Downregulation of the polyamine regulator spermidine/spermine N(1)-acetyltransferase by Epstein-Barr virus in a Burkitt's lymphoma cell line.

Transition of Akata Burkitt's lymphoma (BL) from a malignant to nonmalignant phenotype upon loss of Epstein-Barr virus (EBV) is evidence for a viral contribution to tumorigenesis despite the tight restriction of EBV gene expression in BL. Examination of global cellular gene expression in Akata subclones that retained or lost EBV identified spermidine/spermine N(1)-acetyltransferase (SAT1), an inducible enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes downregulated by EBV. Re-infection of the EBV-negative Akata clone reduced SAT1 mRNA to a level comparable with the parental EBV-positive Akata.

A defective, rearranged Epstein-Barr virus genome in EBER-negative and EBER-positive Hodgkin's disease.

A ubiquitous herpesvirus that establishes life-long infection, the Epstein-Barr virus (EBV) has yielded little insight into how a single agent in general accord with its host can produce diverse pathologies ranging from oral hairy leukoplakia to nasopharyngeal carcinoma, from infectious mononucleosis to Hodgkin's disease (HD) and Burkitt's lymphoma. Its pathogenesis is further confounded by the less than total association of virus with histologically similar tumors. In other viral systems, defective (interfering) viral genomes are known to modulate outcome of infection, with either ameliorating or intensifying effects on disease processes initiated by prototype strains.