Suppressor of cytokine signaling 1 (SOCS1) inhibits antiviral responses to facilitate Senecavirus A infection by regulating the NF-κB signaling pathway

Chen, Yongjie; Zhong, Wenxia; Xie, Zhenxin; Li, Baojian; Li, Huizi; Gao, Kuipeng; Ning, Zhangyong

doi:10.1016/j.virusres.2022.198748

Cited by 8 publications

(9 citation statements)

References 52 publications

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“…Porcine kidney-15 (PK-15) and human embryonic kidney (HEK293T) cells were cultured at 37°C and 5% CO 2 in Dulbecco’s modified Eagle’s medium (DMEM; Gibco) supplemented with 10% fetal bovine serum (FBS; Gibco), 100 IU/mL penicillin, 100 g/mL streptomycin, and 2 mM L-glutamine (Gibco). The SVA strain, CH-GDFS-2018, was isolated by our group and propagated and titrated in PK-15 cells using the Reed–Muench method [ 46 ]. The SVA strain was incubated in a water bath at 70°C for 2 h to generate a heat-inactivated SVA (Heat-SVA).…”

Section: Methodsmentioning

confidence: 99%

“…The PK-15 cell suspension was collected at the indicated time points and viral titration was performed. The 50% tissue culture infective dose (TCID 50 ) was calculated using the Reed–Muench formula [ 46 ]. In brief, PK-15 cells were maintained in 96-well cell culture plates, and virus samples to be titrated were prepared in a 10-fold serial dilution (from 10 −1 to 10 −8 ).…”

Section: Methodsmentioning

confidence: 99%

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Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

Lin

et al. 2023

PLoS Pathog

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Senecavirus A (SVA)-induced porcine idiopathic vesicular disease has caused huge economic losses worldwide. Glucose metabolism in the host cell is essential for SVA proliferation; however, the impact of the virus on glucose metabolism in host cells and the subsequent effects are still unknown. Here, glycolysis induced by SVA is shown to facilitate virus replication by promoting lactate production, which then attenuates the interaction between the mitochondrial antiviral-signaling protein (MAVS) and retinoic acid-inducible gene I (RIG-I). SVA induces glycolysis in PK-15 cells, as indicated by significantly increased expression of hexokinase 2 (HK2), 6-phosphofructokinase (PFKM), pyruvate kinase M (PKM), phosphoglycerate kinase 1 (PGK1), hypoxia-inducible factor-1 alpha (HIF-1α), and superoxide dismutase-2 (SOD2) in a dose-and replication-dependent manner, and enhanced lactate production, while reducing ATP generation. Overexpression of PKM, PGK1, HIF-1α, and PDK3 in PK-15 cells and high glucose concentrations promote SVA replication, while glycolytic inhibitors decrease it. Inhibition of RLR signaling allowed better replication of SVA by promoting lactate production to attenuate the interaction between MAVS and RIG-I, and regulatory effect of glycolysis on replication of SVA was mainly via RIG-I signaling. SVA infection in mice increased expression of PKM and PGK1 in tissues and serum yields of lactate. Mice treated with high glucose and administered sodium lactate showed elevated lactate levels and better SVA replication, as well as suppressed induction of RIG-I, interferon beta (IFNβ), IFNα, interferon-stimulated gene 15 (ISG15), and interleukin 6 (IL-6). The inhibitory effect on interferons was lower in mice administered sodium oxamate and low glucose compared to the high glucose, indicating that RLR signaling was inhibited by SVA infection through lactate in vitro and in vivo. These results provide a new perspective on the relationship between metabolism and innate immunity of the host in SVA infection, suggesting that glycolysis or lactate may be new targets against the virus.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

Lin

et al. 2023

PLoS Pathog

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“…Anti-NF-κB p65, anti-p-NF-κB p65 (Ser536), anti-IκBα, and anti-p-IκBα (Ser32/36) primary antibodies were purchased from Abmart (China), and anti-βactin antibody was obtained from Boiss (China). The rabbit anti-VP2 of SVA was stored in our laboratory [11]. The respective horseradish peroxidase (HRP)-conjugated secondary antibodies were purchased from Abcam (Cambridge, UK).…”

Section: Cells Virus and Reagentsmentioning

confidence: 99%

“…Western blot was performed according to our previous research [11]. Briefly, cellular proteins were extracted from different samples and separated with 10% sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and transferred onto a nitrocellulose membrane (Pall, USA).…”

Section: Western Blotmentioning

confidence: 99%

“…Host factors as passive responders to SVA infection will participate in the process of antiviral responses. It has been reported that suppressor of cytokine signaling 1 (SOCS1) facilitates the replication of SVA by inhibiting the type I IFN signaling pathway [11]; IFN-induced protein with tetratricopeptide repeats 3 (IFIT3) targets SVA entry, assembly, and release mediated by a type I IFN antiviral response [12]. Although some progress has been made on host factors regulating the replication of SVA, the role of Z-DNA binding protein 1 (ZBP1) remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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ZBP1 inhibits the replication of Senecavirus A by enhancing NF-κB signaling pathway mediated antiviral response in porcine alveolar macrophage 3D4/21 cells

Li,

Zheng,

Chen

et al. 2024

Cell Mol Biol Lett

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Background Senecavirus A (SVA) caused porcine idiopathic vesicular disease (PIVD) showing worldwide spread with economic losses in swine industry. Although some progress has been made on host factors regulating the replication of SVA, the role of Z-DNA binding protein 1 (ZBP1) remains unclear. Methods The expression of ZBP1 in SVA-infected 3D/421 cells was analyzed by quantitative real-time PCR (qRT-PCR) and western blot. Western blot and qRT-PCR were used to detect the effects of over and interference expression of ZBP1 on SVA VP2 gene and protein. Viral growth curves were prepared to measure the viral proliferation. The effect on type I interferons (IFNs), interferon-stimulated genes (ISGs), and pro-inflammatory cytokines in SVA infection was analyzed by qRT-PCR. Western blot was used to analysis the effect of ZBP1 on NF-κB signaling pathway and inhibitor are used to confirm. Results ZBP1 is shown to inhibit the replication of SVA by enhancing NF-κB signaling pathway mediated antiviral response. SVA infection significantly up-regulated the expression of ZBP1 in 3D4/21 cells. Infection of cells with overexpression of ZBP1 showed that the replication of SVA was inhibited with the enhanced expression of IFNs (IFN-α, IFN-β), ISGs (ISG15, PKR, and IFIT1) and pro-inflammatory cytokines (IL-6, IL-8, and TNF-α), while, infected-cells with interference expression of ZBP1 showed opposite effects. Further results showed that antiviral effect of ZBP1 is achieved by activation the NF-κB signaling pathway and specific inhibitor of NF-κB also confirmed this. Conclusions ZBP1 is an important host antiviral factor in SVA infection and indicates that ZBP1 may be a novel target against SVA. Graphical Abstract

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CD46 inhibits the replication of swine influenza viruses by promoting the production of type I IFNs in PK-15 cells

Li,

Sun,

Zheng

et al. 2023

Vet Res Commun

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Suppressor of cytokine signaling 1 (SOCS1) inhibits antiviral responses to facilitate Senecavirus A infection by regulating the NF-κB signaling pathway

Cited by 8 publications

References 52 publications

Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

ZBP1 inhibits the replication of Senecavirus A by enhancing NF-κB signaling pathway mediated antiviral response in porcine alveolar macrophage 3D4/21 cells

CD46 inhibits the replication of swine influenza viruses by promoting the production of type I IFNs in PK-15 cells

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