ArticleJournal of cellular physiology2009
Regulation of HIV-1 transcription at 3% versus 21% oxygen concentration.
Article in Journal of cellular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Effect of Kinases in Extracellular Vesicles from HIV-1-Infected Cells on Bystander Cells.Cells · 2025Article
- Article
- The hypoxia-regulated ectonucleotidase CD73 is a host determinant of HIV latency.Cell reports · 2023Article
- Crosstalk between hypoxic cellular micro-environment and the immune system: a potential therapeutic target for infectious diseases.Frontiers in immunology · 2023Article
- HIV-1 infection in sickle cell disease and sickle cell trait: role of iron and innate response.Expert review of hematology · 2022Article
- Disrupting the Cdk9/Cyclin T1 heterodimer of 7SK snRNP for the Brd4 and AFF1/4 guided reconstitution of active P-TEFb.Nucleic acids research · 2022Article
- Impact of Hypoxia over Human Viral Infections and Key Cellular Processes.International journal of molecular sciences · 2021Review
- Establishing Rules for Self-Adhesion and Aggregation ofLangmuir : the ACS journal of surfaces and colloids · 2020Article
- Review
- Hypoxic microenvironment shapes HIV-1 replication and latency.Communications biology · 2020Article
- Article
- Specific Biological Features of Adipose Tissue, and Their Impact on HIV Persistence.Frontiers in microbiology · 2019Review
- Glucose Metabolism and Oxygen Availability Govern Reactivation of the Latent Human Retrovirus HTLV-1.Cell chemical biology · 2017Article
- Increased iron export by ferroportin induces restriction of HIV-1 infection in sickle cell disease.Blood advances · 2016Article
- Phenyl-1-Pyridin-2yl-ethanone-based iron chelators increase IκB-α expression, modulate CDK2 and CDK9 activities, and inhibit HIV-1 transcription.Antimicrobial agents and chemotherapy · 2014Article
- Acute hypoxia affects P-TEFb through HDAC3 and HEXIM1-dependent mechanism to promote gene-specific transcriptional repression.Nucleic acids research · 2014Article
- Role of cellular iron and oxygen in the regulation of HIV-1 infection.Future virology · 2013Article
- Sickle cell disease is associated with decreased HIV but higher HBV and HCV comorbidities in U.S. hospital discharge records: a cross-sectional study.Sexually transmitted infections · 2012Article
- Hypoxia induces the gene expression and extracellular transmission of persistent lymphocytic choriomeningitis virus.Journal of virology · 2011Article
- Diametrically opposed effects of hypoxia and oxidative stress on two viral transactivators.Virology journal · 2010Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
HIV transcription is induced by the HIV-1 Tat protein, in concert with cellular co-factors including CDK9, CDK2, NF-kappaB, and others. The cells of most of the body's organs are exposed to approximately 3-6% oxygen, but most in vitro studies of HIV replication are conducted at 21% oxygen. We hypothesized that activities of host cell factors involved in HIV-1 replication may differ at 3% versus 21% O(2), and that such differences may affect HIV-1 replication. Here we show that Tat-induced HIV-1 transcription was reduced at 3% O(2) compared to 21% O(2). HIV-1 replication was also reduced in acutely or chronically infected cells cultured at 3% O(2) compared to 21% O(2). This reduction was not due the decreased cell growth or increased cellular toxicity and also not due to the induction of hypoxic response. At 3% O(2), the activity of CDK9/cyclin T1 was inhibited and Sp1 activity was reduced, whereas the activity of other host cell factors such as CDK2 or NF-kappaB was not affected. CDK9-specific inhibitor ARC was much less efficient at 3% compared to 21% O(2) and also expression of CDK9/cyclin T1-dependent IkappaB inhibitor alpha was repressed. Our results suggest that lower HIV-1 transcription at 3% O(2) compared to 21% O(2) may be mediated by lower activity of CDK9/cyclin T1 and Sp1 at 3% O(2) and that additional host cell factors such as CDK2 and NF-kappaB might be major regulators of HIV-1 transcription at low O(2) concentrations.
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Registered trials
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