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Study on the Modes of Cell Death in Lung Cancer Epithelial Cells During Acute EBV Infection Using a Co-Culture Model
Xinyue Zhang1, Chenpeng Li2, Shuilian Zhang2
1The First School of Clinical Medicine, Guangdong Pharmaceutical University, Guangzhou, China.
Thoracic Cancer
|April 13, 2026
Summary
Epstein-Barr virus (EBV) infection causes lung cancer cells to undergo necroptosis, a form of programmed cell death. This study clarifies early cell death mechanisms in EBV-associated lung cancers.
Area of Science:
- Oncology
- Virology
- Cell Biology
Background:
- Pulmonary lymphoepithelial carcinoma is linked to Epstein-Barr virus (EBV), but its precise pathogenesis is unclear.
- Early cellular responses and death pathways in lung epithelial cells after acute EBV infection require further investigation.
Purpose of the Study:
- To investigate the modes of cell death in lung epithelial cells following acute Epstein-Barr virus (EBV) infection.
- To elucidate the early pathological changes and cellular fate decisions in EBV-infected lung epithelium.
Main Methods:
- Established an acute EBV infection model by co-culturing EBV-positive Akata cells with lung cancer cells.
- Utilized immunofluorescence staining and confocal laser scanning microscopy to evaluate morphological alterations and cell death modes.
Main Results:
- Acute EBV infection induced significant necroptosis (pMLKL upregulation) in lung cancer cells by 72 hours.
- Apoptosis (cCASP3) and pyroptosis (cGSDMD) were not significantly involved in epithelial cell death.
- ~15.1% of epithelial cells showed "cell-in-cell" structures with internalized B cells undergoing apoptosis, pyroptosis, and necroptosis.
Conclusions:
- Acute EBV infection primarily induces lung cancer epithelial cell death via pMLKL-mediated necroptosis.
- Internalized B cells within "cell-in-cell" structures display diverse death modalities.
- Findings offer new insights into cellular fate in EBV-infected lung epithelium before latency.
