ArticleJournal of virology2009
Transcriptional restriction of human immunodeficiency virus type 1 gene expression in undifferentiated primary monocytes.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
49 citing papers in PubMed, 66 citations in OpenAlex.
- SAMHD1 enhances HIV-1-induced apoptosis in monocytic cells via the mitochondrial pathway.mBio · 2025Article
- Host factor Naf1 restricts HIV-1 infection of myeloid cells and compromises the capacity of dendritic cell to prime CD4Virologica Sinica · 2025Article
- Neurological impact of HIV/AIDS and substance use alters brain function and structure.Frontiers in medicine · 2024Review
- HIV infection of non-classical cells in the brain.Retrovirology · 2023Review
- Synergistic Chromatin-Modifying Treatments Reactivate Latent HIV and Decrease Migration of Multiple Host-Cell Types.Viruses · 2021Article
- N6-methyladenosine modification of HIV-1 RNA suppresses type-I interferon induction in differentiated monocytic cells and primary macrophages.PLoS pathogens · 2021Article
- TRAF6 and TAK1 Contribute to SAMHD1-Mediated Negative Regulation of NF-κB Signaling.Journal of virology · 2021Article
- HIV replication and latency in monocytes and macrophages.Seminars in immunology · 2021Review
- The Polar Region of the HIV-1 Envelope Protein Determines Viral Fusion and Infectivity by Stabilizing the gp120-gp41 Association.Journal of virology · 2019Article
- Host and Viral Factors Influencing Interplay between the Macrophage and HIV-1.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
- Comparative Description of the Expression Profile of Interferon-Stimulated Genes in Multiple Cell Lineages Targeted by HIV-1 Infection.Frontiers in microbiology · 2019Article
- Article
- Scaffold attachment factor B suppresses HIV-1 infection of CD4The Journal of biological chemistry · 2018Article
- SAMHD1 Impairs HIV-1 Gene Expression and Negatively Modulates Reactivation of Viral Latency in CD4Journal of virology · 2018Article
- SAMHD1 suppresses innate immune responses to viral infections and inflammatory stimuli by inhibiting the NF-κB and interferon pathways.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- BET inhibitors RVX-208 and PFI-1 reactivate HIV-1 from latency.Scientific reports · 2017Article
- Naf1 Regulates HIV-1 Latency by Suppressing Viral Promoter-Driven Gene Expression in Primary CD4+ T Cells.Journal of virology · 2017Article
- The HIV-1 Tat Protein: Mechanism of Action and Target for HIV-1 Cure Strategies.Current pharmaceutical design · 2017Review
- Cyclin-dependent kinases as therapeutic targets for HIV-1 infection.Expert opinion on therapeutic targets · 2016Review
- SAMHD1-mediated HIV-1 restriction in cells does not involve ribonuclease activity.Nature medicine · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Monocytes are critical precursors of dendritic cells and macrophages, which play an important role in the pathogenesis of human immunodeficiency virus type 1 (HIV-1). HIV-1 postentry infection is blocked in undifferentiated monocytes in vitro, while the underlying mechanisms are not fully understood. HIV-1 Tat-mediated transactivation of the viral long terminal repeat (LTR) promoter is essential for HIV-1 transcription. Two critical cellular cofactors of HIV-1 Tat, cyclin T1 (CycT1) and cyclin-dependent kinase 9 (CDK9), are required for LTR-directed HIV-1 transcription. In addition to the previously identified restrictions in early viral life cycle, we find that HIV-1 gene expression is impaired in undifferentiated primary monocytes. Transfection of monocytes by nucleofection with HIV-1 proviral DNA could not produce infectious HIV-1. The lack of Tat transactivation of the LTR promoter correlated with the impaired HIV-1 gene expression in monocytes. Interestingly, heterokaryons between primary monocytes and a human embryonic kidney cell line restored Tat transactivation of LTR, suggesting that monocytes lack cellular factors required for Tat transactivation. CycT1 protein was undetectable in freshly isolated monocytes and induced in monocyte-differentiated macrophages, while the expression of CDK9 remained constant. Transient expression of CycT1 in undifferentiated monocytes could not rescue Tat transactivation, suggesting that CycT1 is not the only limiting factor of HIV-1 infection in monocytes. Furthermore, monocyte differentiation into macrophages appeared to enhance the phosphorylation of CDK9, which correlated with significantly increased HIV-1 infection in macrophages. Our results provide new insights into HIV-1 infection and regulation in primary monocytes and viral pathogenesis.
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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.