RESUMO
To investigate the antiviral effect of lithium chloride (LiCl) on the replication of Marek's disease virus (MDV) in chicken embryonic fibroblast (CEF) cells, real-time PCR, Western blotting, plaque counting, and indirect immunofluorescence experiments were performed at different time points of LiCl treated CEF cells with virus infection. The results demonstrated that LiCl could affect multiple steps of virus replication and inhibit viral gene expression and protein synthesis in a dose- and time-dependent manner. Moreover, LiCl could directly affect viral infectivity as well. In addition, LiCl significantly affected the gene expression of IFN-ß related genes in virus-infected cells. These results indicate that LiCl significantly inhibits MDV replication and proliferation in CEF cells and it has the potential to be used as an antiviral agent against MDV.
Assuntos
Antivirais/farmacologia , Herpesvirus Galináceo 2/efeitos dos fármacos , Cloreto de Lítio/farmacologia , Proteínas Oncogênicas Virais/genética , Replicação Viral/efeitos dos fármacos , 2',5'-Oligoadenilato Sintetase/genética , 2',5'-Oligoadenilato Sintetase/metabolismo , Animais , Linhagem Celular , Embrião de Galinha , Galinhas , Relação Dose-Resposta a Droga , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Fibroblastos/virologia , Regulação da Expressão Gênica , Herpesvirus Galináceo 2/genética , Herpesvirus Galináceo 2/metabolismo , Interações Hospedeiro-Patógeno/efeitos dos fármacos , Fator Regulador 7 de Interferon/genética , Fator Regulador 7 de Interferon/metabolismo , Interferon beta/genética , Interferon beta/metabolismo , Proteínas Oncogênicas Virais/antagonistas & inibidores , Proteínas Oncogênicas Virais/metabolismo , Carga Viral/efeitos dos fármacosRESUMO
Marek's disease virus (MDV) infection causes immunosuppression in the host, ultimately inducing tumor formation and causing significant economic losses to the poultry industry. While the abnormal activation of the Wnt/ß-catenin signaling pathway is closely associated with the occurrence and development of tumors. However, the relationship between MDV and the Wnt/ß-catenin pathway remains unclear. In this study, we found that the MDV RB1B strain, but not the MDV vaccine strain CVI988, activated the Wnt/ß-catenin signaling pathway by increasing the phosphorylation level of GSK-3ß in chicken embryo fibroblast (CEF). In vivo infection experiments in SPF chickens also confirmed that the RB1B strain activated the Wnt/ß-catenin signaling pathway, while the CVI988 strain did not lead to its activation. Moreover, unlike the Meq protein encoded by the CVI988 strain, the Meq protein encoded by the RB1B strain specifically activated the Wnt/ß-catenin signaling pathway in CEF cells. The findings from these studies extend our understanding of the regulation of Wnt/ß-catenin signaling by MDV, which make a new contribution to understanding the virus-host interactions of MDV.