Influence of Foot-and-Mouth Disease Virus O/CHN/Mya98/33-P Strain Leader Protein on Viral Replication and Host Innate Immunity

2015 ◽  
Vol 28 (7) ◽  
pp. 360-366 ◽  
Author(s):  
Shaodong Jiang ◽  
Xingwen Bai ◽  
Pinghua Li ◽  
Meng Zhang ◽  
Huifang Bao ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Viral Replication ◽  
Disease Virus ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Leader Protein ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Host Innate Immunity

scholarly journals Advances in Foot-and-Mouth Disease Virus Proteins Regulating Host Innate Immunity

2020 ◽  
Vol 11 ◽  
Author(s):  
Jiangling Peng ◽  
Jiamin Yi ◽  
Wenping Yang ◽  
Jingjing Ren ◽  
Yuan Wen ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Disease Virus ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Host Innate Immunity ◽  
Virus Proteins

scholarly journals Basal Level p53 Suppresses Antiviral Immunity against Foot-and-Mouth Disease Virus

Viruses ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 727
Author(s):  
Zhang ◽  
Chen ◽  
Liu ◽  
Qi ◽  
Gao ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Disease Virus ◽  
Knockout Mice ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Clear Cut ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Immune Related Genes ◽  
Fmdv Replication

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.

scholarly journals Foot-and-mouth disease virus utilizes an autophagic pathway during viral replication

Virology ◽  
2011 ◽  
Vol 410 (1) ◽  
pp. 142-150 ◽  
Author(s):  
Vivian O'Donnell ◽  
Juan M. Pacheco ◽  
Michael LaRocco ◽  
Tom Burrage ◽  
William Jackson ◽  
...  
Keyword(s):  
Viral Replication ◽  
Disease Virus ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Mouth Disease Virus ◽  
Foot And Mouth

scholarly journals The Ability of Integrin αvβ3 To Function as a Receptor for Foot-and-Mouth Disease Virus Is Not Dependent on the Presence of Complete Subunit Cytoplasmic Domains

2001 ◽  
Vol 75 (1) ◽  
pp. 527-532 ◽  
Author(s):  
Sherry Neff ◽  
Barry Baxt
Keyword(s):  
Viral Replication ◽  
Disease Virus ◽  
High Efficiency ◽  
Cultured Cells ◽  
Foot And Mouth Disease ◽  
Integrin Αvβ3 ◽  
Mouth Disease ◽  
Cytoplasmic Domains ◽  
Mouth Disease Virus ◽  
Foot And Mouth

ABSTRACT The integrin αvβ3 has been shown to function as one of the integrin receptors on cultured cells for foot-and-mouth disease virus (FMDV), and high-efficiency utilization of the bovine homolog of this integrin is dependent on the cysteine-rich repeat region of the bovine β3 subunit. In this study we have examined the role of the cytoplasmic domains of the αv and β3 subunits in FMDV infection. We have found that truncations or extensions of these domains of either subunit, including deletions removing almost all of the cytoplasmic domains, had little or no effect on the ability of the integrin to function as a receptor for FMDV. The lysosomotropic agent monensin inhibited viral replication in cells transfected with either intact or cytoplasmic domain-truncated αvβ3. In addition, viral replication in transfected cells was inhibited by an αvβ3 function-blocking antibody but not by function-blocking antibodies to three other RGD-directed integrins, suggesting that these integrins are not involved in the infectious process. These results indicate that alterations to the cytoplasmic domains of either subunit, which lead to the inability of the integrin receptor to function normally, do not abolish the ability of the integrin to bind and internalize this viral ligand.

scholarly journals The Different Tactics of Foot-and-Mouth Disease Virus to Evade Innate Immunity

2018 ◽  
Vol 9 ◽  
Author(s):  
Gisselle N. Medina ◽  
Fayna Díaz-San Segundo ◽  
Carolina Stenfeldt ◽  
Jonathan Arzt ◽  
Teresa de los Santos
Keyword(s):  
Innate Immunity ◽  
Disease Virus ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Mouth Disease Virus ◽  
Foot And Mouth
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