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Fish Shellfish Immunol. 2019 May;88:217-224. doi: 10.1016/j.fsi.2019.02.046. Epub 2019 Feb 23.

Functional analysis of the CXCR1a gene response to SGIV viral infection in grouper.

Author information

1
College of Marine Sciences, South China Agricultural University, Guangzhou, 510642, China.
2
Fisheries Research Institute of Fujian, Xiamen, 361000, People's Republic of China.
3
College of Marine Sciences, South China Agricultural University, Guangzhou, 510642, China. Electronic address: ypyu@scau.edu.cn.
4
College of Marine Sciences, South China Agricultural University, Guangzhou, 510642, China. Electronic address: qinqw@scau.edu.cn.

Abstract

Chemokine receptors are a superfamily of seven-transmembrane domain G-coupled receptors and have important roles in immune surveillance, inflammation, and development. In previous studies, a series of CXCRs in grouper (Epinephelus coioides) was identified; however, the function of CXCR in viral infection has not been studied. To better understand the effect of the CXCR family on the fish immune response, full-length CXCR1a was cloned, and its immune response to Singapore grouper iridovirus (SGIV) was investigated. Grouper CXCR1a shared a seven-transmembrane (7-TM) region and a G protein-coupled receptor (GPCR) family 1 that contained a triaa stretch (DRY motif). Phylogenetic analysis indicated that CXCR1a showed the nearest relationship to Takifugu rubripes, followed by other fish, bird and mammal species. Fluorescence microscopy revealed that CXCR1a was expressed predominantly in the cytoplasm. Overexpression of CXCR1a in grouper cells significantly inhibited the replication of SGIV, demonstrating that CXCR1a delayed the occurrence of cytopathic effects (CPE) induced by SGIV infection and inhibited viral gene transcription. Furthermore, our results also showed that CXCR1a overexpression significantly increased the expression of interferon-related cytokines and activated ISRE and IFN promoter activities. Taken together, the results demonstrated that CXCR1a might have an antiviral function against SGIV infection.

KEYWORDS:

Antiviral; CXCR1a; Grouper; SGIV; Virus replication

PMID:
30807858
DOI:
10.1016/j.fsi.2019.02.046

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