Singapore grouper iridovirus (SGIV) TNFR homolog VP51 functions as a virulence factor via modulating host inflammation response

Yepin Yu; Youhua Huang; Songwei Ni; Lingli Zhou; Jiaxin Liu; Jingcheng Zhang; Xin Zhang; Yin Hu; Xiaohong Huang; Qiwei Qin

doi:10.1016/j.virol.2017.06.025

Singapore grouper iridovirus (SGIV) TNFR homolog VP51 functions as a virulence factor via modulating host inflammation response

Virology. 2017 Nov:511:280-289. doi: 10.1016/j.virol.2017.06.025. Epub 2017 Jul 6.

Authors

Yepin Yu¹, Youhua Huang¹, Songwei Ni², Lingli Zhou², Jiaxin Liu², Jingcheng Zhang², Xin Zhang¹, Yin Hu², Xiaohong Huang³, Qiwei Qin⁴

Affiliations

¹ Joint Laboratory of Guangdong Province and Hong Kong Region on Marine Bioresource Conservation and Exploitation, College of Marine Sciences, South China Agricultural University, 483 Wushan Road, Guangzhou 510642, China.
² Key Laboratory of Tropical Marine Bio-resources and Ecology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, 164 West Xingang Road, Guangzhou 510301, China; University of Chinese Academy of Sciences, Beijing 100049, China.
³ Joint Laboratory of Guangdong Province and Hong Kong Region on Marine Bioresource Conservation and Exploitation, College of Marine Sciences, South China Agricultural University, 483 Wushan Road, Guangzhou 510642, China. Electronic address: huagnxh@scsio.ac.cn.
⁴ Joint Laboratory of Guangdong Province and Hong Kong Region on Marine Bioresource Conservation and Exploitation, College of Marine Sciences, South China Agricultural University, 483 Wushan Road, Guangzhou 510642, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266000, China. Electronic address: qinqw@scau.edu.cn.

PMID: 28689858
DOI: 10.1016/j.virol.2017.06.025

Abstract

Virus encoded tumor necrosis factor receptor (TNFR) homologues are usually involved in immune evasion by regulating host immune response or cell death. Singapore grouper iridovirus (SGIV) is a novel ranavirus which causes great economic losses in aquaculture industry. Previous studies demonstrated that SGIV VP51, a TNFR-like protein regulated apoptotic process in VP51 overexpression cells. Here, we developed a VP51-deleted recombinant virus Δ51-SGIV by replacing VP51 with puro^R-GFP. Deletion of VP51 resulted in the decrease of SGIV virulence, evidenced by the reduced replication in vitro and the decreased cumulative mortalities in Δ51-SGIV challenged grouper compared to WT-SGIV. Moreover, VP51 deletion significantly increased virus induced apoptosis, and reduced the expression of pro-inflammatory cytokines in vitro. In addition, the expression of several pro-inflammatory genes were decreased in Δ51-SGIV infected grouper compared to WT-SGIV. Thus, we speculate that SGIV VP51 functions as a critical virulence factor via regulating host cell apoptosis and inflammation response.

Keywords: Apoptosis; Inflammation response; SGIV; TNFR; Virulence factor.

MeSH terms

Animals
Apoptosis
Cells, Cultured
Cytokines / metabolism
Fish Diseases / pathology
Fish Diseases / virology
Fishes
Gene Deletion
Host-Pathogen Interactions*
Immunologic Factors / genetics
Immunologic Factors / metabolism*
Inflammation / pathology*
Iridovirus / genetics
Iridovirus / pathogenicity*
Iridovirus / physiology
Receptors, Tumor Necrosis Factor / genetics
Receptors, Tumor Necrosis Factor / metabolism*
Survival Analysis
Viral Proteins / genetics
Viral Proteins / metabolism*
Virulence
Virulence Factors / genetics
Virulence Factors / metabolism*
Virus Replication

Substances

Cytokines
Immunologic Factors
Receptors, Tumor Necrosis Factor
Viral Proteins
Virulence Factors