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Porcine reproductive and respiratory syndrome virus infection induces microRNA novel-216 production to facilitate viral-replication by targeting MAVS 3´UTR.
- Source :
-
Veterinary Microbiology . May2024, Vol. 292, pN.PAG-N.PAG. 1p. - Publication Year :
- 2024
-
Abstract
- Porcine reproductive and respiratory syndrome virus (PRRSV) has caused significant economic losses in the swine industry. In this study, the high-throughput sequencing, microRNAs (miRNAs) mimic, and lentivirus were used to screen for potential miRNAs that can promote PRRSV infection in porcine alveolar macrophages or Marc-145 cells. It was observed that novel-216, a previously unidentified miRNA, was upregulated through the p38 signaling pathway during PRRSV infection, and its overexpression significantly increased PRRSV replication. Further analysis revealed that novel-216 regulated PRRSV replication by directly targeting mitochondrial antiviral signaling protein (MAVS), an upstream molecule of type Ⅰ IFN that mediates the production and response of type Ⅰ IFN. The proviral function of novel-216 on PRRSV replication was abolished by MAVS overexpression, and this effect was reversed by the 3′UTR of MAVS, which served as the target site of novel-216. In conclusion, this study demonstrated that PRRSV-induced upregulation of novel-216 served to inhibit the production and response of typeⅠ IFN and facilitate viral replication, providing new insights into viral immune evasion and persistent infection. • Porcine reproductive and respiratory syndrome virus (PRRSV) is characterized by immunosuppression and persistent infection. • PRRSV upregulates novel-216 expression to facilitate self-replication. • Novel-216 targets MAVS to negatively regulates the antiviral activity of type Ⅰ IFN. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 03781135
- Volume :
- 292
- Database :
- Academic Search Index
- Journal :
- Veterinary Microbiology
- Publication Type :
- Academic Journal
- Accession number :
- 176472025
- Full Text :
- https://doi.org/10.1016/j.vetmic.2024.110061