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- W2906650498 abstract "HIV persists in long-lived infected cells that are not affected by antiretroviral treatment. These HIV reservoirs are mainly located in CD4+ T cells, but their distribution is variable in the different subsets. Susceptibility to HIV-1 increases with CD4+ T cell differentiation. We evaluated whether the metabolic programming that supports the differentiation and function of CD4+ T cells affected their susceptibility to HIV-1. We found that differences in HIV-1 susceptibility between naive and more differentiated subsets were associated with the metabolic activity of the cells. Indeed, HIV-1 selectively infected CD4+ T cells with high oxidative phosphorylation and glycolysis, independent of their activation phenotype. Moreover, partial inhibition of glycolysis (1) impaired HIV-1 infection in vitro in all CD4+ T cell subsets, (2) decreased the viability of preinfected cells, and (3) precluded HIV-1 amplification in cells from HIV-infected individuals. Our results elucidate the link between cell metabolism and HIV-1 infection and identify a vulnerability in tackling HIV reservoirs." @default.
- W2906650498 created "2019-01-01" @default.
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- W2906650498 date "2019-03-01" @default.
- W2906650498 modified "2023-10-18" @default.
- W2906650498 title "Cellular Metabolism Is a Major Determinant of HIV-1 Reservoir Seeding in CD4+ T Cells and Offers an Opportunity to Tackle Infection" @default.
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- W2906650498 doi "https://doi.org/10.1016/j.cmet.2018.11.015" @default.
- W2906650498 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30581119" @default.
- W2906650498 hasPublicationYear "2019" @default.
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