title: Proof for EBV's sustaining role in Burkitt's lymphomas.
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.
authors.affiliation: McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, 1400 University Ave., Madison, WI 53706, USA.
authors.forename: David
authors.initials: D
authors.lastname: Vereide
authors.forename: Bill
authors.initials: B
authors.lastname: Sugden
mesh_terms: D000818:Animals; D002051:Burkitt Lymphoma / Q000821:virology*; D020031:Epstein-Barr Virus Infections / Q000821:virology*; D004854:Herpesvirus 4, Human / Q000472:pathogenicity*; D006801:Humans