Major Vault Protein Inhibits Porcine Reproductive and Respiratory Syndrome Virus Infection in CRL2843CD163 Cell Lines and Primary Porcine Alveolar Macrophages

被引：1

作者：

Wu, Xiaoping ^{[1
]}

Fang, Junyang ^{[1
]}

Huang, Qiuping ^{[1
]}

Chen, Xu ^{[1
]}

Guo, Zhongyi ^{[1
]}

Tian, Lingyujia ^{[1
]}

Zhou, Enmin ^{[1
]}

Chen, Jianxin ^{[2
]}

Mu, Yang ^{[1
]}

Du, Taofeng ^{[1
]}

机构：

[1] Northwest A&F Univ, Coll Vet Med, Dept Vet Prevent Med, Yangling 712100, Shaanxi, Peoples R China

[2] South China Agr Univ, Coll Vet Med, Guangdong Prov Key Lab Vet Pharmaceut Dev & Safet, Guangzhou 510642, Peoples R China

来源：

VIRUSES-BASEL | 2021年 / 13卷 / 11期

基金：

中国国家自然科学基金;

关键词：

PRRSV; MVP; host factor; type I interferon; antiviral; NUCLEAR-LOCALIZATION; VIRAL REPLICATION; IMMUNE-RESPONSES; A VIRUS; EXPRESSION; RESISTANCE; CYTOKINE; PRRSV; MVP; PHOSPHATASE;

D O I：

10.3390/v13112267

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Porcine reproductive and respiratory syndrome (PRRS), a significant viral infectious disease that commonly occurs among farmed pigs, leads to considerable economic losses to the swine industry worldwide. Major vault protein (MVP) is a host factor that induces type I interferon (IFN) production. In this study, we evaluated the effect of MVP on PRRSV infection in CRL2843(CD163) cell lines and porcine alveolar macrophages (PAMs). Our results showed that MVP expression was downregulated by PRRSV infection. Adenoviral overexpression of MVP inhibited PRRSV replication, whereas the siRNA knockdown of MVP promoted PRRSV replication. In addition, MVP knockdown has an adverse effect on the inhibitive role of MVP overexpression on PRRSV replication. Moreover, MVP could induce the expression of type I IFNs and IFN-stimulated gene 15 (ISG15) in PRRSV-infected PAMs. Based on these results, MVP may be a potential molecular target of drugs for the effective prevention and treatment of PRRSV infection.

引用

页数：13

共 58 条

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