ifit1 expression patterns induced by h9n2 virus and inactivated viral particle in human umbilical vein endothelial cells and bronchus epithelial cells
Virion
Endothelial Cells
RNA-Binding Proteins
Bronchi
Interferon-beta
Transfection
Virus Replication
Article
Madin Darby Canine Kidney Cells
Dogs
Influenza, Human
Human Umbilical Vein Endothelial Cells
Influenza A Virus, H9N2 Subtype
Animals
Humans
Carrier Proteins
Adaptor Proteins, Signal Transducing
DOI:
10.14348/molcells.2018.2091
Publication Date:
2018-04-05
AUTHORS (7)
ABSTRACT
IFIT1 (also known as ISG56) is a member of the interferon-inducible protein with tetratricopeptide repeats (IFITs) family. IFITs are strongly induced by type I interferon (IFN), double-stranded RNA and virus infection. Here, we investigated IFIT1 expression in human umbilical vein endothelial cells (HUVECs) and in human bronchus epithelial cells (BEAS-2Bs) induced by the H9N2 virus and inactivated viral particle at different time points. We also investigated the effect of H9N2 virus and viral particle infection on IFN-α/β production, and assessed whether hemagglutinin or neuraminidase protein induced IFIT1 expression. Results showed that both H9N2 virus infection and viral particle inoculation induced the expression of IFIT1 at mRNA and protein levels in the two cell lines. Hemagglutinin or neuraminidase protein binding alone is not sufficient to induce IFIT1 expression. Surprisingly, the expression patterns of IFIT1 in response to H9N2 virus and viral particles in the two cell lines were opposite, and production kinetics of IFN-α/β also differed. An additional finding was that induction of IFIT1 in response to H9N2 virus infection or viral particle inoculation was more sensitive in HUVECs than in BEAS-2Bs. Our data offers new insight into the innate immune response of endothelial cells to H9N2 virus infection.
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