ArticleMicrobiology spectrum2025
miR-30a enhanced RIG-I-mediated type I interferon antiviral response by targeting USP14.
Article in Microbiology spectrum, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Investigating the Role of microRNA in Host-Influenza A and Other Respiratory RNA Virus Interactions.Pathogens (Basel, Switzerland) · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
Type I interferon (IFN) signaling plays a prominent role in the host innate immune defense against viral infection. The regulatory roles of miRNAs on the innate immune response remain to be further explored. Although miR-30a has been implicated in the regulation of various viral life cycles, the underlying mechanism on type I IFN signaling remains controversial. Herein, miR-30a was identified as a regulator of type 1 IFN production in macrophages. We observed that miR-30a expression was significantly decreased by vesicular stomatitis virus (VSV) or Sendai virus (SeV) infection in THP-1 cells. In return, overexpression of miR-30a promoted viral infection-triggered IFN and ISGs production to inhibit VSV or SeV replication. Mechanistically, miR-30a inhibited USP14 expression by binding with the 3'UTR of mRNA. USP14 was identified as an inhibitor of IFN signaling by removing the K63-linked ubiquitination from RIG-I, as previously reported. Consequently, miR-30a, by downregulating USP14 expression, enhanced the K63-linked ubiquitination of RIG-I to exert broad-spectrum antiviral effects. Overall, this study revealed a novel antiviral mechanism of miR-30a through the miR-30a-USP14-RIG-I axis and enriched miRNA-innate immunity regulatory networks.IMPORTANCEmiRNAs are involved in the regulation of innate immune responses and affect the life cycle of viruses. In this study, we identified miR-30a as a potent positive regulator of type I IFN signaling. The further mechanistic study revealed that miR-30a, by targeting and inhibiting USP14 expression, promoted RIG-I K63 ubiquitination to enhance type I IFN responses, thereby resulting in broad-spectrum antiviral effects against multiple viruses. As a complex regulatory network, the activation of type I interferon responses could subsequently reduce miR-30a expression to prevent the dysregulated activation. The insights gained could be crucial for developing innovative antiviral strategies to combat viral infections.
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