tetano
Editor, Senior Moderator
J Immunol. 2016 Jun 27. pii: 1501563. [Epub ahead of print]
[h=1]FAT10 Is Critical in Influenza A Virus Replication by Inhibiting Type I IFN.[/h] Zhang Y[SUP]1[/SUP], Tang J[SUP]1[/SUP], Yang N[SUP]1[/SUP], Liu Q[SUP]1[/SUP], Zhang Q[SUP]1[/SUP], Zhang Y[SUP]1[/SUP], Li N[SUP]1[/SUP], Zhao Y[SUP]1[/SUP], Li S[SUP]1[/SUP], Liu S[SUP]1[/SUP], Zhou H[SUP]1[/SUP], Li X[SUP]2[/SUP], Tian M[SUP]2[/SUP], Deng J[SUP]1[/SUP], Xie P[SUP]3[/SUP], Sun Y[SUP]1[/SUP], Lu H[SUP]2[/SUP], Zhang MQ[SUP]4[/SUP], Jin N[SUP]5[/SUP], Jiang C[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The H5N1 avian influenza virus causes severe disease and high mortality, making it a major public health concern worldwide. The virus uses the host cellular machinery for several steps of its life cycle. In this report, we observed overexpression of the ubiquitin-like protein FAT10 following live H5N1 virus infection in BALB/c mice and in the human respiratory epithelial cell lines A549 and BEAS-2B. Further experiments demonstrated that FAT10 increased H5N1 virus replication and decreased the viability of infected cells. Total RNA extracted from H5N1 virus-infected cells, but not other H5N1 viral components, upregulated FAT10, and this process was mediated by the retinoic acid-induced protein I-NF-κB signaling pathway. FAT10 knockdown in A549 cells upregulated type I IFN mRNA expression and enhanced STAT1 phosphorylation during live H5N1 virus infection. Taken together, our data suggest that FAT10 was upregulated via retinoic acid-induced protein I and NF-κB during H5N1 avian influenza virus infection. And the upregulated FAT10 promoted H5N1 viral replication by inhibiting type I IFN.
Copyright ? 2016 by The American Association of Immunologists, Inc.
PMID: 27354218 DOI: 10.4049/jimmunol.1501563
[PubMed - as supplied by publisher]
[h=1]FAT10 Is Critical in Influenza A Virus Replication by Inhibiting Type I IFN.[/h] Zhang Y[SUP]1[/SUP], Tang J[SUP]1[/SUP], Yang N[SUP]1[/SUP], Liu Q[SUP]1[/SUP], Zhang Q[SUP]1[/SUP], Zhang Y[SUP]1[/SUP], Li N[SUP]1[/SUP], Zhao Y[SUP]1[/SUP], Li S[SUP]1[/SUP], Liu S[SUP]1[/SUP], Zhou H[SUP]1[/SUP], Li X[SUP]2[/SUP], Tian M[SUP]2[/SUP], Deng J[SUP]1[/SUP], Xie P[SUP]3[/SUP], Sun Y[SUP]1[/SUP], Lu H[SUP]2[/SUP], Zhang MQ[SUP]4[/SUP], Jin N[SUP]5[/SUP], Jiang C[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The H5N1 avian influenza virus causes severe disease and high mortality, making it a major public health concern worldwide. The virus uses the host cellular machinery for several steps of its life cycle. In this report, we observed overexpression of the ubiquitin-like protein FAT10 following live H5N1 virus infection in BALB/c mice and in the human respiratory epithelial cell lines A549 and BEAS-2B. Further experiments demonstrated that FAT10 increased H5N1 virus replication and decreased the viability of infected cells. Total RNA extracted from H5N1 virus-infected cells, but not other H5N1 viral components, upregulated FAT10, and this process was mediated by the retinoic acid-induced protein I-NF-κB signaling pathway. FAT10 knockdown in A549 cells upregulated type I IFN mRNA expression and enhanced STAT1 phosphorylation during live H5N1 virus infection. Taken together, our data suggest that FAT10 was upregulated via retinoic acid-induced protein I and NF-κB during H5N1 avian influenza virus infection. And the upregulated FAT10 promoted H5N1 viral replication by inhibiting type I IFN.
Copyright ? 2016 by The American Association of Immunologists, Inc.
PMID: 27354218 DOI: 10.4049/jimmunol.1501563
[PubMed - as supplied by publisher]