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- W4294053778 abstract "Abstract Human immunodeficiency virus type 1 (HIV-1) leads to a chronic, incurable infection that causes immune activation, resulting in chronic inflammation in people with HIV-1 (PWH) despite virologic suppression on antiretroviral therapy (ART). The mechanisms underlying this chronic inflammation are multifactorial; literature supports the role of lymphoid structures as reservoirs for viral latency and immune activation. Analysis of the cell type-specific transcriptomic changes induced by HIV-1 infection in lymphoid tissue has not been conducted. Human tonsil explants from four donors were infected with HIV-1 ex vivo. Single-cell RNA sequencing (scRNA Seq) was performed to evaluate the represented cell types and the impact of infection, differential gene expression, and inflammatory signaling pathways. Infected CD4 + T cells exhibited increased respiratory electron transport pathway genes. Myeloid cells with low HIV-1 transcript demonstrated increased NLRP3 inflammasome pathway genes, suggesting that these cells may play a “bystander” role in HIV-associated inflammatory pathogenesis. We propose that HIV-1-infected CD4 + T cells activate oxidative phosphorylation, resulting in excess ATP efflux. Bystander myeloid cells sense the resulting extracellular ATP, thereby triggering NLRP3 inflammasome activation, proinflammatory signaling pathways, and pyroptotic cell death. These observations support important mechanistic understanding to drive the development of therapeutic strategies to eradicate disease in PWH." @default.
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- W4294053778 date "2022-09-01" @default.
- W4294053778 modified "2023-09-27" @default.
- W4294053778 title "HIV-1 infection of human tonsils activates CD4+ T cell oxidative phosphorylation and myeloid NLRP3 inflammasome activation" @default.
- W4294053778 doi "https://doi.org/10.21203/rs.3.rs-1910284/v3" @default.
- W4294053778 hasPublicationYear "2022" @default.
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