Abstract
Wnt/β-catenin signaling is a highly conserved pathway related to a variety of biological processes in different cells. The regulation of replication of various viruses by Wnt/β-catenin signaling pathway has been reported. However, the interaction between the Wnt/β-catenin pathway and avian leukosis virus is unknown. In the present study, we investigated the effect of modulating the Wnt/β-catenin pathway during avian leukosis virus subgroup J (ALV-J) infection. The activation of the Wnt/β-catenin pathway by GSK-3 inhibitor increased ALV-J mRNA, viral protein expression, and virus production in CEF cells. This increase was suppressed by iCRT14, one of the specific inhibitors of the Wnt/β-catenin signaling pathway. Moreover, treatment with iCRT14 reduced virus titer and viral gene expression significantly in CEF and LMH cells in a dose-dependent manner. Inhibition Wnt/β-catenin signaling pathway by knockdown of β-catenin reduced virus proliferation in CEF cells also. Collectively, these results suggested that the status of Wnt/β-catenin signaling pathway modulated ALV-J replication. These studies extend our understanding of the role of Wnt/β-catenin signaling pathway in ALV-J replication and make a new contribution to understanding the virus–host interactions of avian leukosis virus.
Highlights
Avian leukosis virus (ALV) belongs to the genus Alpharetrovirus of the family Retroviridae, which causes immunosuppression, reproductive disorders, and a diverse set of tumors, causing significant economic losses in the poultry industry worldwide [1,2,3]
We first determined the effects of GSK-3 inhibitor X on the Wnt/β-catenin signaling pathway in CEF cells
By using the Wnt/β-catenin signaling TOP/FOP flash reporter assay, we first validated that GSK-3 inhibitor X could activate the Wnt/β-catenin signaling in CEF cells
Summary
Avian leukosis virus (ALV) belongs to the genus Alpharetrovirus of the family Retroviridae, which causes immunosuppression, reproductive disorders, and a diverse set of tumors, causing significant economic losses in the poultry industry worldwide [1,2,3]. Within the five subgroups of exogenous ALVs, subgroup J (ALV-J) is the major ALV affecting poultry health in China. It can induce a spectrum of different neoplasms in meat-type and layer chickens. ALV-J infection is prevalent in the Chinese native breeds of chickens [3,4]. Several groups reported the significance of the host’s innate immune responses during ALV-J infection. These reports demonstrated that interferon-stimulated genes (ISGs) were not induced in birds with hemangioma due to the reduction of IRF1 and STAT1 gene expression [5]. Investigation into the interaction between ALV-J and macrophages by transcriptome analysis [6] showed that
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