ArticleNature microbiology2025
HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Three immunoregulatory signatures define non-productive HIV infection in stem cell memory CD4Nature communications · 2026Article
- Metabolic reprogramming of CD4⁺ T cells by Zaprinast induces HIV-1 latency reversal ex vivo.Retrovirology · 2026Article
- Identification of the cellular factor KLF16 as a novel epigenetic repressor of HIV-1 transcription.Research square · 2026Article
- Preparation, Oral SNEDDS Formulation, and In Vivo Evaluation of the HIV-1 Latency-Reversing Agent EK-16A.Molecules (Basel, Switzerland) · 2026Article
- Article
- Identification of the cellular transcription factor KLF16 as a novel repressive epigenetic repressor of HIV-1 transcription.bioRxiv : the preprint server for biology · 2026Article
- Molecular Regulation of HIV-1 Expression and Persistence Across Diverse Cellular Reservoirs.International journal of molecular sciences · 2026Review
- Three immunoregulatory signatures define non-productive HIV infection in CD4bioRxiv : the preprint server for biology · 2026Article
- Transcriptomic Signatures of Immune Suppression and Cellular Dysfunction Distinguish Latent from Transcriptionally Active HIV-1 Infection in Dendritic Cells.International journal of molecular sciences · 2026Article
- Shaping the founders: naïve CD4 T cell heterogeneity in people with HIV-1 or HIV-2.Frontiers in immunology · 2026Article
- Proteomic profiling of single extracellular vesicles reveals association of CD31Frontiers in immunology · 2026Article
- Identification of Clinical Characteristics and Risk Factors of Invasive Pulmonary Aspergillosis in Patients with Acquired Immunodeficiency Syndrome: A Retrospective Study.Infection and drug resistance · 2026Article
- HIV-induced T cell quiescence and the origins of viral latency.Nature immunology · 2025Article
- HIV infection in microglia leads to senescence, triggering activation of neurotoxicity pathways.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Human immunodeficiency virus (HIV) persists in infected individuals despite effective antiretroviral therapy due to the rapid establishment of latent reservoirs, mainly composed of quiescent memory CD4+ T cells. The mechanisms governing latent reservoir formation remain poorly understood. Here, using single-cell RNA-seq and functional studies in human primary CD4+ T cell models, we show that HIV infection with reporter constructs and laboratory and patient-derived strains triggers transcriptomic remodelling, activating the p53 pathway and a quiescence programme mediated by Krüppel-like factor 2 (KLF2), a key quiescence regulator. Loss- and gain-of-function studies, including unbiased shRNA screens and confirmatory studies in CD4+ T cells from HIV+ donors, demonstrate that HIV infection drives KLF2 and p53 signalling, which downregulate MYC and proliferation pathways, resulting in proviral transcriptional silencing. This enhances latent reservoir formation in T cells, ensuring viral persistence. These findings present a mechanism for forming the latent HIV reservoir and broaden the repertoire of strategies through which viruses control host cells to their advantage.
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Registered trials
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