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 Blood, 1 January 2004, Vol. 103, No. 1, pp. 313-316.
Prepublished online as a Blood First Edition Paper on September 11, 2003; DOI 10.1182/blood-2003-05-1710.

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NEOPLASIA
Brief report

Infection of HHV-8+ primary effusion lymphoma cells with a recombinant Epstein-Barr virus leads to restricted EBV latency, altered phenotype, and increased tumorigenicity without affecting TCL1 expression

Pankaj Trivedi, Kumi Takazawa, Claudia Zompetta, Laura Cuomo, Elena Anastasiadou, Antonino Carbone, Stefania Uccini, Filippo Belardelli, Kenzo Takada, Luigi Frati, and Alberto Faggioni

From the Istituto Pasteur-Fondazione Cenci Bolognetti, Department of Experimental Medicine and Pathology, University of Rome, "La Sapienza," Rome, Italy; Department of Tumor Virology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan; Department of Clinical Pathology, San Filippo Neri Hospital, Rome, Italy; Division of Pathology and Scientific Direction, Centro di Riferimento Oncologico-IRCCS, National Cancer Institute, Aviano, Italy; Laboratory of Virology, Istituto Superiore di Sanità, Rome, Italy; and INM, Neuromed, Pozzilli (IS), Italy.

To investigate the role of Epstein-Barr virus (EBV) in the pathogenesis of primary effusion lymphoma (PEL), we infected human herpesvirus 8 (HHV-8+) but EBV- PEL lines BC-3, CRO-AP/6, and CRO-AP/3 cells with the recombinant Akata EBV strain. All EBV-infected clones expressed EBER-1, EBNA-1, and LMP2A. The expression of LMP1 and LMP2B was variable. None, however, expressed EBNA2-6. The surface markers CD30, CD74, and syndecan-1 were down-regulated in EBV convertants. EBV-infected BC-3 and CRO-AP/6 cells were highly tumorigenic in severe combined immunodeficiency (SCID) mice in contrast to their respective EBV- parental cells. However, neither the parental cells nor the virusconverted counterparts expressed TCL1. The results showing that PEL cells on in vitro EBV infection do not sustain latency III despite the absence of immune pressure indicate that the choice of EBV latent gene expression program is cell dependent. The data suggest an important role of EBV in the pathogenesis of PEL.


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