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• W2095683698 abstract "Significance HIV-1 enters host cells via CD4 and the coreceptors CXCR4 or CCR5. Most HIV-1 variants isolated from newly infected individuals use CCR5 (R5 strains) and infect Th1 cells, among other cell types. In ∼50% of patients, R5 strains shift to X4 strains (which use CXCR4) and infect mainly Th2 cells, leading to poor prognosis and rapid disease progression. In Th2 cells, CD4 and CXCR4 levels resemble those of Th1 cells, but they express little CCR5. We report that CCR5 expression in CD4 + T cells reduced X4 strain cell entry and infection; the molecular mechanism involves CD4/CXCR4/CCR5 oligomer formation. CCR5 expression altered CD4/CXCR4 heterodimer conformation, blocking virus binding. Oligomeric complexes should thus be considered a target for reducing HIV-1 binding and infection." @default.
• W2095683698 created "2016-06-24" @default.
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• W2095683698 date "2014-04-28" @default.
• W2095683698 modified "2023-10-06" @default.
• W2095683698 title "CCR5/CD4/CXCR4 oligomerization prevents HIV-1 gp120_IIIBbinding to the cell surface" @default.
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• W2095683698 doi "https://doi.org/10.1073/pnas.1322887111" @default.
• W2095683698 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4024905" @default.
• W2095683698 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24778234" @default.
• W2095683698 hasPublicationYear "2014" @default.
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