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, Alberto Faggioni

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)313-316
Number of pages4
JournalBlood
Volume103
Issue number1
DOIs
Publication statusPublished - Jan 1 2004

ASJC Scopus subject areas

  • Hematology

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