tetano
Editor, Senior Moderator
PLoS Pathog. 2017 Apr 5;13(4):e1006305. doi: 10.1371/journal.ppat.1006305. [Epub ahead of print]
[h=1]miR-144 attenuates the host response to influenza virus by targeting the TRAF6-IRF7 signaling axis.[/h] Rosenberger CM[SUP]1[/SUP], Podyminogin RL[SUP]1[/SUP], Diercks AH[SUP]1[/SUP], Treuting PM[SUP]2[/SUP], Peschon JJ[SUP]1[/SUP], Rodriguez D[SUP]1[/SUP], Gundapuneni M[SUP]3[/SUP], Weiss MJ[SUP]4[/SUP], Aderem A[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that suppress protein levels by binding target sequences on their cognate mRNA. Here, we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses in primary mouse lung epithelial cells: influenza virus, EMCV, and VSV. We identified the transcriptional network regulated by miR-144 and demonstrate that miR-144 post-transcriptionally suppresses TRAF6 levels. In vivo ablation of miR-144 reduced influenza virus replication in the lung and disease severity. These data suggest that miR-144 reduces the antiviral response by attenuating the TRAF6-IRF7 pathway to alter the cellular antiviral transcriptional landscape.
PMID: 28380049 DOI: 10.1371/journal.ppat.1006305
[h=1]miR-144 attenuates the host response to influenza virus by targeting the TRAF6-IRF7 signaling axis.[/h] Rosenberger CM[SUP]1[/SUP], Podyminogin RL[SUP]1[/SUP], Diercks AH[SUP]1[/SUP], Treuting PM[SUP]2[/SUP], Peschon JJ[SUP]1[/SUP], Rodriguez D[SUP]1[/SUP], Gundapuneni M[SUP]3[/SUP], Weiss MJ[SUP]4[/SUP], Aderem A[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that suppress protein levels by binding target sequences on their cognate mRNA. Here, we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses in primary mouse lung epithelial cells: influenza virus, EMCV, and VSV. We identified the transcriptional network regulated by miR-144 and demonstrate that miR-144 post-transcriptionally suppresses TRAF6 levels. In vivo ablation of miR-144 reduced influenza virus replication in the lung and disease severity. These data suggest that miR-144 reduces the antiviral response by attenuating the TRAF6-IRF7 pathway to alter the cellular antiviral transcriptional landscape.
PMID: 28380049 DOI: 10.1371/journal.ppat.1006305