replication is still unclear. Here, we have generated data in SIV-infected rhesus macaques (RMs) that suggest that CD4+ T cells are essential in establishing control of virus replication during acute infection. To directly assess the role of CD4+ T cells during primary SIV infection, we in vivo depleted these cells from RMs prior to infecting the primates with a pathogenic strain of SIV. Compared with undepleted animals, CD4+ lymphocyte-depleted RMs showed a similar peak of viremia, but did not manifest any post-peak de</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Nov</publication><modification>2025-04-21T18:14:12.19Z</modification><creation>2019-03-27T00:45:31Z</creation></dates><accession>S-EPMC3204830</accession><cross_references><pubmed>22005304</pubmed><doi>10.1172/jci46023</doi><doi>10.1172/JCI46023</doi></cross_references></HashMap>