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Review
. 2009 Dec;19(6):389-93.
doi: 10.1016/j.semcancer.2009.07.006. Epub 2009 Jul 21.

Proof for EBV's sustaining role in Burkitt's lymphomas

David Vereide  1 , Bill Sugden
Affiliations
Review

Proof for EBV's sustaining role in Burkitt's lymphomas

David Vereide et al. Semin Cancer Biol. 2009 Dec.

Abstract

We have found that not all Epstein-Barr viral (EBV) plasmids are duplicated each cell cycle. This inefficiency is intrinsic to EBV's mechanism of DNA synthesis in latently infected cells and necessarily leads to a loss of EBV plasmids from proliferating cells. If EBV provides its host cells advantages that allow those cells that retain EBV to outgrow those that lose it, then such proliferating populations will be EBV-positive. EBV-associated human tumors are EBV-positive. Thus, the presence of EBV plasmids in most cells of a tumor demonstrates that EBV sustains these tumors in vivo. The virus can provide multiple selective advantages to tumor cells, including promoting cell proliferation and inhibiting cell death. In the case of Burkitt's lymphomas (BL), most current evidence indicates that the tumor requires the virus minimally to block apoptosis.

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Conflict of interest statement

Conflict of Interest statement: The authors declare that there are no conflicts of interest.

Figures

Figure 1
Figure 1. A model of the synthesis and partitioning of EBV plasmids
Shown is one cell in the G2 phase of the cell cycle with EBV plasmids identified with letters. Four plasmids were duplicated in the prior S phase to yield co-localized pairs of plasmids (AA1, BB1, CC1, and DD1); one was not (E). Studies with EBV plasmids visualized in live cells have shown that 16% of the plasmids fail to be duplicated each S-phase [21]. These studies have also shown that during mitosis (M-phase) 88% of the co-localized plasmids are partitioned symmetrically. This partitioning is represented here as plasmids A and A1, B and B1, and C and C1 each being distributed to separate daughter cells in G1 phase. The 12% of the co-localized plasmids that do not partition symmetrically, represented by D and D1, and the 16% of the plasmids that are not duplicated in S phase, represented by E, partition randomly. In the example depicted here, all three plasmids (D, D1, A) have been distributed to the same daughter cell. These defects in synthesis and partitioning lead to daughter cells having increased numbers of plasmids as shown for the upper cell in G1 and decreased numbers of plasmids as shown for the lower cell in G1 relative to the parental cell in G2. The defect in plasmid synthesis leads to the loss of plasmids from a population of proliferating cells. The parental cell prior to S-phase had five plasmids; the two daughter cells have only nine plasmids or four and one-half plasmids per cell.
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