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Epstein-Barr virus-infected marmoset cells do not form lymphomas in mice with severe combined immunodeficiency

B Z Katz1, B Salimi, U Saini

  • 1Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06510.

Pediatric Research
|October 1, 1994
PubMed

Insights

The cellular environment, not Epstein-Barr virus (EBV) replication, determines tumor formation in SCID mice. Marmoset cells, permissive for EBV replication, did not form tumors, unlike human cells.

Area of Science:

  • Virology
  • Immunology
  • Oncology

Background:

  • Epstein-Barr virus (EBV) is linked to human cancers.
  • Marmoset B lymphocytes support EBV lytic replication, unlike human B cells.
  • Severe combined immunodeficiency (SCID) mice are susceptible to EBV-induced lymphomagenesis.

Purpose of the Study:

  • To investigate the role of the cellular environment versus EBV replication permissiveness in EBV-induced lymphomagenesis.
  • To compare tumor formation in SCID mice using human versus marmoset lymphoblastoid cells infected with EBV.

Main Methods:

  • SCID mice were inoculated with EBV-infected human and marmoset lymphoblastoid cells.
  • Marmoset cells were treated with acyclovir or anti-natural killer cell antibody.
  • Human lymphoblastoid cells engineered for lytic EBV replication were also used.

Main Results:

  • Marmoset lymphoblastoid cells did not form lymphomas in SCID mice, even with interventions.
  • Human lymphoblastoid cells consistently formed lymphomas within 8 weeks.
  • Engineered human cells permitting lytic EBV replication also formed tumors.

Conclusions:

  • The cellular milieu, not EBV isolate or lytic replication capacity, is critical for lymphomagenesis in this SCID mouse model.
  • Host cell permissiveness for EBV lytic replication does not dictate tumor formation.
  • SCID mouse models can differentiate the impact of cellular factors on EBV-driven diseases.

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