ArticleViruses2025
TRIM38 Inhibits Zika Virus by Upregulating RIG-I/MDA5 Pathway and Promoting Ubiquitin-Mediated Degradation of Viral NS3 Protein.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- TRIM23 prevents adenovirus replication by p62-mediated selective autophagic degradation of viral E1A protein.PLoS pathogens · 2026Article
- Article
- TRIM38 Suppresses Breast Cancer Progression via Modulating SQSTM1 Ubiquitination and Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracellular Vesicles from Probiotic and BeneficialPharmaceutics · 2026Article
- Host protein cleavage by Dengue and Zika virus NS3 proteases: from substrate identification to potential biological consequences.Frontiers in cellular and infection microbiology · 2026Review
- Ubiquitin-specific protease 5 promotes EV-A71 replication by de-ubiquitinating MAVS and IRF3.Virologica Sinica · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Members of the tripartite motif (TRIM)-containing protein family play crucial roles in regulating immune system responses. The TRIM38 protein regulates host innate immunity and directly degrades some viral proteins through its E3 ubiquitin ligase activity. This study demonstrated that Zika virus (ZIKV) infection can promote the expression of TRIM38 in human glioma cells (U251). TRIM38 overexpression restricted ZIKV replication in U251 cells, while TRIM38 knockout enhanced ZIKV replication. TRIM38 overexpression upregulated the RIG-I/MDA5 pathway and promoted the level of IFN-β early during viral infection, while TRIM38 knockout had the opposite effect. In addition, TRIM38 interacts with ZIKV non-structural protein 3 (NS3) and degrades the NS3 protein through a lysosome-dependent manner via the E3 ligase activity of TRIM38. Deletion of the RING domain of TRIM38 abrogates its interaction with NS3 and impairs the antiviral activity of TRIM38. Our results indicate that TRIM38 is a novel antiviral protein against ZIKV, and it exerts antiviral activity by upregulating the RIG-I/MDA5 pathway, increasing IFN-β levels, and degrading the viral NS3 protein.
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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.