CXCL10 Induces Lytic Reactivation of EBV through EXTL1  

作　　者：Bei-Ning Ding Yi-Lin Wu You-Yu Zhang Yong-Guo Li Bei-Ning Ding;Yi-Lin Wu;You-Yu Zhang;Yong-Guo Li(Department of Infectious Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China)

机构地区：[1]Department of Infectious Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China

出　　处：《Advances in Bioscience and Biotechnology》2024年第10期621-635,共15页生命科学与技术进展（英文）

摘　　要：Epstein-Barr virus (EBV) infects over 90% of the global population, establishing latent infections in most individuals. Under specific conditions like inflammation and immune suppression, EBV can be reactivated, leading to the initiation and progression of related diseases. While inflammation is known to induce EBV reactivation, the precise mechanisms underlying this phenomenon remain unclear. Chemokine (C-X-C motif) ligand (CXCL10), a key inflammatory factor, plays a significant role in various infectious diseases. In this study, we investigated how CXCL10 levels regulate the transition between the latent and lytic replication phases of the EBV lifecycle using cell culture, Western blot, fluorescent quantitative PCR, immunofluorescence, and flow cytometric apoptosis assays. Our findings indicate that CXCL10 induces EBV transition from latency to lytic replication through its receptor CXCR3 by regulating the downstream effector, exostosis-like glycosyltransferase 1. Additionally, CXCL10 activates the JAK2/STAT3 pathway. This study confirms the role of CXCL10 in promoting EBV lytic replication, providing crucial insights into the pathogenic mechanisms of inflammation-triggered EBV reactivation.Epstein-Barr virus (EBV) infects over 90% of the global population, establishing latent infections in most individuals. Under specific conditions like inflammation and immune suppression, EBV can be reactivated, leading to the initiation and progression of related diseases. While inflammation is known to induce EBV reactivation, the precise mechanisms underlying this phenomenon remain unclear. Chemokine (C-X-C motif) ligand (CXCL10), a key inflammatory factor, plays a significant role in various infectious diseases. In this study, we investigated how CXCL10 levels regulate the transition between the latent and lytic replication phases of the EBV lifecycle using cell culture, Western blot, fluorescent quantitative PCR, immunofluorescence, and flow cytometric apoptosis assays. Our findings indicate that CXCL10 induces EBV transition from latency to lytic replication through its receptor CXCR3 by regulating the downstream effector, exostosis-like glycosyltransferase 1. Additionally, CXCL10 activates the JAK2/STAT3 pathway. This study confirms the role of CXCL10 in promoting EBV lytic replication, providing crucial insights into the pathogenic mechanisms of inflammation-triggered EBV reactivation.

关 键 词：Epstein-Barr Virus REACTIVATION Inflammation Chemokine (C-X-C Motif) Ligand 10 EXTL1 

分 类 号：R73[医药卫生—肿瘤]