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Epstein-Barr virus (EBV) infection of endothelial cells via endocytosis is associated with a poor prognosis in nasopharyngeal carcinoma

  • 0Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor (Guangxi Medical University), Ministry of Education, Guangxi, China.
Microbiology Spectrum +

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July 9, 2025

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July 9, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Epstein-Barr virus (EBV) infects endothelial cells (ECs) by engulfing infected lymphocytes, worsening nasopharyngeal carcinoma (NPC) and lymphatic metastasis. This EBV infection mechanism in ECs is linked to poor patient outcomes and immune changes.

Area Of Science

  • Oncology
  • Virology
  • Immunology

Background

  • Epstein-Barr virus (EBV) is linked to several cancers, but its endothelial cell (EC) infection and role in nasopharyngeal carcinoma (NPC) are unclear.
  • Understanding EBV's interaction with ECs is crucial for elucidating cancer progression and developing targeted therapies.

Purpose Of The Study

  • To investigate the mechanism of EBV infection in endothelial cells (ECs).
  • To determine the clinical significance of EBV-encoded small RNAs (EBERs) in ECs of NPC patients.
  • To explore the impact of EBV-infected ECs on the tumor microenvironment and patient prognosis.

Main Methods

  • Analysis of 99 NPC clinical samples for EBERs positivity in ECs.
  • Immunological profiling of patients with EBERs-positive ECs.
  • In vitro modeling using EBV particle infection, Transwell coculture, and direct-contact systems.
  • RT-PCR to detect EBV oncogenes and endocytosis-related genes.
  • Ultrastructural electron microscopy to observe cellular interactions.

Main Results

  • EBERs positivity in ECs significantly correlates with advanced N stage, M stage, and overall clinical stage of NPC.
  • Patients with EBERs-positive ECs show reduced B-cell proportions, indicating an altered immune status.
  • In vitro studies show ECs internalize EBV-infected lymphocytes, expressing EBV oncogenes and upregulating endocytosis genes.
  • Phagocytosis of infected lymphocytes by ECs is identified as a primary EBV entry mechanism.

Conclusions

  • Endothelial cell infection by EBV, via phagocytosis of infected lymphocytes, is a significant factor in NPC progression.
  • EBERs-positive ECs are potential biomarkers for advanced NPC and poor clinical outcomes.
  • EBV infection of ECs contributes to an immunosuppressive tumor microenvironment, requiring further investigation into molecular pathways.

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