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• W2235523204 abstract "The mechanism behind the selective depletion of CD4(+) cells in HIV infections remains undetermined. Although HIV selectively infects CD4(+) cells, the relatively few infected cells in vivo cannot account for the extent of CD4(+) T cell depletion, suggesting indirect or bystander mechanisms. The role of virus replication, Env glycoprotein phenotype, and immune activation (IA) in this bystander phenomenon remains controversial. Using samples derived from HIV-infected patients, we demonstrate that, although IA in both CD4(+) and CD8(+) subsets correlates with CD4 decline, apoptosis in CD4(+) and not CD8(+) cells is associated with disease progression. Because HIV-1 Env glycoprotein has been implicated in bystander apoptosis, we cloned full-length Envs from plasma of viremic patients and tested their apoptosis-inducing potential (AIP). Interestingly, AIP of HIV-1 Env glycoproteins were found to correlate inversely with CD4:CD8 ratios, suggesting a role of Env phenotype in disease progression. In vitro mitogenic stimulation of PBMCs resulted in upregulation of IA markers but failed to alter the CD4:CD8 ratio. However, coculture of normal PBMCs with Env-expressing cells resulted in selective CD4 loss that was significantly enhanced by IA. Our study demonstrates that AIP of HIV-1 Env and IA collectively determine CD4 loss in HIV infection." @default.
• W2235523204 created "2016-06-24" @default.
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• W2235523204 date "2016-02-15" @default.
• W2235523204 modified "2023-10-11" @default.
• W2235523204 title "HIV-1 Env Glycoprotein Phenotype along with Immune Activation Determines CD4 T Cell Loss in HIV Patients" @default.
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• W2235523204 doi "https://doi.org/10.4049/jimmunol.1501588" @default.
• W2235523204 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4744550" @default.
• W2235523204 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26764036" @default.
• W2235523204 hasPublicationYear "2016" @default.
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