SynthesisRetrovirology2015
Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.
Synthesis in Retrovirology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Meta-analysis of transcriptomic variation in T-cell populations reveals both variable and consistent signatures of gene expression and splicing.RNA (New York, N.Y.) · 2020Pooled it
- Pharmacological and genetic modulation of IL-32 expression in intestinal epithelial cells does not impact HIV-1 outgrowth in co-cultured CD4Frontiers in immunology · 2026Article
- Medications for opioid use disorder shape immune responses during chronic HIV infection.Cell reports. Medicine · 2025Article
- Article
- The Complex Dysregulations of CD4 T Cell Subtypes in HIV Infection.International journal of molecular sciences · 2024Review
- Detection of CLCF1 protein expression by flow cytometry.Scientific reports · 2024Article
- IL-32 Drives the Differentiation of Cardiotropic CD4+ T Cells Carrying HIV DNA in People With HIV.The Journal of infectious diseases · 2024Article
- Metformin Enhances Antibody-Mediated Recognition of HIV-Infected CD4bioRxiv : the preprint server for biology · 2024Article
- A Canadian Survey of Research on HIV-1 Latency-Where Are We Now and Where Are We Heading?Viruses · 2024Review
- Article
- Identification of aryl hydrocarbon receptor as a barrier to HIV-1 infection and outgrowth in CD4Cell reports · 2023Article
- Closing the Door with CRISPR: Genome Editing of CCR5 and CXCR4 as a Potential Curative Solution for HIV.Biotech (Basel (Switzerland)) · 2022Review
- Anti-inflammatory effects of recreational marijuana in virally suppressed youth with HIV-1 are reversed by use of tobacco products in combination with marijuana.Retrovirology · 2022Article
- CXCR3 Expression Pattern on CD4+ T Cells and IP-10 Levels with Regard to the HIV-1 Reservoir in the Gut-Associated Lymphatic Tissue.Pathogens (Basel, Switzerland) · 2022Article
- HIV Infection and Spread between ThViruses · 2022Review
- Endothelial Cells Promote Productive HIV Infection of Resting CD4AIDS research and human retroviruses · 2022Article
- Th17 CD4+ T-Cell as a Preferential Target for HIV Reservoirs.Frontiers in immunology · 2022Review
- Flow Cytometry Sorting of Memory CCR6Methods in molecular biology (Clifton, N.J.) · 2022Article
- Th22 Cells Are a Major Contributor to the Mycobacterial CD4Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Exaggerated IL-17A activity in human in vivo recall responses discriminates active tuberculosis from latent infection and cured disease.Science translational medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe HIV-1 infection is characterized by profound CD4(+) T cell destruction and a marked Th17 dysfunction at the mucosal level. Viral suppressive antiretroviral therapy restores Th1 but not Th17 cells. Although several key HIV dependency factors (HDF) were identified in the past years via genome-wide siRNA screens in cell lines, molecular determinants of HIV permissiveness in primary Th17 cells remain to be elucidated.
resultsIn an effort to orient Th17-targeted reconstitution strategies, we investigated molecular mechanisms of HIV permissiveness in Th17 cells. Genome-wide transcriptional profiling in memory CD4(+) T-cell subsets enriched in cells exhibiting Th17 (CCR4(+)CCR6(+)), Th1 (CXCR3(+)CCR6(-)), Th2 (CCR4(+)CCR6(-)), and Th1Th17 (CXCR3(+)CCR6(+)) features revealed remarkable transcriptional differences between Th17 and Th1 subsets. The HIV-DNA integration was superior in Th17 versus Th1 upon exposure to both wild-type and VSV-G-pseudotyped HIV; this indicates that post-entry mechanisms contribute to viral replication in Th17. Transcripts significantly enriched in Th17 versus Th1 were previously associated with the regulation of TCR signaling (ZAP-70, Lck, and CD96) and Th17 polarization (RORγt, ARNTL, PTPN13, and RUNX1). A meta-analysis using the NCBI HIV Interaction Database revealed a set of Th17-specific HIV dependency factors (HDFs): PARG, PAK2, KLF2, ITGB7, PTEN, ATG16L1, Alix/AIP1/PDCD6IP, LGALS3, JAK1, TRIM8, MALT1, FOXO3, ARNTL/BMAL1, ABCB1/MDR1, TNFSF13B/BAFF, and CDKN1B. Functional studies demonstrated an increased ability of Th17 versus Th1 cells to respond to TCR triggering in terms of NF-κB nuclear translocation/DNA-binding activity and proliferation. Finally, RNA interference studies identified MAP3K4 and PTPN13 as two novel Th17-specific HDFs.
conclusionsThe transcriptional program of Th17 cells includes molecules regulating HIV replication at multiple post-entry steps that may represent potential targets for novel therapies aimed at protecting Th17 cells from infection and subsequent depletion in HIV-infected subjects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.