Enhanced susceptibility of B lymphoma cells to measles virus by Epstein-Barr virus type III latency that upregulates CD150/signaling lymphocytic activation molecule.
Bottom Line: Among EBV-encoded genes, latent membrane protein 1 was responsible for the CD150 upregulation.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.
Affiliation: AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan.Show MeSH
Related in: MedlinePlus
Mentions: To assess the effect of EBV latency on MV susceptibility, we examined the efficiencies of MV-induced cytolysis in two EBV-negative B lymphoma cell lines BL41 and BJAB, and compared them with their EBV-positive counterparts. Infection of EBV 95-8 strain yields type III latency in both cell lines.(36,37) In BL41 cells, the LD50 values of all MV strains were above the limit of detection (Fig. 2a). In contrast, EBV-positive BL41 cells showed susceptibilities to Schwarz and the WT MV, with LD50 values of 0.4 and 0.15, respectively (Fig. 2a). In BJAB cells, Schwarz and the WT MV were not able to kill cells. However, CAM-70 showed substantial cytolytic activity (LD50 < 0.02) in BJAB cells (Fig. 2b). In accordance with BL41 cells, EBV-positive BJAB cells were more susceptible to MV than EBV-negative counterparts as represented by the enhanced susceptibility to WT MV (LD50 2.0) (Fig. 2b). These data suggested that type III EBV latency in B lymphoma cells augments the susceptibility to MV-induced cytolysis, although the magnitude of augmentation varies among cell types and the MV strains.
Affiliation: AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan.