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Fish Cholesterol 25-Hydroxylase Inhibits Virus Replication via Regulating Interferon Immune Response or Affecting Virus Entry
Zhang, Ya; Wang, Liqun1,2; Huang, Xiaohong; Wang, Shaowen; Huang, Youhua; Qin, Qiwei3
2019
Source PublicationFRONTIERS IN IMMUNOLOGY
ISSN1664-3224
Volume10Pages:322
AbstractCholesterol 25-hydroxylase (CH25H) is an interferon (IFN)-induced gene that catalyzes the oxidation of cholesterol to 25-hydroxycholesterol (25HC), which exerts broad-spectrum antiviral function. To investigate the roles of fi sh CH25H in Singapore grouper iridovirus (SGIV) and red-spotted grouper nervous necrosis virus (RGNNV) infection, we cloned and characterized a CH25H homolog from orange-spotted grouper (Epinephelus coioides) (EcCH25H). EcCH25H encoded a 271-amino-acid polypeptide, with 86 and 59% homology with yellow croaker (Larimichthys crocea) and humans, respectively. EcCH25H contained a conserved fatty acid (FA) hydroxylase domain and an ERG3 domain. EcCH25H expression was induced by RGNNV or SGIV infection, lipopolysaccharide (LPS) or poly (I:C) treatment in vitro. Subcellular localization showed that EcCH25H and mutant EcCH25H-M were distributed in the cytoplasm and partly colocalized with the endoplasmic reticulum. SGIV and RGNNV replication was decreased by EcCH25H overexpression, which was re fl ected in the reduced severity of the cytopathic effect and a decrease in viral gene transcription, but replication of both viruses was increased by knockdown of EcCH25H. Besides, the antiviral activity was dependent on its enzymatic activity. Treatment with 25HC signi fi cantly inhibited replication of SGIV and RGNNV. EcCH25H overexpression positively regulated the IFN-related molecules and proin fl ammatory cytokines, and increased both IFN and ISRE promoter activities. Moreover, 25HC treatment signi fi cantly suppressed SGIV and RGNNV entry into host cells. The similar inhibitory effect on SGIV entry was observed in EcCH25H overexpression cells. Taken together, our fi ndings demonstrated that EcCH25H inhibited SGIV and RGNNV infection by regulating IFN signaling molecules, and might also in fl uence viral entry via an effect on cholesterol.
DepartmentLMB
Keywordcholesterol 25-hydroxylase grouper Singapore grouper iridovirus red-spotted grouper nervous necrosis virus viral replication interferon-stimulated gene viral entry
DOI10.3389/fimmu.2019.00322
Citation statistics
Cited Times:3[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.scsio.ac.cn/handle/344004/17879
Collection中科院海洋生物资源可持续利用重点实验室
Affiliation1.South China Agr Univ, Coll Marine Sci, Guangzhou, Guangdong, Peoples R China
2.Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, Guangzhou, Guangdong, Peoples R China
3.Univ Chinese Acad Sci, Beijing, Peoples R China
4.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China
Recommended Citation
GB/T 7714
Zhang, Ya,Wang, Liqun,Huang, Xiaohong,et al. Fish Cholesterol 25-Hydroxylase Inhibits Virus Replication via Regulating Interferon Immune Response or Affecting Virus Entry[J]. FRONTIERS IN IMMUNOLOGY,2019,10:322.
APA Zhang, Ya,Wang, Liqun,Huang, Xiaohong,Wang, Shaowen,Huang, Youhua,&Qin, Qiwei.(2019).Fish Cholesterol 25-Hydroxylase Inhibits Virus Replication via Regulating Interferon Immune Response or Affecting Virus Entry.FRONTIERS IN IMMUNOLOGY,10,322.
MLA Zhang, Ya,et al."Fish Cholesterol 25-Hydroxylase Inhibits Virus Replication via Regulating Interferon Immune Response or Affecting Virus Entry".FRONTIERS IN IMMUNOLOGY 10(2019):322.
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