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Learn MoreEnterovirus 71 (EV71) infection causes a profound shutoff of cellular protein synthesis. Deep RNA-sequencing and ribosome profiling were employed to systematically analyze messenger RNA and ribosome-protected RNA in EV71-infected rhabdomyosarcoma cells at progressive time points following infection. The analysis characterized the dynamic transcriptional and translational landscapes of both the virus and host cells. The results indicated that reduced translation of cellular mRNAs played a key role in EV71-induced host shutoff rather than mRNA depletion. During the host shutoff, EV71 protein was preferably synthesized through both a translational advantage and abundant mRNA production. Moreover, a small number of cellular genes were resistant to the host shutoff through both transcriptional and translational regulation, including genes in mitogen-activated protein kinase (MAPK) signaling pathway that is important for EV71 replication. These results indicated selective cellular protein synthesis during EV71-induced host shutoff as a mechanism the virus utilizes to benefit its replication. SOURCE: Yongquan Lin (circleleen@hotmail.com) - Nankai University
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