ArticleRetrovirology2015
HIV-1 transcriptional silencing caused by TRIM22 inhibition of Sp1 binding to the viral promoter.
Article in Retrovirology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- Methaneseleninic acid, a circadian-modulating agent, reactivates latent HIV-1 infection without cellular activation or proliferation.Journal of virology · 2026Article
- Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions.Frontiers in immunology · 2026Review
- TRIM proteins: A 'swiss army knife' of antiviral immunity.PLoS pathogens · 2025Review
- Article
- Review
- Mechanism of autophagy induced by activation of the AMPK/ERK/mTOR signaling pathway after TRIM22-mediated DENV-2 infection of HUVECs.Virology journal · 2022Article
- Neuropathogenesis of HIV-1: insights from across the spectrum of acute through long-term treated infection.Seminars in immunopathology · 2022Review
- Host Restriction Factors Modulating HIV Latency and Replication in Macrophages.International journal of molecular sciences · 2022Review
- Updating on Roles of HIV Intrinsic Factors: A Review of Their Antiviral Mechanisms and Emerging Functions.Intervirology · 2022Review
- Methamphetamine induces transcriptional changes in cultured HIV-infected mature monocytes that may contribute to HIV neuropathogenesis.Frontiers in immunology · 2022Article
- The roles and targeting options of TRIM family proteins in tumor.Frontiers in pharmacology · 2022Review
- Insights Into Persistent HIV-1 Infection and Functional Cure: Novel Capabilities and Strategies.Frontiers in microbiology · 2022Review
- TRIM22 genotype is not associated with markers of disease progression in children with HIV-1 infection.AIDS (London, England) · 2021Article
- HIV-1 persistence in the CNS: Mechanisms of latency, pathogenesis and an update on eradication strategies.Virus research · 2021Review
- TRIM22 inhibits the proliferation of gastric cancer cells through the Smad2 protein.Cell death discovery · 2021Article
- TRIM22. A Multitasking Antiviral Factor.Cells · 2021Review
- Plasmacytoid dendritic cells have divergent effects on HIV infection of initial target cells and induce a pro-retention phenotype.PLoS pathogens · 2021Article
- Knockdown of TRIM22 Relieves Oxygen-Glucose Deprivation/Reoxygenation-Induced Apoptosis and Inflammation Through Inhibition of NF-κB/NLRP3 Axis.Cellular and molecular neurobiology · 2021Article
- Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracellular defense proteins, also referred to as restriction factors, are capable of interfering with different steps of the viral life cycle. Among these, we have shown that Tripartite motif 22 (TRIM22) suppresses basal as well as phorbol ester-induced HIV-1 long terminal repeat (LTR)-mediated transcription, independently of its E3 ubiquitin ligase activity, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) binding to the U3 region and Tat interaction with the TAR region of the HIV-1 LTR. As basal HIV-1 transcription is driven by the transcription factor specificity protein 1 (Sp1), we have investigated whether TRIM22 could interfere with Sp1-driven transcriptional activation of the HIV-1 LTR.
findings293T cells, devoid of endogenous TRIM22 expression, were transfected with a TRIM22-expressing plasmid together with reporter plasmids driven by the HIV-1 LTR promoter either containing or lacking Sp1 binding sites or with reporter plasmids driven by non-viral promoter sequences either containing or lacking the three Sp1 binding sites from the HIV-1 LTR. These reporter assays showed that TRIM22 efficiently inhibited Sp1-driven transcription. Knocking down TRIM22 expression in the CD4(+) SupT1 T cell line increased the replication of Sp1-dependent HIV-1 variants. TRIM22 did not interact with Sp1, but prevented binding of Sp1 to the HIV-1 promoter, as demonstrated in protein-DNA pull down and chromatin immunoprecipitation assays.
conclusionTRIM22 acts as a suppressor of basal HIV-1 LTR-driven transcription by preventing Sp1 binding to the HIV-1 promoter.
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