Japan Health Science Foundation. Japanese Ministry of Health, Labor, and Welfare (H23-Shinko-Ippan-028 and H25-Shinko-Ippan-010). Japanese Ministry of Education, Culture, Sports, Science and Technology (24310146).
Enhanced susceptibility of B lymphoma cells to measles virus by Epstein–Barr virus type III latency that upregulates CD150/signaling lymphocytic activation molecule
Article first published online: 12 JAN 2014
© 2013 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Volume 105, Issue 2, pages 211–218, February 2014
How to Cite
Cancer Sci 105 (2014) 211–218
- Issue published online: 10 FEB 2014
- Article first published online: 12 JAN 2014
- Accepted manuscript online: 15 NOV 2013 11:45AM EST
- Manuscript Accepted: 13 NOV 2013
- Manuscript Revised: 5 NOV 2013
- Manuscript Received: 18 SEP 2013
- Japan Health Science Foundation
- Japanese Ministry of Health, Labor, and Welfare
- Japanese Ministry of Education, Culture, Sports, Science and Technology. Grant Number: 24310146
- B-cell lymphoma;
- CD150/signaling lymphocytic activation molecule;
- Epstein–Barr virus;
- latent membrane protein 1;
- measles virus oncolytic virotherapy
Measles virus (MV) is one of the candidates for the application of oncolytic virotherapy (OVT). Although an advanced clinical study has been reported on a T-cell lymphoma, the potential of MV OVT against B-cell lymphomas remains to be clarified. We found that an EBV-transformed B lymphoblastoid cell line, a model for diffuse large B-cell lymphoma, and EBV-positive Burkitt's lymphoma cells bearing type III latency were highly susceptible to the cytolysis induced by an MV vaccine strain CAM-70. As analyzed by EBV-positive and -negative counterparts of the same cytogenetic background, type III EBV latency, not type I, was shown to augment the susceptibility of B lymphoma cells to MV-induced cytolysis. Cell surface levels of CD150/signaling lymphocytic activation molecule, a receptor of MV, were upregulated in B lymphoma cell lines with type III EBV latency by 3.8-fold, on average. The cytolytic activity of CD150-tropic WT MV was akin to that of CD46- and CD150-tropic CAM-70, suggesting that CD150 is critical for the susceptibility to MV-induced cytolysis. Among EBV-encoded genes, latent membrane protein 1 was responsible for the CD150 upregulation. It was notable that the majority of B lymphoma cell lines of type III EBV latency showed higher susceptibility to the non-Edmonston-derived CAM-70 than to the Edmonston-derived Schwarz strain. This is the first report indicating the potential of non-Edmonston MV strain for the application of OVT. Furthermore, a cellular regulator of MV replication was implicated that functions in a vaccine strain-specific fashion. Altogether, the MV OVT should serve as an alternative therapy against EBV-positive diffuse large B-cell lymphoma with type III EBV latency.