Isolation and identification of bovine nasopharyngeal mucosal epithelial cells and establishment of cell models of acute infection by foot-and-mouth disease virus

2018 ◽  
Vol 54 (4) ◽  
pp. 287-294
Author(s):  
Wan-fu Bai ◽  
Lu Li ◽  
Ting Zhang ◽  
Xiao-hu Su ◽  
Yong-wei Wang ◽  
...  
2010 ◽  
Vol 84 (18) ◽  
pp. 9149-9160 ◽  
Author(s):  
Pradyot Dash ◽  
Paul V. Barnett ◽  
Michael S. Denyer ◽  
Terry Jackson ◽  
Catrina M. A. Stirling ◽  
...  

ABSTRACT Three-dimensional (3D) porcine nasal mucosal and tracheal mucosal epithelial cell cultures were developed to analyze foot-and-mouth disease virus (FMDV) interactions with mucosal epithelial cells. The cells in these cultures differentiated and polarized until they closely resemble the epithelial layers seen in vivo. FMDV infected these cultures predominantly from the apical side, primarily by binding to integrin αvβ6, in an Arg-Gly-Asp (RGD)-dependent manner. However, FMDV replicated only transiently without any visible cytopathic effect (CPE), and infectious progeny virus could be recovered only from the apical side. The infection induced the production of beta interferon (IFN-β) and the IFN-inducible gene Mx1 mRNA, which coincided with the disappearance of viral RNA and progeny virus. The induction of IFN-β mRNA correlated with the antiviral activity of the supernatants from both the apical and basolateral compartments. IFN-α mRNA was constitutively expressed in nasal mucosal epithelial cells in vitro and in vivo. In addition, FMDV infection induced interleukin 8 (IL-8) protein, granulocyte-macrophage colony-stimulating factor (GM-CSF), and RANTES mRNA in the infected epithelial cells, suggesting that it plays an important role in modulating the immune response.


2017 ◽  
Vol 1 (1) ◽  
pp. 33-47 ◽  
Author(s):  
Samia Ahmed Kamal ◽  
Randa Abd El-Rahman Hassan

Some strains of Foot and mouth disease virus (FMDV) are endemic in Egypt. The present study was performed on cattle and buffaloes (ages: 3 months up to 1.5 years old, of years 2015 and 2016), which were suffering foot and mouth disease (FMD). Sera and tissues samples were tested by different techniques including serum and virus neutralization tests (SNT, VNT), virus isolation and identification by tissue culture methods, Enzyme linked immune-Sorbent Assays (ELISA); and by the pathological and hematology techniques. The results showed the predominance of FMDV serotype O with the presence of serotypes SAT2 and A. The results showed the pathologic picture of FMD was similar regardless its specific subtypes, as apparently the studied strains produces same pathological and hematological changes. Microscopic examination reveals severe hydropic degenerations and necrosis in most affected organs, accompanied by significant changes in blood parameters which indicate severity and direct effects of FMDV on the hematopoietic system. These findings indicates the mode of pathogenesis of FMD virus in its way to exhibits the characteristic symptoms of illness. However, the investigation showed the presence of FMDV type O, A and SAT2 in the studied areas of delta governorates. It is important to focus on producing of vaccines which have only these serotypes as solution to get rid of the endemic behavior of FMDV in delta of Egypt.


Viruses ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 53 ◽  
Author(s):  
Florian Pfaff ◽  
Sara Hägglund ◽  
Martina Zoli ◽  
Sandra Blaise-Boisseau ◽  
Eve Laloy ◽  
...  

