scholarly journals The Causative Agent of FMD Disease

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.

2002 ◽  
Vol 150 (23) ◽  
pp. 724-727 ◽  
Author(s):  
G. J. Hughes ◽  
V. Mioulet ◽  
R. P. Kitching ◽  
S. Alexandersen ◽  
A. I. Donaldson ◽  
...  

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.


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

2021 ◽  
Author(s):  
Lucy Gordon ◽  
Neil Mabbott ◽  
Joanna Wells ◽  
Liudmila Kulik ◽  
Nick Juleff ◽  
...  

AbstractPrevious studies have shown after the resolution of acute infection and viraemia, foot- and-mouth disease virus (FMDV) capsid proteins and/or genome are localised in the light zone of germinal centres of lymphoid tissue in cattle and African buffalo. The pattern of staining for FMDV proteins was consistent with the virus binding to follicular dendritic cells (FDCs). We have now demonstrated a similar pattern of FMDV protein staining in mouse spleens after acute infection and showed FMDV proteins are colocalised with FDCs. Blocking antigen binding to complement receptor type 2 and 1 (CR2/CR1) prior to infection with FMDV significantly reduced the detection of viral proteins on FDCs and FMDV genomic RNA in spleen samples. Blocking the receptors prior to infection also significantly reduced neutralising antibody titres. Therefore, the binding of FMDV to FDCs and sustained induction of neutralising antibody responses are dependent on FMDV binding to CR2/CR1 in mice.Author SummaryFoot and mouth disease virus causes a highly contagious acute vesicular disease, resulting in more than 50% of cattle, regardless of vaccination status, and almost 100% of African buffalo becoming persistently infected for long periods (months) of time. Yet, the mechanisms associated with establishment of persistent infections are still poorly understood. Infected animals are characterised by the presence of long-lived neutralising antibody titres, which contrast with the short-lived response induced by vaccination. We have used a mouse model to understand how foot and mouth disease virus is trapped and retained in the spleen for up to 28 days post infection and how the absence of antigen in the germinal centre prevents a sustainable neutralising antibody response, in the mouse. Our results highlight the importance of targeting antigen to FDCs to stimulate potent neutralising antibody responses after vaccination.


Author(s):  
S. S. Breese ◽  
H. L. Bachrach

Models for the structure of foot-and-mouth disease virus (FMDV) have been proposed from chemical and physical measurements (Brown, et al., 1970; Talbot and Brown, 1972; Strohmaier and Adam, 1976) and from rotational image-enhancement electron microscopy (Breese, et al., 1965). In this report we examine the surface structure of FMDV particles by high resolution electron microscopy and compare it with that of particles in which the outermost capsid protein VP3 (ca. 30, 000 daltons) has been split into smaller segments, two of which VP3a and VP3b have molecular weights of about 15, 000 daltons (Bachrach, et al., 1975).Highly purified and concentrated type A12, strain 119 FMDV (5 mg/ml) was prepared as previously described (Bachrach, et al., 1964) and stored at 4°C in 0. 2 M KC1-0. 5 M potassium phosphate buffer at pH 7. 5. For electron microscopy, 1. 0 ml samples of purified virus and trypsin-treated virus were dialyzed at 4°C against 0. 2 M NH4OAC at pH 7. 3, deposited onto carbonized formvar-coated copper screens and stained with phosphotungstic acid, pH 7. 3.


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