ArticlePLoS pathogens2021
Tripartite Motif 22 (TRIM22) protein restricts herpes simplex virus 1 by epigenetic silencing of viral immediate-early genes.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- IL-19 Modulates Antiviral Immunity and Inflammation via IL-20RB/STAT3/TRIM22 Signaling Pathway.Journal of medical virology · 2026Article
- SUMOylation and ubiquitination reciprocally regulate SMCHD1 antiviral activity against herpes simplex virus 1.PLoS pathogens · 2026Article
- Induction of TRIM22 promotes autophagy and apoptosis of colorectal cancer through reactive oxygen species generation.Journal of translational medicine · 2026Article
- TRIM22 mechanism promoting KAT2A ubiquitination degradation to regulate ferroptosis in hepatocellular carcinoma cell invasion and metastasis.Histology and histopathology · 2025Article
- Kaposi's sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production.Nature microbiology · 2025Article
- TRIMming down Flavivirus Infections.Viruses · 2024Review
- Local Power: The Role of Tissue-Resident Immunity in Human Genital Herpes Simplex Virus Reactivation.Viruses · 2024Review
- Histone H2A variant H2A.B is enriched in transcriptionally active and replicating HSV-1 lytic chromatin.Journal of virology · 2024Article
- Exploring TRIM proteins' role in antiviral defense against influenza A virus and respiratory coronaviruses.Frontiers in cellular and infection microbiology · 2024Review
- Genome-Wide CRISPR-Cas9 Screen Identifies SMCHD1 as a Restriction Factor for Herpesviruses.mBio · 2023Article
- Mechanism of autophagy induced by activation of the AMPK/ERK/mTOR signaling pathway after TRIM22-mediated DENV-2 infection of HUVECs.Virology journal · 2022Article
- CHAF1A/B mediate silencing of unintegrated HIV-1 DNAs early in infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Herpesvirus-mediated stabilization of ICP0 expression neutralizes restriction by TRIM23.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Review
- TRIM22. A Multitasking Antiviral Factor.Cells · 2021Review
- Tissue-Resident-Memory CD8Frontiers in immunology · 2021Article
- Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man.Frontiers in immunology · 2021Review
- Constitutive TRIM22 Expression in the Respiratory Tract Confers a Pre-Existing Defence Against Influenza A Virus Infection.Frontiers in cellular and infection microbiology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Intrinsic resistance is a crucial line of defense against virus infections, and members of the Tripartite Ring Interaction Motif (TRIM) family of proteins are major players in this system, such as cytoplasmic TRIM5α or nuclear promyelocytic leukemia (PML/TRIM19) protein. Previous reports on the antiviral function of another TRIM protein, TRIM22, emphasized its innate immune role as a Type I and Type II interferon-stimulated gene against RNA viruses. This study shows that TRIM22 has an additional intrinsic role against DNA viruses. Here, we report that TRIM22 is a novel restriction factor of HSV-1 and limits ICP0-null virus replication by increasing histone occupancy and heterochromatin, thereby reducing immediate-early viral gene expression. The corresponding wild-type equivalent of the virus evades the TRIM22-specific restriction by a mechanism independent of ICP0-mediated degradation. We also demonstrate that TRIM22 inhibits other DNA viruses, including representative members of the β- and γ- herpesviruses. Allelic variants in TRIM22 showed different degrees of anti-herpesviral activity; thus, TRIM22 genetic variability may contribute to the varying susceptibility to HSV-1 infection in humans. Collectively, these results argue that TRIM22 is a novel restriction factor and expand the list of restriction factors functioning in the infected cell nucleus to counter DNA virus infection.
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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.