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Oncogene. 2014 Mar 6;33(10):1258-64. doi: 10.1038/onc.2013.71. Epub 2013 Mar 18.

Epstein-Barr virus maintains lymphomas via its miRNAs.

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McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI, USA.
1] Research Unit Gene Vectors, DZIF German Centre for Infection Research, Munich, Munich, Germany [2] Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany.
Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.


Epstein-Barr virus (EBV) has evolved exquisite controls over its host cells, human B lymphocytes, not only directing these cells during latency to proliferate and thereby expand the pool of infected cells, but also to survive and thereby persist for the lifetime of the infected individual. Although these activities ensure the virus is successful, they also make the virus oncogenic, particularly when infected people are immunosuppressed. Here we show, strikingly, that one set of EBV's microRNAs (miRNAs) both sustain Burkitt's lymphoma (BL) cells in the absence of other viral oncogenes and promote the transformation of primary B lymphocytes. BL cells were engineered to lose EBV and found to die by apoptosis and could be rescued by constitutively expressing viral miRNAs in them. Two of these EBV miRNAs were found to target caspase 3 to inhibit apoptosis at physiological concentrations.

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