Calmodulin-like 5 promotes PEDV replication by regulating late-endosome synthesis and innate immune response
作者机构:National Key Laboratory of Veterinary Public Health and SafetyCollege of Veterinary MedicineChina Agricultural UniversityBeijing 100193China College of Animal Science and TechnologyChina Agricultural UniversityBeijing 100193China Beijing General Station of Animal Husbandry Service(South Section)Beijing102218China
出 版 物:《Virologica Sinica》 (中国病毒学(英文版))
年 卷 期:2024年第39卷第3期
页 面:501-512页
核心收录:
学科分类:1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学]
基 金:supported by the National Key R&D Program of China(2023YFD1801100) the National Natural Science Foundation of China(32172821) a CAU-Grant for the Prevention and Control of Immunosuppressive Disease in Animals(CAU-G-PCIDA)of the China Agricultural University
主 题:Porcine epidemic diarrhea virus(PEDV) EF-hand protein calmodulin-like 5(CALML5) Late endosomes Innate immune response
摘 要:The infection caused by porcine epidemic diarrhea virus(PEDV)is associated with high mortality in piglets *** factors involved in the efficient replication of PEDV,however,remain largely *** recent proteomic study in the virus-host interaction network revealed a significant increase in the accumulation of CALML5(EF-hand protein calmodulin-like 5)following PEDV infection.A further study unveiled a biphasic increase of CALML5 in 2 and 12 h after viral *** trends were observed in the intestines of piglets in the early and late stages of the PEDV ***,CALML5 depletion reduced PEDV mRNA and protein levels,leading to a one-order-of-magnitude decrease in virus *** the early stage of PEDV infection,CALML5 affected the endosomal trafficking pathway by regulating the expression of endosomal sorting complex related cellular ***5 depletion also suppressed IFN-βand IL-6 production in the PEDV-infected cells,thereby indicating its involvement in negatively regulating the innate immune *** study reveals the biological function of CALML5 in the virology field and offers new insights into the PEDV-host cell interaction.