Computational prediction of intracellular targets of wild-type or mutant vesicular stomatitis matrix protein.

While both viruses significantly upregulated TNFAIP3 transcription as predicted by the model ( Fig 6 ), there was slightly significant statistical evidence that the magnitude of this upregulation was lower in cells infected by 22–25 (p<0.1) 4 Discussion We constructed a mechanistic regulatory circuit model of the intracellular signaling pathways governing Type I IFN response to VSV infection based on causal relationships between the RIG-I and NFκB pathways documented in published scientific literature and experimental observations.

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