tetano
Editor, Senior Moderator
Sci Signal. 2015 Dec 8;8(406):ra126. doi: 10.1126/scisignal.aab3183.
[h=1]The microRNA miR-485 targets host and influenza virus transcripts to regulate antiviral immunity and restrict viral replication.[/h] Ingle H[SUP]1[/SUP], Kumar S[SUP]1[/SUP], Raut AA[SUP]2[/SUP], Mishra A[SUP]2[/SUP], Kulkarni DD[SUP]2[/SUP], Kameyama T[SUP]3[/SUP], Takaoka A[SUP]3[/SUP], Akira S[SUP]4[/SUP], Kumar H[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] MicroRNAs (miRNAs) are small noncoding RNAs that are responsible for dynamic changes in gene expression, and some regulate innate antiviral responses. Retinoic acid-inducible gene I (RIG-I) is a cytosolic sensor of viral RNA; RIG-I activation induces an antiviral immune response. We found that miR-485 of the host was produced in response to viral infection and targeted RIG-I mRNA for degradation, which led to suppression of the antiviral response and enhanced viral replication. Thus, inhibition of the expression of mir-485 markedly reduced the replication of Newcastle disease virus (NDV) and the H5N1 strain of influenza virus in mammalian cells. Unexpectedly, miR-485 also bound to the H5N1 gene PB1 (which encodes an RNA polymerase required for viral replication) in a sequence-specific manner, thereby inhibiting replication of the H5N1 virus. Furthermore, miR-485 exhibited bispecificity, targeting RIG-I in cells with a low abundance of H5N1 virus and targeting PB1 in cells with increased amounts of the H5N1 virus. These findings highlight the dual role of miR-485 in preventing spurious activation of antiviral signaling and restricting influenza virus infection.
Copyright ? 2015, American Association for the Advancement of Science.
PMID: 26645583 [PubMed - in process]
[h=1]The microRNA miR-485 targets host and influenza virus transcripts to regulate antiviral immunity and restrict viral replication.[/h] Ingle H[SUP]1[/SUP], Kumar S[SUP]1[/SUP], Raut AA[SUP]2[/SUP], Mishra A[SUP]2[/SUP], Kulkarni DD[SUP]2[/SUP], Kameyama T[SUP]3[/SUP], Takaoka A[SUP]3[/SUP], Akira S[SUP]4[/SUP], Kumar H[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] MicroRNAs (miRNAs) are small noncoding RNAs that are responsible for dynamic changes in gene expression, and some regulate innate antiviral responses. Retinoic acid-inducible gene I (RIG-I) is a cytosolic sensor of viral RNA; RIG-I activation induces an antiviral immune response. We found that miR-485 of the host was produced in response to viral infection and targeted RIG-I mRNA for degradation, which led to suppression of the antiviral response and enhanced viral replication. Thus, inhibition of the expression of mir-485 markedly reduced the replication of Newcastle disease virus (NDV) and the H5N1 strain of influenza virus in mammalian cells. Unexpectedly, miR-485 also bound to the H5N1 gene PB1 (which encodes an RNA polymerase required for viral replication) in a sequence-specific manner, thereby inhibiting replication of the H5N1 virus. Furthermore, miR-485 exhibited bispecificity, targeting RIG-I in cells with a low abundance of H5N1 virus and targeting PB1 in cells with increased amounts of the H5N1 virus. These findings highlight the dual role of miR-485 in preventing spurious activation of antiviral signaling and restricting influenza virus infection.
Copyright ? 2015, American Association for the Advancement of Science.
PMID: 26645583 [PubMed - in process]