Abstract
BackgroundEndothelial cells are believed to play an important role in response to virus infection. Our previous microarray analysis showed that H9N2 virus infection and inactivated viral particle inoculation increased the expression of interferon-inducible transmembrane protein 1 (IFITM1) in human umbilical vein endothelial cells (HUVECs). In present study, we deeply investigated the expression patterns of IFITM1 and IFITM1-mediated antiviral response induced by H9N2 virus infection and inactivated viral particle inoculation in HUVECs. Epithelial cells that are considered target cells of the influenza virus were selected as a reference control.MethodsFirst, we quantified the expression levels of IFITM1 in HUVECs induced by H9N2 virus infection or viral particle inoculation using quantitative real-time PCR and western blot. Second, we observed whether hemagglutinin or neuraminidase affected IFITM1 expression in HUVECs. Finally, we investigated the effect of induced-IFITM1 on the antiviral state in HUVECs by siRNA and activation plasmid transfection.ResultsBoth H9N2 virus infection and viral particle inoculation increased the expression of IFITM1 without elevating the levels of interferon-ɑ/β in HUVECs. HA or NA protein binding alone is not sufficient to increase the levels of IFITM1 and interferon-ɑ/β in HUVECs. IFITM1 induced by viral particle inoculation significantly decreased the virus titers in culture supernatants of HUVECs.ConclusionsOur results showed that inactivated viral particle inoculation increased the expression of IFITM1 at mRNA and protein levels. Moreover, the induction of IFITM1 expression mediated the antiviral state in HUVECs.
Highlights
Endothelial cells are believed to play an important role in response to virus infection
The results showed that both H9N2 virus infection and viral particle inoculation significantly increased the expression of interferon-inducible transmembrane protein 1 (IFITM1) at mRNA and protein levels, and the IFITM1 protein induced by viral particle inoculation significantly enhanced the antiviral state of human umbilical vein endothelial cells (HUVECs) against H9N2 virus infection
H9N2 virus infection and viral particle inoculation increased the expression of IFITM1 According to our previous microarray results, both H9N2 virus infection and inactivated viral particle inoculation upregulate the expression of IFITM1 at transcriptional level
Summary
Endothelial cells are believed to play an important role in response to virus infection. Our previous microarray analysis showed that H9N2 virus infection and inactivated viral particle inoculation increased the expression of interferon-inducible transmembrane protein 1 (IFITM1) in human umbilical vein endothelial cells (HUVECs). H9N2 viruses provide their six inner genes to contribute to the evolution of the H7N9, H10N8 and H5N6 viruses that cause severe human respiratory infections in China [11,12,13]. All these features indicate that H9N2 virus has a considerable public health threat. It is valuable to reveal the pathogenesis of H9N2 influenza virus infection and the innate immune responses of host to the H9N2 viruses
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