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- W3109535314 abstract "Abstract Clonal expansion of infected CD4 + T cells is a major mechanism of HIV-1 persistence and a barrier to cure. Potential causes are homeostatic proliferation, effects of HIV-1 integration, and interaction with antigens. Here we show that it is possible to link antigen responsiveness, full proviral sequence, integration site, and T cell receptor β-chain (TCRβ) sequence to examine the role of recurrent antigenic exposure in maintaining the HIV-1 reservoir. We isolated Cytomegalovirus (CMV)- and Gag-responding CD4 + T cells from 10 treated individuals. Proviral populations in CMV-responding cells were dominated by large clones, including clones harboring replication-competent proviruses. TCRβ repertoires showed high clonality driven by converging adaptive responses. Although some proviruses were in genes linked to HIV-1 persistence ( BACH2 , STAT5B, MKL1 ), proliferation of infected cells under antigenic stimulation occurred regardless of the site of integration. Paired TCRβ-integration site analysis showed that infection could occur early or late in the course of a clone’s response to antigen and could generate infected cell populations too large to be explained solely by homeostatic proliferation. Together these findings implicate antigen-driven clonal selection as a major factor in HIV-1 persistence, a finding that will be a difficult challenge to eradication efforts." @default.
- W3109535314 created "2020-12-07" @default.
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- W3109535314 date "2020-12-01" @default.
- W3109535314 modified "2023-10-18" @default.
- W3109535314 title "Antigen-driven clonal selection shapes the persistence of HIV-1 infected CD4+T cellsin vivo" @default.
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