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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  CD 150/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  CD 150‐tropic  WT MV  was akin to that of  CD 46‐ and  CD 150‐tropic  CAM ‐70, suggesting that  CD 150 is critical for the susceptibility to  MV ‐induced cytolysis. Among  EBV ‐encoded genes, latent membrane protein 1 was responsible for the  CD 150 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.

cancer science

Enhanced susceptibility of  B  lymphoma cells to measles virus by  E pstein– B arr virus type  III  latency that upregulates  CD 150/signaling lymphocytic activation molecule