Novel Role for miR-1290 in Host Species Specificity of Influenza A Virus

The role of microRNA (miRNA) in influenza A virus (IAV) host species specificity is not well understood as yet. Here, we show that a host miRNA, miR-1290, is induced through the extracellular signal-regulated kinase (ERK) pathway upon IAV infection and is associated with increased viral titers in hu...

Full description

Saved in:
Bibliographic Details
Published in:Molecular therapy. Nucleic acids 2019-09, Vol.17, p.10-23
Main Authors: Huang, Sheng-Yu, Huang, Chih-Heng, Chen, Chi-Jene, Chen, Ting-Wen, Lin, Chun-Yuan, Lin, Yueh-Te, Kuo, Shu-Ming, Huang, Chung-Guei, Lee, Li-Ang, Chen, Yi-Hsiang, Chen, Mei-Feng, Kuo, Rei-Lin, Shih, Shin-Ru
Format: Article
Language:English
Subjects:
Animal models
Binding sites
Cell culture
Experiments
Extracellular signal-regulated kinase
ferret
Gene expression
host species-specificity
Infections
Influenza
Influenza A
influenza A virus
Mammals
Metabolic pathways
MicroRNAs
miR-1290
miRNA
Proteins
Species
Statistical analysis
Vimentin
Viral infections
viral ribonucleoprotein
virus
Viruses
vRNP
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The role of microRNA (miRNA) in influenza A virus (IAV) host species specificity is not well understood as yet. Here, we show that a host miRNA, miR-1290, is induced through the extracellular signal-regulated kinase (ERK) pathway upon IAV infection and is associated with increased viral titers in human cells and ferret animal models. miR-1290 was observed to target and reduce expression of the host vimentin gene. Vimentin binds with the PB2 subunit of influenza A virus ribonucleoprotein (vRNP), and knockdown of vimentin expression significantly increased vRNP nuclear retention and viral polymerase activity. Interestingly, miR-1290 was not detected in either chicken cells or mouse animal models, and the 3′ UTR of the chicken vimentin gene contains no binding site for miR-1290. These findings point to a host species-specific mechanism by which IAV upregulates miR-1290 to disrupt vimentin expression and retain vRNP in the nucleus, thereby enhancing viral polymerase activity and viral replication. [Display omitted]
ISSN:2162-2531
2162-2531
DOI:10.1016/j.omtn.2019.04.028