Infection with foot-and-mouth disease virus (FMDV) induces a natural killer (NK) cell response in cattle that is lacking following vaccination

2014 ◽  
Vol 37 (4) ◽  
pp. 249-257 ◽  
Author(s):  
Jared R. Patch ◽  
Pervaiz A. Dar ◽  
Ryan Waters ◽  
Felix N. Toka ◽  
Jose Barrera ◽  
...  
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.


2009 ◽  
Vol 29 (3) ◽  
pp. 179-192 ◽  
Author(s):  
Felix N. Toka ◽  
Charles K. Nfon ◽  
Harry Dawson ◽  
D. Mark Estes ◽  
William T. Golde

2016 ◽  
Vol 97 (9) ◽  
pp. 2201-2209 ◽  
Author(s):  
Clare F. J. Grant ◽  
B. Veronica Carr ◽  
Nagendrakumar B. Singanallur ◽  
Jacqueline Morris ◽  
Simon Gubbins ◽  
...  

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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