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Duck RIG-I restricts duck enteritis virus infection. Vet Microbiol. 2019 Mar;230:78-85

Huo H , Wang Y , Wang D , Wang Y , Chen X , Zhao L , Chen H .

Vet Microbiol. 2019 Mar;230:78-85. doi: 10.1016/j.vetmic.2019.01.014. Epub 2019 Jan 15.

 

Abstract

Retinoic acid-inducible gene I (RIG-I) is a nucleic acid sensor that plays a key role in host antiviral defenses. Duck viral enteritis (DEV) is a DNA virus that causes significant economic losses to the poultry industry worldwide. Although RIG-I is known to be involved in a common antiviral signaling pathway triggered by RNA viruses, its role in DEV infection remains unclear. In this study, we demonstrated that DEV infection increased the expression levels of interferon β (IFN-β) and RIG-I in ducks both in vivo and in vitro. Furthermore, overexpression of duck RIG-I significantly upregulated the expression of interferon-stimulated genes, including myxovirus resistance protein (Mx), Interferon-induced oligodenylate synthetase-like (OASL) and IFN-β. We therefore used overexpression and knockdown methods to determine if RIG-I affected DEV infection in ducks. Viral infection was inhibited by RIG-I, and enhanced by knockdown of RIG-I expression using small interfering RNA. RIG-I overexpression also activated signal transducer and activator of transcription 1 (STAT1), as a member of the JAK-STAT family. The combined results following STAT1 knockdown and RIG-I overexpression suggested that the antiviral activity of RIG-I was STAT1-dependent. Overall, these findings indicate that RIG-I effectively restricts DEV replication and may play a vital role in the host immune response to DEV infection in ducks.

Copyright © 2019 Elsevier B.V. All rights reserved.

 

KEYWORDS:

Antiviral response; Duck enteritis virus; IFN-β; RIG-I; STAT1

 

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