ArticleNature communications2017
HIV-1-mediated insertional activation of STAT5B and BACH2 trigger viral reservoir in T regulatory cells.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 116 citations in OpenAlex.
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- CD19-targeting CAR T cell immunotherapy outcomes correlate with genomic modification by vector integration.The Journal of clinical investigation · 2020Trial
- Intact HIV-1 proviruses accumulate at distinct chromosomal positions during prolonged antiretroviral therapy.The Journal of clinical investigation · 2019Trial
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Single-cell analysis of HIV expression and integration sites reveals robust viral expression across diverse chromatin environments.Microbiology spectrum · 2026Article
- Clonal dynamics of HIV-infected and uninfected T cells.EBioMedicine · 2026Article
- Immune correlates of HIV-1 rebound during broadly neutralizing antibody treatment in young children.The Journal of clinical investigation · 2026Article
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- Development and validation of HIV SMRTcap for the characterization of HIV-1 reservoirs across tissues and subtypes.PLoS pathogens · 2026Article
- Transcription factor BACH2 shapes tissue-resident memory T cell programs to promote HIV-1 persistence.Immunity · 2025Article
- CRISPR-based gene therapy for huntington's disease: current advances and future prospects.Neurogenetics · 2025Review
- The STAT Signaling Pathway in HIV-1 Infection: Roles and Dysregulation.International journal of molecular sciences · 2025Review
- BACH2 promotes seeding and establishment of long-lived HIV-1 reservoir in memory CD4Cell reports. Medicine · 2025Article
- Impacts of immune checkpoint inhibitors use on the HIV reservoir are linked to provirus sequences but not integration sites.Scientific reports · 2025Article
- Proviruses in CD4Science translational medicine · 2025Article
- In vitro HIV DNA integration in STAT3 drives T cell persistence-A model of HIV-associated T cell lymphoma.PLoS pathogens · 2025Article
- Dysregulation of the tumor suppressor Menin and its target Bach2 in HTLV-1 infection.Retrovirology · 2025Article
- Barcoded HIV-1 reveals viral persistence driven by clonal proliferation and distinct epigenetic patterns.Nature communications · 2025Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1 insertions targeting BACH2 or MLK2 are enriched and persist for decades in hematopoietic cells from patients under combination antiretroviral therapy. However, it is unclear how these insertions provide such selective advantage to infected cell clones. Here, we show that in 30/87 (34%) patients under combination antiretroviral therapy, BACH2, and STAT5B are activated by insertions triggering the formation of mRNAs that contain viral sequences fused by splicing to their first protein-coding exon. These chimeric mRNAs, predicted to express full-length proteins, are enriched in T regulatory and T central memory cells, but not in other T lymphocyte subsets or monocytes. Overexpression of BACH2 or STAT5B in primary T regulatory cells increases their proliferation and survival without compromising their function. Hence, we provide evidence that HIV-1-mediated insertional activation of BACH2 and STAT5B favor the persistence of a viral reservoir in T regulatory cells in patients under combination antiretroviral therapy.HIV insertions in hematopoietic cells are enriched in BACH2 or MLK2 genes, but the selective advantages conferred are unknown. Here, the authors show that BACH2 and additionally STAT5B are activated by viral insertions, generating chimeric mRNAs specifically enriched in T regulatory cells favoring their persistence.
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