Research Papers: Pathology:

Classical swine fever virus Shimen infection increases p53 signaling to promote cell cycle arrest in porcine alveolar macrophages

Pengbo Ning _, Congxia Hu, Xuepeng Li, Yulu Zhou, Aoxue Hu, Ya Zhang, Lifang Gao, Cunmei Gong, Kangkang Guo, Xianghan Zhang and Yanming Zhang

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Oncotarget. 2017; 8:55938-55949. https://doi.org/10.18632/oncotarget.18997

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Pengbo Ning1,2,3, Congxia Hu4, Xuepeng Li1, Yulu Zhou3, Aoxue Hu1, Ya Zhang5, Lifang Gao3, Cunmei Gong3, Kangkang Guo6, Xianghan Zhang1,2 and Yanming Zhang6

1 School of Life Science and Technology, Xidian University, Xi’an, Shaanxi, PR China

2 Engineering Research Center of Molecular and Neuro Imaging Ministry of Education, Xi’an, Shaanxi, PR China

3 College of Science, Northwest A&F University, Yangling, Shaanxi, PR China

4 Bio-ID Center, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, PR China

5 Shaanxi Provincial People’s Hospital, Xi’an, Shaanxi, PR China

6 College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, PR China

Correspondence to:

Pengbo Ning, email:

Keywords: CSFV Shimen, p53 pathway, p21, cell cycle dysregulation, macrophages, Pathology Section

Received: February 08, 2017 Accepted: June 18, 2017 Published: July 05, 2017


Classical swine fever virus (CSFV) replicates in macrophages and causes persistent infection. Despite its role in disastrous economic losses in swine industries, the molecular mechanisms underlying its pathogenesis are poorly understood. The virus evades the neutralizing immune response, subverting the immune system to ensure its own survival and persistence.Our genome-wide analysis of porcine alveolar macrophage transcriptional responses to CSFV Shimen infection using the Solexa/Illumina digital gene expression system revealed that p53 pathway components and cell cycle molecules were differentially regulated during infection compared to controls. Further, we investigated the molecular changes in macrophages infected with CSFV Shimen, focusing on the genes involved in the p53 pathway. CSFV Shimen infection led to phosphorylation and accumulation of p53 in a time-dependent manner. Furthermore, CSFV Shimen infection upregulated cyclin-dependent kinase inhibitor 1A (p21) mRNA and protein. In addition, CSFV Shimen infection induced cell cycle arrest at the G1 phase, as well as downregulation of cyclin E1 and cyclin-dependent kinase 2 (CDK2). The expression of genes in the p53 pathway did not change significantly after p53 knockdown by pifithrin-α during CSFV Shimen infection. Our data suggest that CSFV Shimen infection increases expression of host p53 and p21, and inhibits expression of cyclin E1 and CDK2, leading to cell cycle arrest at the G1 phase. CSFV may utilize this strategy to subvert the innate immune response and proliferate in host cells.

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