Announcement

Collapse
No announcement yet.

The highly pathogenic H5N1 influenza A virus down-regulated several cellular MicroRNAs which target viral genome

Collapse
X
  • Filter
  • Time
  • Show
Clear All
new posts

  • The highly pathogenic H5N1 influenza A virus down-regulated several cellular MicroRNAs which target viral genome

    J Cell Mol Med. 2017 Jun 13. doi: 10.1111/jcmm.13219. [Epub ahead of print]
    The highly pathogenic H5N1 influenza A virus down-regulated several cellular MicroRNAs which target viral genome.

    Wang R1, Zhang YY1,2, Lu JS1, Xia BH1, Yang ZX1, Zhu XD1, Zhou XW1, Huang PT1.
    Author information

    Abstract

    Higher and prolonged viral replication is critical for the increased pathogenesis of the highly pathogenic avian influenza (HPAI) subtype of H5N1 influenza A virus (IAV) over the lowly pathogenic H1N1 IAV strain. Recent studies highlighted the considerable roles of cellular miRNAs in host defence against viral infection. In this report, using a 3'UTR reporter system, we identified several putative miRNA target sites buried in the H5N1 virus genome. We found two miRNAs, miR-584-5p and miR-1249, that matched with the PB2 binding sequence. Moreover, we showed that these miRNAs dramatically down-regulated PB2 expression, and inhibited replication of H5N1 and H1N1 IAVs in A549 cells. Intriguingly, these miRNAs expression was differently regulated in A549 cells infected with the H5N1 and H1N1 viruses. Furthermore, transfection of miR-1249 inhibitor enhanced the PB2 expression and promoted the replication of H5N1 and H1N1 IAVs. These results suggest that H5N1 virus may have evolved a mechanism to escape host-mediated inhibition of viral replication through down-regulation of cellular miRNAs, which target its viral genome.
    2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.


    KEYWORDS:

    H1N1; H5N1 HPAI; MicroRNAs; host defence; virus replication

    PMID: 28609011 DOI: 10.1111/jcmm.13219
Working...
X