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

Bibliographic Details
Title: Basal Level p53 Suppresses Antiviral Immunity Against Foot-And-Mouth Disease Virus
Authors: Tianliang Zhang, Haotai Chen, Xinsheng Liu, Linlin Qi, Xin Gao, Kailing Wang, Kaishen Yao, Jie Zhang, Yuefeng Sun, Yongguang Zhang, Run Wu
Source: Viruses, Vol 11, Iss 8, p 727 (2019)
Publisher Information: MDPI AG, 2019.
Publication Year: 2019
Collection: LCC:Microbiology
Subject Terms: p53, MDM2, foot-and-mouth disease virus, innate immunity, interferon, Microbiology, QR1-502
More Details: 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.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1999-4915
Relation: https://www.mdpi.com/1999-4915/11/8/727; https://doaj.org/toc/1999-4915
DOI: 10.3390/v11080727
Access URL: https://doaj.org/article/a804627ab47c48218cd7d956e2e8e976
Accession Number: edsdoj.804627ab47c48218cd7d956e2e8e976
Database: Directory of Open Access Journals
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More Details
ISSN:19994915
DOI:10.3390/v11080727
Published in:Viruses
Language:English