tetano
Editor, Senior Moderator
Elife. 2016 Aug 15;5. pii: e18311. doi: 10.7554/eLife.18311. [Epub ahead of print]
[h=1]A systematic view on Influenza induced host shut-off.[/h] Bercovich-Kinori A[SUP]1[/SUP], Tai J[SUP]1[/SUP], Gelbart IA[SUP]1[/SUP], Shitrit A[SUP]1[/SUP], Ben-Moshe S[SUP]2[/SUP], Drori Y[SUP]3[/SUP], Itzkovitz S[SUP]2[/SUP], Mandelboim M[SUP]4[/SUP], Stern-Ginossar N[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Host shutoff is a common strategy used by viruses to repress cellular mRNA translation and concomitantly allow the efficient translation of viral mRNAs. Here we use RNA-sequencing and ribosome profiling to explore the mechanisms that are being utilized by Influenza A virus (IAV) to induce host shutoff. We show that viral transcripts are not preferentially translated and instead the decline in cellular protein synthesis is mediated by viral takeover on the mRNA pool. Our measurements also uncover strong variability in the levels of cellular transcripts reduction, revealing that short transcripts are less affected by IAV. Interestingly, these mRNAs that are refractory to IAV infection are enriched in cell maintenance processes such as oxidative phosphorylation. Furthermore we show that the continuous oxidative phosphorylation activity is important for viral propagation. Our results advance our understanding of IAV-induced shutoff, and suggest a mechanism that facilitates the translation of genes with important housekeeping functions.
[h=4]KEYWORDS:[/h] computational biology; human; infectious disease; microbiology; systems biology
PMID: 27525483 DOI: 10.7554/eLife.18311
[PubMed - as supplied by publisher]
[h=1]A systematic view on Influenza induced host shut-off.[/h] Bercovich-Kinori A[SUP]1[/SUP], Tai J[SUP]1[/SUP], Gelbart IA[SUP]1[/SUP], Shitrit A[SUP]1[/SUP], Ben-Moshe S[SUP]2[/SUP], Drori Y[SUP]3[/SUP], Itzkovitz S[SUP]2[/SUP], Mandelboim M[SUP]4[/SUP], Stern-Ginossar N[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Host shutoff is a common strategy used by viruses to repress cellular mRNA translation and concomitantly allow the efficient translation of viral mRNAs. Here we use RNA-sequencing and ribosome profiling to explore the mechanisms that are being utilized by Influenza A virus (IAV) to induce host shutoff. We show that viral transcripts are not preferentially translated and instead the decline in cellular protein synthesis is mediated by viral takeover on the mRNA pool. Our measurements also uncover strong variability in the levels of cellular transcripts reduction, revealing that short transcripts are less affected by IAV. Interestingly, these mRNAs that are refractory to IAV infection are enriched in cell maintenance processes such as oxidative phosphorylation. Furthermore we show that the continuous oxidative phosphorylation activity is important for viral propagation. Our results advance our understanding of IAV-induced shutoff, and suggest a mechanism that facilitates the translation of genes with important housekeeping functions.
[h=4]KEYWORDS:[/h] computational biology; human; infectious disease; microbiology; systems biology
PMID: 27525483 DOI: 10.7554/eLife.18311
[PubMed - as supplied by publisher]