Abstract
BackgroundInterferon (IFN) inhibits viruses by inducing several hundred cellular genes, aptly named ‘interferon (IFN)-stimulated genes’ (ISGs). The only two RNA viruses of the Pneumovirus genus of the Paramyxoviridae family, namely Respiratory Syncytial Virus (RSV) and Pneumonia Virus of Mice (PVM), each encode two nonstructural (NS) proteins that share no sequence similarity but yet suppress IFN. Since suppression of IFN underlies the ability of these viruses to replicate in the host cells, the mechanism of such suppression has become an important area of research. This Short Report is an important extension of our previous efforts in defining this mechanism.ResultsWe show that, like their PVM counterparts, the RSV NS proteins also target multiple members of the ISG family. While significantly extending the substrate repertoire of the RSV NS proteins, these results, unexpectedly, also reveal that the target preferences of the NS proteins of the two viruses are entirely different. This is surprising since the two Pneumoviruses are phylogenetically close with similar genome organization and gene function, and the NS proteins of both also serve as suppressors of host IFN response.ConclusionThe finding that the NS proteins of the two highly similar viruses suppress entirely different members of the ISG family raises intriguing questions of pneumoviral NS evolution and mechanism of action.
Highlights
IFN is recognized as an antiviral cytokine that uses Signal transducers and activators of transcription (STAT)-family transcription factors to induce a few hundred IFN-stimulated genes (ISGs), many of which have been shown to be antiviral [1, 2]
We have been following this property in selected members of this family [5,6,7,8,9], focusing on the Pneumovirus genus, which is comprised of two members that are severe respiratory pathogens, namely Respiratory Syncytial Virus (RSV), a human virus, and Pneumonia Virus of Mice (PVM), a mouse virus [10, 11]
To start with, we examined the effect of RSV NS proteins on six major human ISGs, and the immunoblot results are shown (Fig. 1)
Summary
IFN is recognized as an antiviral cytokine that uses STAT-family transcription factors to induce a few hundred IFN-stimulated genes (ISGs), many of which have been shown to be antiviral [1, 2]. We have been following this property in selected members of this family [5,6,7,8,9], focusing on the Pneumovirus genus, which is comprised of two members that are severe respiratory pathogens, namely RSV, a human virus, and PVM, a mouse virus [10, 11]. The only two RNA viruses of the Pneumovirus genus of the Paramyxoviridae family, namely Respiratory Syncytial Virus (RSV) and Pneumonia Virus of Mice (PVM), each encode two nonstructural (NS) proteins that share no sequence similarity but yet suppress IFN. Since suppression of IFN underlies the ability of these viruses to replicate in the host cells, the mechanism of such suppression has become an important area of research. This Short Report is an important extension of our previous efforts in defining this mechanism
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