Seneca Valley virus induces proinflammatory cytokine and chemokine response in vitro.

IF 1.1 Q3 VETERINARY SCIENCES
Jianguo Dong, Mingrui Chen, Linyang Yu, Dan Rao, Ning Zhang, Feng Cong
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引用次数: 0

Abstract

Seneca Valley virus (SVV) is an oncolytic virus, which belongs to the Picornaviridae family, that causes blisters on the nose and hooves, affecting the production performance of pigs. However, the function of proinflammatory cytokines and chemokines in SVV infection is still unclear. In our study, SVV infection could induce a high expression of proinflammatory cytokines interleukin (IL)-1α, IL-1β, and tumor necrosis factor α (TNF-α) and chemokines, including chemokine (C-C motif) ligand 2 (CCL2), chemokine (C-C motif) ligand 5 (CCL5), and chemokine (C-X-C motif) ligand 10 (CXCL10). Interfered genes of IL-1α, IL-1β, and TNF-α inhibited virus replication, but interfered genes of CCL2, CCL5, and CXCL10 promoted virus replication. These results indicate that proinflammatory cytokines and chemokines are involved in SVV infection; this will be beneficial to explore the pathogenesis and cytokine therapy of SVV.

Seneca Valley病毒在体外诱导促炎细胞因子和趋化因子反应。
Seneca Valley病毒(SVV)是一种溶瘤病毒,属于小核糖核酸病毒科,会在猪的鼻子和蹄上引起水泡,影响猪的生产性能。然而,促炎细胞因子和趋化因子在SVV感染中的作用尚不清楚。在我们的研究中,SVV感染可诱导促炎细胞因子白细胞介素(IL)-1α、IL-1β和肿瘤坏死因子α(TNF-α。受干扰的IL-1α、IL-1β和TNF-α基因抑制病毒复制,但受干扰的CCL2、CCL5和CXCL10基因促进病毒复制。这些结果表明,促炎细胞因子和趋化因子参与SVV感染;这将有助于探讨SVV的发病机制和细胞因子治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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