Early Pattern of Epstein-Barr Virus Infection in Gastric Epithelial Cells by "Cell-in-cell".
Cell Line
Cell-in-Cell Formation
Cytokines
/ immunology
Epithelial Cells
/ immunology
Fluorescence
Gastrointestinal Tract
/ cytology
Green Fluorescent Proteins
HSP72 Heat-Shock Proteins
/ metabolism
Herpesvirus 4, Human
/ genetics
Humans
Immunity, Innate
In Situ Hybridization
Inflammation
Microscopy, Electron, Transmission
NF-kappa B
/ metabolism
Cell-in-cell infection
Epstein-Barr virus (EBV)
Gastric epithelial cells
Inflammatory response
Journal
Virologica Sinica
ISSN: 1995-820X
Titre abrégé: Virol Sin
Pays: Netherlands
ID NLM: 101514185
Informations de publication
Date de publication:
Jun 2019
Jun 2019
Historique:
received:
16
10
2018
accepted:
18
02
2019
pubmed:
27
3
2019
medline:
14
8
2019
entrez:
27
3
2019
Statut:
ppublish
Résumé
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 carcinomas. How EBV enters an epithelial cell has been an interesting project for investigation. "Cell-in-cell" infection was recently reported an efficient way for the entry of EBV into nasopharynx epithelial cells. The present approach was to explore the feasibility of this mode for EBV infection in gastric epithelial cells and the dynamic change of host inflammatory reaction. The 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 microscopies. Real-time quantitative PCR and Western-blotting assay were employed to detect the expression of a few specific cytokines and inflammatory factors. The results demonstrated that EBV could get into gastric epithelial cells by "cell-in-cell" infection but not fully successful due to the host fighting. IL-1β, IL-6 and IL-8 played prominent roles in the cellular response to the infection. The activation of NF-κB and HSP70 was also required for the host antiviral response. The 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.
Identifiants
pubmed: 30911896
doi: 10.1007/s12250-019-00097-1
pii: 10.1007/s12250-019-00097-1
pmc: PMC6599502
doi:
Substances chimiques
Cytokines
0
HSP72 Heat-Shock Proteins
0
NF-kappa B
0
Green Fluorescent Proteins
147336-22-9
Types de publication
Journal Article
Langues
eng
Pagination
253-261Références
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