A central example of this is the latent reservoir concept, in which some HIV proviruses are thought to persist by maintaining a quiescent state that spares their host cells from virus- or immune-mediated killing 2. Understanding how HIV persists during antiretroviral therapy (ART) can advance the search for a safe and scalable HIV cure. These findings reveal that HIV-infected memory CD4 T cells under antiretroviral therapy are a distinctive population with host gene expression patterns that favour HIV silencing, cell survival and cell proliferation, with important implications for the development of HIV cure strategies. These genes ( n = 145) accounted for just 0.81% of the measured transcriptome and included negative regulators of HIV transcription that were higher in HIV-DNA + cells, positive regulators of HIV transcription that were lower in HIV-DNA + cells, and other genes involved in RNA processing, negative regulation of mRNA translation, and regulation of cell state and fate. Moreover, two groups of genes identified by network co-expression analysis were significantly associated with HIV-DNA + cells. HIV-DNA + memory CD4 T cells in the blood from people receiving antiretroviral therapy showed inhibition of six transcriptomic pathways, including death receptor signalling, necroptosis signalling and antiproliferative Gα12/13 signalling. Here we address this challenge using a microfluidic technology that isolates the transcriptomes of HIV-infected cells based solely on the detection of HIV DNA. Rare CD4 T cells that contain HIV under antiretroviral therapy represent an important barrier to HIV cure 1, 2, 3, but the infeasibility of isolating and characterizing these cells in their natural state has led to uncertainty about whether they possess distinctive attributes that HIV cure-directed therapies might exploit. Nature volume 614, pages 318–325 ( 2023) Cite this article

HIV silencing and cell survival signatures in infected T cell reservoirs

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