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Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
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Proof for EBV's sustaining role in Burkitt's lymphomas.

David Vereide1, Bill Sugden

  • 1McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, 1400 University Ave., Madison, WI 53706, USA.

Seminars in Cancer Biology
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Epstein-Barr virus (EBV) DNA replication is inefficient, causing plasmid loss in dividing cells. Tumors retaining EBV likely benefit from viral advantages, such as blocked apoptosis in Burkitt

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Area of Science:

  • Virology
  • Molecular Biology
  • Oncology

Background:

  • Epstein-Barr virus (EBV) establishes lifelong latent infections.
  • EBV DNA exists as extrachromosomal plasmids in infected cells.
  • The replication dynamics of EBV plasmids during host cell division are not fully understood.

Purpose of the Study:

  • To investigate the replication efficiency of Epstein-Barr viral (EBV) plasmids during host cell proliferation.
  • To determine the consequences of EBV plasmid replication inefficiency on infected cell populations.
  • To elucidate the role of EBV in sustaining tumor growth, particularly in EBV-associated malignancies.

Main Methods:

  • Analysis of EBV plasmid copy number in latently infected proliferating cells.
  • Comparative studies of EBV-positive and EBV-negative cell populations.
  • Investigation of cellular mechanisms affected by EBV presence in tumor cells.

Main Results:

  • Not all Epstein-Barr viral (EBV) plasmids are duplicated in each cell cycle.
  • This replication inefficiency leads to a progressive loss of EBV plasmids in proliferating cells.
  • EBV-positive cells demonstrate enhanced proliferation and resistance to apoptosis, suggesting viral-mediated tumor support.

Conclusions:

  • EBV plasmid loss is an inherent feature of its replication strategy in latent infection.
  • The selective advantage conferred by EBV to infected cells drives the enrichment of EBV-positive cells in proliferating populations.
  • The presence of EBV plasmids in tumors indicates its role in sustaining tumor growth, notably by inhibiting apoptosis in Burkitt's lymphomas (BL).