SPONTANEOUS LOSS OF VIRAL EPISOMES ACCOMPANYING EPSTEIN-BARR-VIRUS REACTIVATION IN A BURKITTS-LYMPHOMA CELL-LINE

Life-long viral persistence is a hallmark of human herpesvirus infecti on. In the Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) c ell line, Mutu, spontaneous loss of all viral episomes accompanied pro ductive viral DNA replication. The molecular configuration of intracel lular 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, rearra nged 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 viral genome in expanding maligna nt cell clones.