ArticleFrontiers in cellular and infection microbiology2026
Identification of extracellular vesicle microRNAs as potential facilitators of interferon-alpha escape in Marek's disease virus infection.
Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Marek's disease virus (MDV) is a highly immunosuppressive alphaherpesvirus. However, whether and how MDV exploits extracellular vesicles (EVs) to evade host immunity, particularly the critical type I interferon (IFN-I) response, remains unknown. We hypothesized that MDV reprograms the EV microRNA (miRNA) cargo to facilitate its escape from the IFN-I-mediated antiviral state. Methods: Small RNA (sRNA) sequencing was conducted to profile and compare the expression patterns of EV miRNAs in chicken embryo fibroblast (DF-1) cells under four conditions: control, MDV infection, chicken interferon-alpha (chIFN-α) treatment and MDV-chIFN-α co-treatment. Integrative bioinformatic analyzes were employed to identify key differentially expressed miRNAs (DEMs) and predict their target genes within the IFN-I signaling network. Results: MDV infection and chIFN-α treatment induced fundamentally distinct EV miRNA profiles. Strikingly, MDV infection counteracted the specific EV miRNA signature triggered by chIFN-α. We identified 65 key DEMs with the potential to cooperatively target multiple nodes of the IFN-I pathway. Among these, gga-miR-20a-5p and gga-miR-148a-3p were experimentally validated to directly target the 3' untranslated regions of the key innate immune sensors cGAS and TLR3, respectively, leading to a significant suppression of downstream IFN-I signaling activation. Conclusion: This study identifies dysregulated EV miRNAs during MDV-interferon antagonism, validating their direct targeting of innate immune sensors. These findings provide new insights into viral pathogenesis and pinpoint specific miRNA-target axes as potential avenues for antiviral intervention.
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