Early Pattern of Epstein-Barr Virus Infection in Gastric Epithelial Cells by “Cell-in-cell”
Early Pattern of Epstein-Barr Virus Infection in Gastric Epithelial Cells by “Cell-in-cell”作者机构:NHC Key Laboratory of CarcinogenesisThe Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education. Xiangya HospitalCentral South UniversityChangsha 410080China Department of MicrobiologySchool of Basic Medical ScienceCentral South UniversityChangsha 410078China Department of Biological ScienceFlorida State UniversityTallahasseeFL 32306USA
出 版 物:《Virologica Sinica》 (中国病毒学(英文版))
年 卷 期:2019年第34卷第3期
页 面:253-261页
核心收录:
学科分类:0710[理学-生物学] 07[理学] 09[农学]
基 金:supported by the National Key Research & Development Program National Natural Science Foundations of China (2017YFC1200204, 31670171, 81728011) Innovation Foundations for Postgraduates of Central South University (2018zzts817)
主 题:Epstein-Barr virus(EBV) Cell-in-cell infection Gastric epithelial cells Inflammatory response
摘 要:Epstein-Barr virus(EBV)is an important human dsDNA virus,which has been shown to be associated with several malignancies including about 10%of gastric *** EBV enters an epithelial cell has been an interesting project for investigation.Cell-in-cellinfection was recently reported an efficient way for the entry of EBV into nasopharynx epithelial *** present approach was to explore the feasibility of this mode for EBV infection in gastric epithelial cells and the dynamic change of host inflammatory *** EBV-positive lymphoblastic cells of Akata containing a GFP tag in the viral genome were co-cultured with the gastric epithelial cells(GES-1).The infection situation was observed under fluorescence and electron ***-time quantitative PCR and Western-blotting assay were employed to detect the expression of a few specific cytokines and inflammatory *** results demonstrated that EBV could get into gastric epithelial cells bycell-in-cellinfection but not fully successful due to the host ***-1β,IL-6 and IL-8 played prominent roles in the cellular response to the *** activation of NF-κB and HSP70 was also required for the host antiviral *** results imply that the gastric epithelial cells could powerfully resist the virus invader via cell-in-cell at the early stage through inflammatory and innate immune responses.