Toll-like receptor 3 pathway restricts Marek’s disease virus infection

// Haitao Zou 1, 2 , Ruixue Su 1, 2 , Jing Ruan 1, 2 , Hongxia Shao 1, 2, 3 , Kun Qian 1, 2, 3 , Jianqiang Ye 1, 2, 3 and Aijian Qin 1, 2, 3 1 Ministry of Education Key Lab for Avian Preventive Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, P.R. China 2 Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, 225009, P.R. China 3 Jiangsu Key Lab of Zoonosis, Yangzhou, Jiangsu, 225009, P.R. China Correspondence to: Aijian Qin, email: aijian@yzu.edu.cn Keywords: Marek’s disease virus, toll-like receptor 3, poly (I:C), interferon-β, inflammatory cytokines Abbreviations: IRF3: interferon regulatory factor3, IKKα: IκB kinase α, TANK: TRAF family member-associated NFκB activator Received: April 04, 2017      Accepted: July 12, 2017      Published: August 07, 2017 ABSTRACT Marek’s disease virus (MDV) is an α-herpesvirus that causes immune suppression and T lymphoma in chickens. Toll-like receptor 3 (TLR3) is critical for the host immune response against MDV infection. Previously, our team demonstrated that pre-treatment of TLR3 agonist poly (I:C) inhibited Marek’s disease virus infection in chicken embryo fibroblasts (CEFs). However, whether TLR3 inhibits the aggravation of MDV infection is unknown. In the current study, we found that TLR3 activation in MDV-infected CEFs effectively inhibited virus spread. Using pharmacological approaches, we revealed that pro-inflammatory cytokines and interferon-β induced by TLR3 could restrict Marek’s disease virus infection. This study contributes to elucidating the function and mechanism of the TLR3 pathway in host immune responses against MDV infection.