Next Article in Journal
MiR-125b Suppression Inhibits Apoptosis and Negatively Regulates Sema4D in Avian Leukosis Virus-Transformed Cells
Next Article in Special Issue
The T-Cell Response to Type 2 Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)
Previous Article in Journal
Genetic Diversity of Sapoviruses among Inpatients in Germany, 2008−2018
Previous Article in Special Issue
Aerosol Detection and Transmission of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV): What Is the Evidence, and What Are the Knowledge Gaps?
Open AccessArticle

Basal Level p53 Suppresses Antiviral Immunity Against Foot-And-Mouth Disease Virus

by Tianliang Zhang 1,2,†, Haotai Chen 2,3,†, Xinsheng Liu 2,3, Linlin Qi 2,3, Xin Gao 2, Kailing Wang 2, Kaishen Yao 1,2, Jie Zhang 2,3, Yuefeng Sun 2,3,*, Yongguang Zhang 2,3,* and Run Wu 1,*
College of Veterinary Medicine, Gansu Agricultural University, Lanzhou 730070, China
State Key Laboratory of Veterinary Etiological Biology, OIE/National Foot and Mouth Disease Reference Laboratory, Key Laboratory of Animal Virology of Ministry of Agriculture, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, China
Authors to whom correspondence should be addressed.
Those authors contribute equally to the work.
Viruses 2019, 11(8), 727;
Received: 25 June 2019 / Revised: 1 August 2019 / Accepted: 6 August 2019 / Published: 7 August 2019
(This article belongs to the Special Issue Porcine Viruses 2019)
Tumor suppressor protein p53 (p53) is a master transcription factor that plays key roles in cell cycle arrest, apoptosis, senescence, and metabolism, as well as regulation of innate immunity during virus infection. In order to facilitate their replication and spreading, viruses have evolved to manipulate p53 function through different strategies, with some requiring active p53 while others demand reduction/inhibition of p53 activity. However, there are no clear-cut reports about the roles of p53 during the infection of foot-and-mouth disease virus (FMDV), the causative agent of a highly contagious foot-and-mouth disease (FMD) of cloven-hoofed animals. Here we showed that p53 level was dynamically regulated during FMDV infection, being degraded at the early infection stage but recovered to the basal level at the late stage. Cells depleted of p53 showed inhibited FMDV replication and enhanced expression of the immune-related genes, whereas overexpression of p53 didn’t affect the viral replication. Viral challenge assay with p53 knockout mice obtained similar results, with viral load decreased, histopathological changes alleviated, and lifespan extended in the p53 knockout mice. Together, these data demonstrate that basal level p53 is required for efficient FMDV replication by suppressing the innate immunity. View Full-Text
Keywords: p53; MDM2; foot-and-mouth disease virus; innate immunity; interferon p53; MDM2; foot-and-mouth disease virus; innate immunity; interferon
Show Figures

Figure 1

MDPI and ACS Style

Zhang, T.; Chen, H.; Liu, X.; Qi, L.; Gao, X.; Wang, K.; Yao, K.; Zhang, J.; Sun, Y.; Zhang, Y.; Wu, R. Basal Level p53 Suppresses Antiviral Immunity Against Foot-And-Mouth Disease Virus. Viruses 2019, 11, 727.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop