Transcriptomic profiles of human foreskin fibroblast cells in response to orf virus
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Daxiang Chen1, Mingjian Long1, Bin Xiao2, Yufeng xiong1, Huiqin Chen1, Yu Chen1, Zhenzhan Kuang1, Ming Li1,3, Yingsong Wu1,3, Daniel L. Rock4, Daoyuan Gong5, Yong Wang5, Haijian He5, Fang Liu6, Shuhong Luo1,5 and Wenbo Hao1,3
1Institute of Antibody Engineering, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, 510515, P.R. China
2Department of Laboratory Medicine, Guangzhou General Hospital of Guangzhou Military Command of PLA, Guangzhou, 510010, P.R. China
3Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, P.R. China
4Department of Pathobiology, College of Veterinary Medicine, University of Illinois at Champaign-Urbana, Urbana, IL 61802 USA
5Department of Laboratory Medicine, School of Stomatology and Medicine, Foshan University, Chancheng District, Foshan, Guangdong Province, 528000 P.R. China
6Department of Pathophysiology, School of Stomatology and Medicine, Foshan University, Chancheng District, Foshan, Guangdong Province, 528000 P.R. China
Shuhong Luo, email: email@example.com
Wenbo Hao, email: firstname.lastname@example.org
Keywords: orf virus, transcriptomic profiles, apoptosis, antiviral immune response, cell cycle
Received: January 18, 2017 Accepted: March 20, 2017 Published: April 25, 2017
Orf virus has been utilized as a safe and efficient viral vector against not only diverse infectious diseases, but also against tumors. However, the nature of the genes triggered by the vector in human cells is poorly characterized. Using RNA sequencing technology, we compared speciﬁc changes in the transcriptomic proﬁles in human foreskin fibroblast cells following infection by the orf virus. The results indicated that orf virus upregulates or downregulates expression of a variety of genes, including genes involved in antiviral immune response, apoptosis, cell cycle and a series of signaling pathways, such as the IFN and p53-signaling pathways. The orf virus stimulates or inhibits immune gene expression such as chemokines, chemokine receptors, cytokines, cytokine receptors, and molecules involved in antigen uptake and processing after infection. Expression of pro-apoptotic genes increased at 8 hours post-infection. The p53 signaling pathway was activated to induce apoptosis at the same time. However, the cell cycle program was promoted after infection, which may be due to the immunomodulatory genes of the orf virus. This presents the first description of transcription profile changes in human foreskin fibroblast cells after orf virus infection and provides an in-depth analysis of the interaction between the host and orf virus. These data offer new insights into the understanding of the mechanisms of infection by orf virus and identify potential targets for future studies.
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