Type 1 Interferon Responses Underlie Tumor-Selective Replication of Oncolytic Measles Virus.

ABSTRACT: The mechanism of tumor-selective replication of oncolytic measles virus (MV) is poorly understood. Using a stepwise model of cellular transformation, in which oncogenic hits were additively expressed in human bone marrow-derived mesenchymal stromal cells, we show that MV-induced oncolysis increased progressively with transformation. The type 1 interferon (IFN) response to MV infection was significantly reduced and delayed, in accordance with the level of transformation. Consistently, we observed delayed and reduced signal transducer and activator of transcription (STAT1) phosphorylation in the fully transformed cells. Pre-treatment with IFNβ restored resistance to MV-mediated oncolysis. Gene expression profiling to identify the genetic correlates of susceptibility to MV oncolysis revealed

SUBMITTER: Aref S 

PROVIDER: S-EPMC7132605 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature