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Humanized Mouse Models of Epstein Barr Virus Infection.

Saskia Gertrud von Boxberg1, Kristin Gehrmann1, Svenja Luisa Nopper1

  • 1Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.

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|November 25, 2025
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Summary

This study details a humanized mouse model for Epstein-Barr virus (EBV) infection, enabling the study of infectious mononucleosis (IM) and EBV-driven lymphomas. The model allows for analysis of viral loads, immune responses, and potential therapeutic interventions.

Keywords:
B‐cell lymphomaEpstein Barr virus (EBV)T‐cell responseshuman immune system reconstitutionimmunocompromised micenatural killer (NK)‐cell responsesxenograft

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Area of Science:

  • Immunology
  • Virology
  • Pathogenesis

Background:

  • Epstein-Barr virus (EBV) is a human herpesvirus causing infectious mononucleosis (IM) and implicated in various cancers.
  • Studying EBV pathogenesis requires a suitable animal model, as EBV primarily infects human B cells.
  • Existing models often necessitate the transfer of human immune components into immunocompromised hosts.

Purpose of the Study:

  • To establish and validate a humanized mouse model for studying EBV infection and associated diseases.
  • To enable the investigation of EBV's primary infection, latency, and oncogenic potential in vivo.
  • To provide a platform for evaluating immune responses and therapeutic strategies against EBV.

Main Methods:

  • Neonatal transfer of CD34+ hematopoietic progenitor cells into immune-compromised NOD-scid γc-/- (NSG) mice to reconstitute the human immune system.
  • Infection of humanized mice with a recombinant EBV strain (B95-8) via intraperitoneal or intranasal routes.
  • Monitoring of viral loads, B-cell lymphoproliferation, T-cell responses (CD8+ T-cell lymphocytosis), and lymphoma development using techniques like immunohistochemistry and spectral flow cytometry.

Main Results:

  • Successful reconstitution of human immune system components, including B cells, in NSG mice.
  • EBV infection in humanized mice mimicked symptomatic primary infection (infectious mononucleosis) with high viral loads.
  • Development of clonal EBV-induced B-cell lymphoproliferations resembling large B-cell lymphomas with EBV latency III program.
  • Characterization of CD8+ T-cell expansion and viral load dynamics post-infection.

Conclusions:

  • The developed humanized mouse model provides a robust platform for studying EBV pathogenesis, including IM and EBV-associated lymphomas.
  • This model facilitates research into EBV-mediated immune responses and the evaluation of potential vaccines and therapies.
  • The model has been instrumental in exploring EBV mutant infections, co-infections (HIV, KSHV), and antibody-mediated protection.