期刊
JOURNAL OF IMMUNOLOGY
卷 209, 期 10, 页码 1918-1929出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2200025
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资金
- National Natural Science Foundation of China [31725026, 31972832]
- Laboratory of Lingnan Modern Agriculture Project [NT2021008]
This study reveals the virus-host combat mechanism between Cyprinid herpesvirus 3 (CyHV-3) and its host. It shows that CyHV-3 evades host antiviral immunity through its ORF89 protein, while the upregulated host miR-722 targets ORF89 to impede CyHV-3 replication.
Cyprinid herpesvirus 3 (CyHV-3) has caused severe economic losses to carp culture, but its pathogenicity is far from clear. Our previous study has revealed that microRNA (miR)-722 was upregulated during CyHV-3 infection, indicating that miR-722 might play an important role in CyHV-3 replication. In this study, we found that overexpression of miR-722 inhibited CyHV-3 replication and promoted IFN expression. The putative target gene of miR-722 was searched over the CyHV-3 genome, and ORF89 was identified and validated as a target gene of miR-722. Overexpression of ORF89 markedly reduced the expression of IFN and IFN-stimulated genes. Mechanistically, ORF89 interacted with and degraded IFN regulatory factor 3 (IRF3), and inhibited the entry of IRF3 into the nucleus by suppressing the dimerization of IRF3. Moreover, ORF89-mediated suppression of IFN expression could be restored by adding miR-722. To our knowledge, our findings confirm a novel virus-host combat, in which CyHV-3 evades host antiviral immunity by its ORF89 protein, whereas host miR-722, upregulated on CyHV-3 infection, targets ORF89 to impede CyHV-3 replication.
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