부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.semcancer.2009.07.006 Byline: David Vereide, Bill Sugden Keywords: Burkitt's lymphoma; Epstein-Barr virus; Tumor virus; Tumor survival Abbreviations: EBV, Epstein-Barr virus; BL, Burkitt's lymphoma; EBNA, Epstein-Barr nuclear antigen; LMP, latent membrane protein; DS, dyad symmetry; FR, family of repeats; IPTG, isopropyl-[beta]-d-thiogalactoside 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. Author Affiliation: McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, 1400 University Ave., Madison, WI 53706, United States