Porcine 2′, 5′-oligoadenylate synthetase 2 inhibits porcine reproductive and respiratory syndrome virus replication in vitro

Zhao, Mengmeng; Wan, Bo; Li, Huawei; He, Jing; Chen, Xinxin; Wang, Linjian; Wang, Yinbiao; Xie, Sha; Qiao, Songlin; Zhang, Gaiping

doi:10.1016/j.micpath.2017.08.011

Cited by 18 publications

(11 citation statements)

References 35 publications

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“…OAS1 and OAS3 restricted DENV and HCV through activating RNase L activity [15,16]. Previous studied also revealed that porcine OAS2 controlled JEV and PRRSV replication through OAS/RNase L pathway [21,22]. In addition, OAS can also regulate virus replication through RNase L-independent pathway.…”

Section: Discussionmentioning

confidence: 98%

“…Several studies have shown that the expression levels of OAS2 were elevated in the sera of patients with viral infections and after IFNs therapy [18][19][20]. In addition, OAS2 has been found to inhibit the replication of JEV and pathological PRRS virus (PRRSV) [21,22]. Although the antiviral effects of other OAS proteins have been well-studied, it is still unknown whether and how OAS2 affects ZIKV replication.…”

Section: Introductionmentioning

confidence: 99%

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2′, 5′-Oligoadenylate Synthetase 2 (OAS2) Inhibits Zika Virus Replication through Activation of Type Ι IFN Signaling Pathway

Liao

Xie

et al. 2020

Viruses

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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 IFNβ 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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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

2′, 5′-Oligoadenylate Synthetase 2 (OAS2) Inhibits Zika Virus Replication through Activation of Type Ι IFN Signaling Pathway

Liao

Xie

et al. 2020

Viruses

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“…In the current study, we demonstrated that TRIM25 functions by restricting PRRSV replication, and that it could act as a host-derived inhibitor of the virus. Previously, many host factors that result in cellular resistance to PRRSV via different mechanisms were identified Song et al, 2017;Wang et al, 2016;Zhao et al, 2018Zhao et al, , 2017. For example, cholesterol 25-hydroxylase protects against PRRSV infection by converting cholesterol to 25-hydroxycholesterol, which can be used as a natural antiviral agent to combat PRRSV infection (Song et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Nucleocapsid protein of porcine reproductive and respiratory syndrome virus antagonizes the antiviral activity of TRIM25 by interfering with TRIM25-mediated RIG-I ubiquitination

Zhao

Jiang

et al. 2019

Veterinary Microbiology

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Porcine reproductive and respiratory syndrome (PRRS) is caused by PRRS virus (PRRSV), and is characterized by respiratory diseases in piglet and reproductive disorders in sow. Identification of sustainable and effective measures to mitigate PRRSV transmission is a pressing problem. The nucleocapsid (N) protein of PRRSV plays a crucial role in inhibiting host innate immunity during PRRSV infection. In the current study, a new host-restricted factor, tripartite motif protein 25 (TRIM25), was identified as an inhibitor of PRRSV replication. Coimmunoprecipitation assay indicated that the PRRSV N protein interferes with TRIM25-RIG-I interactions by competitively interacting with TRIM25. Furthermore, N protein inhibits the expression of TRIM25 and TRIM25mediated RIG-I ubiquitination to suppress interferon β production. Furthermore, with increasing TRIM25 expression, the inhibitory effect of N protein on the ubiquitination of RIG-I diminished. These results indicate for the first time that TRIM25 inhibits PRRSV replication and that the N protein antagonizes the antiviral activity by interfering with TRIM25-mediated RIG-I ubiquitination. This not only provides a theoretical basis for the development of drugs to control PRRSV replication, but also better explains the mechanism through which the PRRSV N protein inhibits innate immune responses of the host. ⁎

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“…OAS2 is known to encode a member of the 2-5A synthetase family, which comprises essential proteins involved in the innate immune responses to viral infection; it promotes viral RNA degradation and inhibition of viral replication [63]. Furthermore, it was reported that OAS2 overexpression in PAMs inhibited PRRSV (North American strain BJ-4) replication [64].…”

Section: Host-gene Modulations During Prrsv Infectionmentioning

confidence: 99%

Integrated time-serial transcriptome networks reveal common innate and tissue-specific adaptive immune responses to PRRSV infection

Lim

Kim

lim

et al. 2020

Vet Res

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Porcine reproductive and respiratory syndrome virus (PRRSV) infection is the most important viral disease causing severe economic losses in the swine industry. However, mechanisms underlying gene expression control in immunity-responsible tissues at different time points during PRRSV infection are poorly understood. We constructed an integrated gene co-expression network and identified tissue- and time-dependent biological mechanisms of PRRSV infection through bioinformatics analysis using three tissues (lungs, bronchial lymph nodes [BLNs], and tonsils) via RNA-Seq. Three groups with specific expression patterns (i.e., the 3-dpi, lung, and BLN groups) were discovered. The 3 dpi-specific group showed antiviral and innate-immune signalling similar to the case for influenza A infection. Moreover, we observed adaptive immune responses in the lung-specific group based on various cytokines, while the BLN-specific group showed down-regulated AMPK signalling related to viral replication. Our study may provide comprehensive insights into PRRSV infection, as well as useful information for vaccine development.

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Porcine 2′, 5′-oligoadenylate synthetase 2 inhibits porcine reproductive and respiratory syndrome virus replication in vitro

Cited by 18 publications

References 35 publications

2′, 5′-Oligoadenylate Synthetase 2 (OAS2) Inhibits Zika Virus Replication through Activation of Type Ι IFN Signaling Pathway

2′, 5′-Oligoadenylate Synthetase 2 (OAS2) Inhibits Zika Virus Replication through Activation of Type Ι IFN Signaling Pathway

Nucleocapsid protein of porcine reproductive and respiratory syndrome virus antagonizes the antiviral activity of TRIM25 by interfering with TRIM25-mediated RIG-I ubiquitination

Integrated time-serial transcriptome networks reveal common innate and tissue-specific adaptive immune responses to PRRSV infection

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