Porcine reproductive and respiratory syndrome virus infection induces microRNA novel-216 production to facilitate viral-replication by targeting MAVS 3´UTR.
Vet Microbiol
; 292: 110061, 2024 May.
Article
em En
| MEDLINE
| ID: mdl-38547545
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 â
IFN that mediates the production and response of type â
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 typeâ
IFN and facilitate viral replication, providing new insights into viral immune evasion and persistent infection.
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Base de dados:
MEDLINE
Assunto principal:
Doenças dos Suínos
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Vírus da Síndrome Respiratória e Reprodutiva Suína
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Síndrome Respiratória e Reprodutiva Suína
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MicroRNAs
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article