ArticleScientific reports2019
TGF-β1 increases viral burden and promotes HIV-1 latency in primary differentiated human bronchial epithelial cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- SMAD4-BPIFA1 Axis Governs Airway Antiviral Defense in Myhre Syndrome.Biomolecules · 2026Article
- Review
- CircRNA profiles of extracellular vesicle-enriched fractions from ART suppressed pregnant women living with HIV identifies interactome networks key to inflammation and viral latency.Journal of translational medicine · 2026Article
- Epigenetic mechanisms of retroviral regulation: a comparative review.Epigenetics & chromatin · 2026Review
- HIV disrupts the lung molecular clock, leading to lung inflammation and features of emphysema.Communications biology · 2026Article
- Transcriptomic Analysis Reveals Key Pathways Influenced by HIV-2 Vpx.International journal of molecular sciences · 2025Article
- Proinflammatory Biomarkers and Clinical Factors Associated with Long-Term Mortality in People with HIV.Viruses · 2025Article
- No Association Between HIV-1 Subtype and Primary Resistance Mutations with CD4 Reconstitution During Effective Antiretroviral Treatment: An Observational, Cohort Study.International journal of molecular sciences · 2025Observational
- HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus.Frontiers in immunology · 2025Review
- Double, double toil and trouble: transforming growth factor beta (TGF-β) in HIV infection.Frontiers in immunology · 2025Review
- Article
- Emerging roles of senolytics/senomorphics in HIV-related co-morbidities.Biochemical pharmacology · 2024Review
- TGF-β blockade drives a transitional effector phenotype in T cells reversing SIV latency and decreasing SIV reservoirs in vivo.Nature communications · 2024Article
- Human Immunodeficiency Virus as a Risk Factor for Cardiovascular Disease.Cardiovascular toxicology · 2024Review
- Circadian-Coupled Genes Expression and Regulation in HIV-Associated Chronic Obstructive Pulmonary Disease (COPD) and Lung Comorbidities.International journal of molecular sciences · 2023Review
- Roles of TGF-β1 in Viral Infection during Pregnancy: Research Update and Perspectives.International journal of molecular sciences · 2023Review
- An Evaluation on the Role of Non-Coding RNA in HIV Transcription and Latency: A Review.HIV/AIDS (Auckland, N.Z.) · 2023Review
- NK cell subsets and dysfunction during viral infection: a new avenue for therapeutics?Frontiers in immunology · 2023Review
- Blockade of TGF-β signaling reactivates HIV-1/SIV reservoirs and immune responses in vivo.JCI insight · 2022Article
- The role of CD101-expressing CD4 T cells in HIV/SIV pathogenesis and persistence.PLoS pathogens · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Combination antiretroviral therapy (cART) has increased the life expectancy of HIV patients. However, the incidence of non-AIDS associated lung comorbidities, such as COPD and asthma, and that of opportunistic lung infections have become more common among this population. HIV proteins secreted by the anatomical HIV reservoirs can have both autocrine and paracrine effects contributing to the HIV-associated comorbidities. HIV has been recovered from cell-free bronchoalveolar lavage fluid, alveolar macrophages, and intrapulmonary lymphocytes. We have recently shown that ex-vivo cultured primary bronchial epithelial cells and the bronchial brushings from human subjects express canonical HIV receptors CD4, CCR5 and CXCR4 and can be infected with HIV. Together these studies suggest that the lung tissue can serve as an important reservoir for HIV. In this report, we show that TGF-β1 promotes HIV latency by upregulating a transcriptional repressor BLIMP-1. Furthermore, we identify miR-9-5p as an important intermediate in TGF-β-mediated BLIMP-1 upregulation and consequent HIV latency. The transcriptionally suppressed HIV can be reactivated by common latency reactivating agents. Together our data suggest that in patients with chronic airway diseases, TGF-β can elevate the HIV viral reservoir load that could further exacerbate the HIV associated lung comorbidities.
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Registered trials
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