Newcastle Disease Virus V Protein Promotes Viral Replication in HeLa Cells through the Activation of MEK/ERK Signaling

Viruses

Kejia Lu¹  Haijin Liu¹  Sa Xiao¹  Jiangang Ma¹  Xiaoqin Li²  Xinglong Wang²  Caiying Wang²  Zhili Chu²  Zengqi Yang² 

[1] F University, Yangling 712100, China;;College of Veterinary Medicine, Northwest A &

关键词: NDV;    V protein;    MEK/ERK pathway;    p-ERK1/2;    antivirals;    viral replication;    infection;   

DOI  :  10.3390/v10090489

来源: DOAJ

【 摘 要 】

Newcastle disease virus (NDV) can infect a wide range of domestic and wild bird species. The non-structural V protein of NDV plays an important role in antagonizing innate host defenses to facilitate viral replication. However, there is a lack of knowledge related to the mechanisms through which the V protein regulates viral replication. The extracellular signal-regulated kinase (ERK) signaling pathway in the host is involved in a variety of functions and is activated by several stimuli, including viral replication. In this study, we show that both the lentogenic strain, La Sota, and the velogenic strain, F48E9, of NDV activate the mitogen-activated protein kinase (MEK)/ERK signaling pathway. The pharmacological inhibition of ERK1/2 phosphorylation using the highly selective inhibitors U0126 and SCH772984 resulted in the reduced levels of NDV RNA in cells and virus titers in the cell supernatant, which established an important role for the MEK/ERK signaling pathway in NDV replication. Moreover, the overexpression of the V protein in HeLa cells increased the phosphorylation of ERK1/2 and induced the transcriptional changes in the genes downstream of the MEK/ERK signaling pathway. Taken together, our results demonstrate that the V protein is involved in the ERK signaling pathway-mediated promotion of NDV replication and thus, can be investigated as a potential antiviral target.

【 授权许可】

Unknown