Foot-and-mouth disease (FMD) is the most devastating disease of cloven-hoofed livestock, with a crippling economic burden in endemic areas and immense costs associated with outbreaks in free countries. Foot-and-mouth disease virus (FMDV), a picornavirus, will spread rapidly in naïve populations, reaching morbidity rates of up to 100% in cattle. Even after recovery, over 50% of cattle remain subclinically infected and infectious virus can be recovered from the nasopharynx. The pathogen and host factors that contribute to FMDV persistence are currently not understood. Using for the first time primary bovine soft palate multilayers in combination with proteogenomics, we analyzed the transcriptional responses during acute and persistent FMDV infection. During the acute phase viral RNA and protein was detectable in large quantities and in response hundreds of interferon-stimulated genes (ISG) were overexpressed, mediating antiviral activity and apoptosis. Although the number of pro-apoptotic ISGs and the extent of their regulation decreased during persistence, some ISGs with antiviral activity were still highly expressed at that stage. This indicates a long-lasting but ultimately ineffective stimulation of ISGs during FMDV persistence. Furthermore, downregulation of relevant genes suggests an interference with the extracellular matrix that may contribute to the skewed virus-host equilibrium in soft palate epithelial cells.


PLoS ONE ◽  
2016 ◽  
Vol 11 (12) ◽  
pp. e0167163 ◽  
Author(s):  
Rajeev Ranjan ◽  
Jitendra K. Biswal ◽  
Saravanan Subramaniam ◽  
Karam Pal Singh ◽  
Carolina Stenfeldt ◽  
...  

PLoS ONE ◽  
2009 ◽  
Vol 4 (5) ◽  
pp. e5659 ◽  
Author(s):  
Fayna Díaz-San Segundo ◽  
Teresa Rodríguez-Calvo ◽  
Ana de Avila ◽  
Noemí Sevilla

2009 ◽  
Vol 16 (12) ◽  
pp. 1738-1749 ◽  
Author(s):  
Felix N. Toka ◽  
Charles Nfon ◽  
Harry Dawson ◽  
William T. Golde

ABSTRACT Natural killer (NK) cells provide one of the initial barriers of cellular host defense against pathogens, in particular intracellular pathogens. The role of these cells in foot-and-mouth disease virus (FMDV) infection is unknown. Previously, we characterized the phenotype and function of NK cells from swine (F. N. Toka et al., J. Interferon Cytokine Res. 29:179-192, 2009). In the present study, we report the analysis of NK cells isolated from animals infected with FMDV and tested ex vivo and show that NK-dependent cytotoxic activity against tumor cells as targets was impaired. More relevantly to this infection, the killing of target cells infected with FMDV also was inhibited. Further, the proportion of NK cells capable of producing gamma interferon and storing perforin was reduced. Peripheral blood mononuclear cells isolated from infected animals are not productively infected, but virus exposure in vivo resulted in the significant induction of NKp30 and Toll-like receptor 3 expression and the moderate activation of SOCS3 and interleukin-15 receptor mRNA. However, there was little alteration of mRNA expression from a number of other receptor genes in these cells, including SH2D1B and NKG2A (inhibitory) as well as NKp80, NKp46, and NKG2D (activating). These data indicate that this virus infection influences the ability of NK cells to recognize and eliminate FMDV-infected cells. In addition, a reduction in NK cell cytotoxicity coincided with the increase in virus titers, indicating the virus blocking of NK cell-associated innate responses, albeit temporarily. These effects likely culminate in brief but effective viral immune evasion, allowing the virus to replicate and disseminate within the host.


2021 ◽  
Author(s):  
Yaxin Wang ◽  
Meijun Liu

Foot-and-mouth disease (FMD) is an acute infection of cloven-hoofed animals caused by foot-and-mouth disease virus (FMDV). It is one of the most serious infectious diseases affecting animal husbandry and a major impediment to international trade in livestock and their products. Foot-and-mouth disease virus (FMDV), a member of the Picornaviridae family of Aphthovirus, is an icosahedral virus without envelope, 25–30 nm in diameter, containing about 8.4 kb of positive-sense single-stranded RNA. The virus exists in seven different serotypes: A, O, C, Asia1, SAT1, SAT2, and SAT3, but a large number of subtypes have evolved in each serotype. This chapter reviews the genome, structure, serotype, and epidemiology of FMDV, which will help people to further explore the mechanism of the interaction between foot-and-mouth disease virus and host and provide reference for scientific prevention and control of FMDV.


2008 ◽  
Vol 21 (1) ◽  
pp. 68-77 ◽  
Author(s):  
Charles K. Nfon ◽  
Geoffrey S. Ferman ◽  
Felix N. Toka ◽  
Douglas A. Gregg ◽  
William T. Golde

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