Epstein-Barr virus infection leads to partial phenotypic reversion of terminally differentiated malignant B cells.

Abstract:

:The B cell lymphomas associated with Epstein-Barr virus (EBV) are not limited to any specific stage of B cell differentiation but covers widely different B cell phenotypes. In vitro infection of the virus negative tumors with a recombinant EBV strain has provided important insights into virus-tumor interaction. Here, we investigated the interaction between EBV and terminally differentiated tumor derived B cells, namely multiple myeloma (MM). The in vitro EBV infected MM expressed restricted viral latency. Acquisition of the virus was accompanied by a partial reprogramming to a mature B cell phenotype. Thus, the plasma cell markers syndecan-1 (CD138), Blimp1 and MUM1 were downregulated, while expression of HLADR, CIITA and TCL1, which are normally not expressed in plasmacytoid cells, was upregulated. The silenced transcription factor gene encoding Pax5 and its target BLNK were activated. Significantly, the free lambda light chains secreted in the medium were reduced in EBV infected MM clones. Collectively, these results suggest that the restricted EBV latency can cause at least partial phenotypic reversion of terminally differentiated B tumor cells. We suggest that the restricted EBV latent gene expression may not only be the consequence but the cause of the mature B cell phenotype, actively participating in the virus persistence.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Anastasiadou E,Vaeth S,Cuomo L,Boccellato F,Vincenti S,Cirone M,Presutti C,Junker S,Winberg G,Frati L,Wade PA,Faggioni A,Trivedi P

doi

10.1016/j.canlet.2009.04.025

subject

Has Abstract

pub_date

2009-11-01 00:00:00

pages

165-74

issue

2

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(09)00293-6

journal_volume

284

pub_type

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