Crimean-Congo hemorrhagic fever virus infection triggers the upregulation of the Wnt signaling pathway inhibitor genes

被引:2
|
作者
Papp, Henrietta [1 ,2 ]
Zeghbib, Safia [1 ,2 ]
Foldes, Fanni [1 ,2 ]
Banfai, Krisztina [3 ,4 ]
Madai, Monika [1 ,2 ]
Kemenesi, Gabor [1 ,2 ]
Urban, Peter [2 ,5 ]
Kvell, Krisztian [3 ,4 ]
Jakab, Ferenc [1 ,2 ]
机构
[1] Univ Pecs, Szentagothai Res Ctr, BSL 4 Lab, Virol Res Grp, Ifjusag Utja 20, H-7624 Pecs, Hungary
[2] Univ Pecs, Fac Sci, Inst Biol, Pecs, Hungary
[3] Univ Pecs, Szentagothai Res Ctr, Wnt Signaling Res Grp, Pecs, Hungary
[4] Univ Pecs, Fac Pharm, Dept Pharmaceut Biotechnol, Pecs, Hungary
[5] Univ Pecs, Szentagothai Res Ctr, Bioinformat Res Grp, Pecs, Hungary
基金
欧盟地平线“2020”;
关键词
Hemorrhagic fever virus; Gene expression; Wnt; ss-catenin signaling pathway; A549; Highly pathogenic; Immunofluorescence; CATENIN; REPLICATION; EXPRESSION;
D O I
10.1007/s11262-020-01759-z
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
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, beta-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/beta-catenin signaling. Additionally, infected cells expressed less beta-catenin. Our findings suggest that CCHFV blocks the Wnt/beta-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.
引用
收藏
页码:508 / 514
页数:7
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