Journal
VIRUSES-BASEL
Volume 12, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/v12040418
Keywords
OAS2; ZIKV replication; IFN beta; Jak/STAT signaling pathway
Categories
Funding
- CAMS Initiative for Innovative Medicine [CAMS-2016-I2M-3-025]
- Ministry of Science and Technology of China [2018YFE0107500]
- Science and Technology Partnership Program, Ministry of Science and Technology of China [KY201904011]
- Natural Science Foundation of China [NSFC 81871661]
- Sichuan Provincial Science and Technology Department Funding [2019YJ0281]
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Background: 2', 5'-oligoadenylate synthetase 2 (OAS2) has been known as an antiviral interferon-stimulated gene (ISG). However, the role of OAS2 on Zika virus (ZIKV) replication is still unknown. In this study, we sought to explore the effect of OAS2 on ZIKV replication and its underlying mechanism. Methods: We performed RNA-Seq in A549 cells with or without ZIKV infection. OAS2 or RIG-I was overexpressed by plasmid transfection or knocked down by siRNA in A549 cells. Expression levels of mRNA and protein of selected genes were detected by RT-qPCR and Western Blot, respectively. Interferon stimulated response element (ISRE) activity was examined by dual luciferase assay. Results: We found that ZIKV infection induced OAS2 expression through a RIG-I-dependent pathway. OAS2 overexpression inhibited ZIKV replication, while OAS2 knockdown increased ZIKV replication. We observed that OAS2 inhibited ZIKV replication through enhanced IFN beta expression, leading to the activation of the Jak/STAT signaling pathway. Conclusion: ZIKV infection induced OAS2 expression, which in turn exerted its anti-ZIKV activities through the IFN-activated Jak/STAT signaling pathway.
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