The highly pathogenic H5N1 influenza A virus down‐regulated several cellular Micro RNA s which target viral genome
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 mi RNA s in...
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Published in | Journal of cellular and molecular medicine Vol. 21; no. 11; pp. 3076 - 3086 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Chichester
John Wiley & Sons, Inc
01.11.2017
|
Subjects | |
Online Access | Get full text |
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Summary: | 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 mi
RNA
s in host defence against viral infection. In this report, using a 3′
UTR
reporter system, we identified several putative mi
RNA
target sites buried in the H5N1 virus genome. We found two mi
RNA
s, miR‐584‐5p and miR‐1249, that matched with the
PB
2 binding sequence. Moreover, we showed that these mi
RNA
s dramatically down‐regulated
PB
2 expression, and inhibited replication of H5N1 and H1N1
IAV
s in A549 cells. Intriguingly, these mi
RNA
s expression was differently regulated in A549 cells infected with the H5N1 and H1N1 viruses. Furthermore, transfection of miR‐1249 inhibitor enhanced the
PB
2 expression and promoted the replication of H5N1 and H1N1
IAV
s. These results suggest that H5N1 virus may have evolved a mechanism to escape host‐mediated inhibition of viral replication through down‐regulation of cellular mi
RNA
s, which target its viral genome. |
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ISSN: | 1582-1838 1582-4934 |
DOI: | 10.1111/jcmm.13219 |