TY - JOUR
T1 - Spontaneous loss of viral episomes accompanying Epstein-Barr virus reactivation in a Burkitt's lymphoma cell line
AU - Srinivas, Shamala K.
AU - Sample, Jeffery T.
AU - Sixbey, John W.
N1 - Funding Information:
Received 20 August 1997; revised 17 December 1997. Financial support: Public Health Service (CA-67372), Cancer Center Support (CORE grant CA-21765 from the National Cancer Institute), and CA-56639 (J.T.S.); American Lebanese Syrian Associated Charities. Reprints or correspondence: Dr. John W. Sixbey, Depts. of Infectious Diseases and Virology & Molecular Biology, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN 38105-2729 ([email protected]).
PY - 1998
Y1 - 1998
N2 - Life-long viral persistence is a hallmark of human herpesvirus infection. In the Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) cell line, Mutu, spontaneous loss of all viral episomes accompanied productive vital DNA replication. The molecular configuration of intracellular EBV DNA evolved from monoclonal episomes in cells retaining the original tumor phenotype to predominantly replicating linear DNA and, subsequently, only integrated forms in BL cells that had acquired the lymphoblastoid cell phenotype. Transient appearance of deleted, rearranged WZhet EBV DNA capable of disrupting viral latency, along with the integration of viral DNA into human chromosomes, indicates a genetic instability in the host cell which, if duplicated in vivo, may affect configuration and persistence of the vital genome in expanding malignant cell clones.
AB - Life-long viral persistence is a hallmark of human herpesvirus infection. In the Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) cell line, Mutu, spontaneous loss of all viral episomes accompanied productive vital DNA replication. The molecular configuration of intracellular EBV DNA evolved from monoclonal episomes in cells retaining the original tumor phenotype to predominantly replicating linear DNA and, subsequently, only integrated forms in BL cells that had acquired the lymphoblastoid cell phenotype. Transient appearance of deleted, rearranged WZhet EBV DNA capable of disrupting viral latency, along with the integration of viral DNA into human chromosomes, indicates a genetic instability in the host cell which, if duplicated in vivo, may affect configuration and persistence of the vital genome in expanding malignant cell clones.
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U2 - 10.1086/517427
DO - 10.1086/517427
M3 - Article
C2 - 9607853
AN - SCOPUS:0031750736
SN - 0022-1899
VL - 177
SP - 1705
EP - 1709
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 6
ER -
