Crimean-Congo hemorrhagic fever virus infection triggers the upregulation of the Wnt signaling pathway inhibitor genes.
A549
Gene expression
Hemorrhagic fever virus
Highly pathogenic
Immunofluorescence
Wnt/ß-catenin signaling pathway
Journal
Virus genes
ISSN: 1572-994X
Titre abrégé: Virus Genes
Pays: United States
ID NLM: 8803967
Informations de publication
Date de publication:
Aug 2020
Aug 2020
Historique:
received:
12
12
2019
accepted:
16
04
2020
pubmed:
27
4
2020
medline:
28
1
2021
entrez:
27
4
2020
Statut:
ppublish
Résumé
Crimean-Congo hemorrhagic fever virus (CCHFV) is a highly pathogenic agent. Thus far, vaccines and specific antiviral therapies are not available against the threat of infection. Our knowledge regarding its pathogenesis is indeed limited, and thus, developing effective antiviral therapies is hampered. Several studies have demonstrated that the CCHFV infection has an impact on numerous signal transduction pathways. In parallel, the Wnt signaling pathway components are responsible for different important biological processes including cell fate determination, cell migration and cell polarity. Moreover, its implication among several virus infections has been proven, yet little is known in reference to which components of the Wnt pathway are being activated/inhibited as a response to the infection. Our aim was to elicit the influence of the CCHFV infection on adenocarcinomic human alveolar basal epithelial cells in vitro regarding the Wnt signaling pathway-related genes. Gene-expression changes of 92 Wnt-associated genes were examined 48 h post-infection. Furthermore, β-catenin levels were compared in the infected and uninfected cells. Significant changes were observed in the case of 13 genes. The majority of the upregulated genes are associated with the inhibition of the Wnt/β-catenin signaling. Additionally, infected cells expressed less β-catenin. Our findings suggest that CCHFV blocks the Wnt/β-catenin pathway. Our study corroborates the link between CCHFV infection and the Wnt signaling pathways. In addition, it broadens our knowledge in the CCHFV pathomechanism.
Identifiants
pubmed: 32335793
doi: 10.1007/s11262-020-01759-z
pii: 10.1007/s11262-020-01759-z
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM