ArticleJournal of virology2011
Association of TRIM22 with the type 1 interferon response and viral control during primary HIV-1 infection.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 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
- Identification of RING E3 pseudoligases in the TRIM protein family.Nature communications · 2025Article
- Genetic determinants of host- and virus-derived insertions for hepatitis E virus replication.Nature communications · 2024Article
- Targeting Viral Transcription for HIV Cure Strategies.Microorganisms · 2024Review
- MicroRNA-376b-3p Promotes Porcine Reproductive and Respiratory Syndrome Virus Replication by Targeting Viral Restriction Factor TRIM22.Journal of virology · 2022Article
- TRIM22 genotype is not associated with markers of disease progression in children with HIV-1 infection.AIDS (London, England) · 2021Article
- Differential Inhibition of HIV Replication by the 12 Interferon Alpha Subtypes.Journal of virology · 2021Article
- Long Noncoding RNA LINC01207 Promotes Colon Cancer Cell Proliferation and Invasion by Regulating miR-3125/TRIM22 Axis.BioMed research international · 2020Article
- Transcriptome Sequencing of Peripheral Blood Mononuclear Cells from Elite Controller-Long Term Non Progressors.Scientific reports · 2019Article
- TRIM Proteins and Their Roles in Antiviral Host Defenses.Annual review of virology · 2018Review
- Retracted Article: TRIM22 functions as an oncogene in gliomas through regulating the Wnt/β-catenin signaling pathway.RSC advances · 2018Article
- miR-215 Enhances HCV Replication by Targeting TRIM22 and Inactivating NF-κB Signaling.Yonsei medical journal · 2018Article
- Mannose Receptor 1 Restricts HIV Particle Release from Infected Macrophages.Cell reports · 2018Article
- Intracellular Antiviral Immunity.Advances in virus research · 2018Review
- Advances in anti-viral immune defence: revealing the importance of the IFN JAK/STAT pathway.Cellular and molecular life sciences : CMLS · 2017Review
- Mechanisms of HIV-1 Control.Current HIV/AIDS reports · 2017Review
- Dynamic Modulation of Expression of Lentiviral Restriction Factors in Primary CD4Journal of virology · 2017Article
- Tripartite Motif 22 and Class II Transactivator Restriction Factors: Unveiling Their Concerted Action against Retroviruses.Frontiers in immunology · 2017Review
- Specific and Novel microRNAs Are Regulated as Response to Fungal Infection in Human Dendritic Cells.Frontiers in microbiology · 2017Article
- Genome-wide scan in two groups of HIV-infected patients treated with dendritic cell-based immunotherapy.Immunologic research · 2016Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Type 1 interferons (IFNs) induce the expression of the tripartite interaction motif (TRIM) family of E3 ligases, but the contribution of these antiviral factors to HIV pathogenesis is not completely understood. We hypothesized that the increased expression of select type 1 IFN and TRIM isoforms is associated with a significantly lower likelihood of HIV-1 acquisition and viral control during primary HIV-1 infection. We measured IFN-α, IFN-β, myxovirus resistance protein A (MxA), human TRIM5α (huTRIM5α), and TRIM22 mRNA levels in peripheral blood mononuclear cells (PBMCs) of high-risk, HIV-1-uninfected participants and HIV-1-positive study participants. Samples were available for 32 uninfected subjects and 28 infected persons, all within 1 year of infection. HIV-1-positive participants had higher levels of IFN-β (P = 0.0005), MxA (P = 0.007), and TRIM22 (P = 0.01) and lower levels of huTRIM5α (P < 0.001) than did HIV-1-negative participants. TRIM22 but not huTRIM5α correlated positively with type 1 IFN (IFN-α, IFN-β, and MxA) (all P < 0.0001). In a multivariate model, increased MxA expression showed a significant positive association with viral load (P = 0.0418). Furthermore, TRIM22 but not huTRIM5α, IFN-α, IFN-β, or MxA showed a negative correlation with plasma viral load (P = 0.0307) and a positive correlation with CD4(+) T-cell counts (P = 0.0281). In vitro studies revealed that HIV infection induced TRIM22 expression in PBMCs obtained from HIV-negative donors. Stable TRIM22 knockdown resulted in increased HIV-1 particle release and replication in Jurkat reporter cells. Collectively, these data suggest concordance between type 1 IFN and TRIM22 but not huTRIM5α expression in PBMCs and that TRIM22 likely acts as an antiviral effector in vivo.
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