ライフサイエンスコーパス: FMDV

1 FMDV protein 2C is part of the replication complex and t

2 FMDV structural and nonstructural proteins were localize

3 FMDV-specific antibody-secreting cells (ASC), predominan

4 ity to infect CHO cells by type O and Asia-1 FMDV.

5 over a nearly 7-month period during the 2001 FMDV outbreak in the United Kingdom.

6 PCs) loaded with peptides derived from all 7 FMDV serotypes, suggesting that CD8(+) T cells recognizi

7 RF7/3(5D) inhibited the replication of all 7 FMDV serotypes.

8 of representative samples from each of the 7 FMDV serotypes showed that the putative epitope is highl

9 We developed a FMDV mutant virus that could not bind DCTN3.

10 sest relative from outside of Bulgaria was a FMDV collected during 2010 in Bursa (Anatolia, Turkey).

11 n alphavbeta6 and two tissue culture adapted FMDV strains by cryo-electron microscopy.

12 hat subsequently identified three additional FMDV-infected livestock premises by serosurveillance, as

13 ambda3, exhibited antiviral activity against FMDV in bovine cell culture.

14 N-gamma) also has antiviral activity against FMDV in cell culture and that, in combination with pIFN-

15 iremia, virus shedding or antibodies against FMDV nonstructural proteins.

16 the innate immune response of cattle against FMDV.

17 and resulted in complete protection against FMDV challenge at 6, 24, or 48 h posttreatment.

18 are pivotal in providing protection against FMDV infection.

19 approach to induce rapid protection against FMDV, we have examined the ability of VRPs containing ei

20 , is directly involved in protection against FMDV.

21 al activities in protection of swine against FMDV.

22 he development of effective vaccines against FMDV.

23 d5-poIRF7/3(5D) in vitro and in vivo against FMDV.

24 y and absence of proofreading activity allow FMDV to rapidly mutate and adapt to dynamic environments

25 Using an FMDV replicon in complementation experiments, our data d

26 Comprehending the cross-talk between DC and FMDV will provide valuable information towards understan

27 ct of ITAFs on the conformations of EMCV and FMDV IRESs by comparing their influence on hydroxyl radi

28 demonstrated that IRES elements of HRV2 and FMDV severely attenuated the neurovirulence of VSV witho

29 Moreover, PKD inhibitors also block PV and FMDV replication.

30 can inhibit the replication of HRV, PV, and FMDV, and therefore, PKD may represent a novel antiviral

31 and AUG2 PPMOs), showed high levels of anti-FMDV activity.

32 le effectively promotes the presence of anti-FMDV ASC in lymphoid tissues associated with the respira

33 that IC could dynamically influence the anti-FMDV immune response and that this may explain why the e

34 e containment of infectious diseases such as FMDV as its strongly enhanced sensitivity may facilitate

35 tification and/or abrogation of asymptomatic FMDV infection.

36 timization as a strategy to safely attenuate FMDV and further develop live attenuated vaccine candida

37 exploited for the development of attenuated FMDV vaccine candidates that are safer and more stable t

38 r 10(10) PFU of Ad5-poIRF7/3(5D) 24 h before FMDV challenge were fully protected from FMD clinical si

39 e assay could reliably differentiate between FMDV and other vesicular viruses, such as swine vesicula

40 ated that the subclinical divergence between FMDV carriers and animals that cleared the infection had

41 wth, suggesting that the interaction between FMDV 2C and cellular vimentin is essential for virus rep

42 ese results suggest that interaction between FMDV 2C and host protein Beclin1 could be essential for

43 These results indicate that HS-binding FMDV enters the cells via the caveola-mediated endocytos

44 ding specific antibodies to integrin-binding FMDV at neutralizing or subneutralizing IgG concentratio

45 susceptible to infection by integrin-binding FMDV but were susceptible to culture-adapted virus.

46 P) or poIFN-alpha (VRP-poIFN-alpha) to block FMDV replication in vitro and in vivo.

47 en processing functions were not affected by FMDV exposure.

48 However, induction of autophagosomes by FMDV appeared to differ from starvation, as the generati

49 imately 50% of the autophagosomes induced by FMDV colocalized with VP1.

50 nse orientation limited host cell killing by FMDV and restricted viral propagation.

51 and alphavbeta5) that, although not used by FMDV, have the potential to be used as receptors; howeve

52 shifting the infected cells to 37 degrees C, FMDV capsid proteins were detected within 15 min after t

53 nt harboring the same mutations in O1 Campos FMDV (O1C3A-PLDGv).

54 -specific ASCs in the absence of circulating FMDV-specific ASCs, indicating the presence of short-liv

55 herapeutic strategy so far tested to control FMDV in cattle.

56 dicating a direct role of PKR in controlling FMDV replication in the natural host.

57 ip is emphasized by the inability of current FMDV vaccines to provide long-term protection and the re

58 lued and 50/dynamitin, resulted in decreased FMDV replication in infected cells.

59 hat the local lymphoid tissue had detectable FMDV-specific ASCs in the absence of circulating FMDV-sp

60 beta6 cells were more effective at detecting FMDV in clinical samples, supporting their use as a more

61 uential vaccination regime of four different FMDV serotypes.

62 viral RNA shed in oropharyngeal fluid during FMDV persistence were similar in vaccinated and nonvacci

63 containing viral proteins is not seen during FMDV infection, a process that is stimulated by Beclin1;

64 , a metabolic pathway required for efficient FMDV replication.

65 ered by either UV-inactivated virus or empty FMDV capsids, suggesting that autophagosome formation wa

66 ranslation and that a genetically engineered FMDV lacking the leader proteinase coding region (A12-LL

67 at use of an especially proficient 'extended FMDV 2A' coding region allows production of two independ

68 post-translational remnants of the extended FMDV 2A peptide localize correctly to various cellular c

69 ed for their compatibility with the extended FMDV 2A peptide.

70 demonstration of the utility of the extended FMDV 2A system, confocal fluorescence microscopy is used

71 g5, suggesting that autophagy may facilitate FMDV infection.

72 characterized poliovirus polymerase fibrils, FMDV fibrils are narrower, are composed of both protein

73 inical signs, and immune responses following FMDV infection.

74 For FMDV SAT2 viruses, studies have shown that at least two

75 a novel separation-of-function activity for FMDV L(pro).

76 gnostic sensitivity of the mRT-PCR assay for FMDV was 93.9% (95% confidence interval [CI], 89.8 to 96

77 erized real-time RT-PCR (rRT-PCR) assays for FMDV.

78 pathway, which was shown to be important for FMDV replication.

79 aVbeta6 integrin is a principal receptor for FMDV, we transduced a bovine kidney cell line to stably

80 istence of nonintegrin, non-HS receptors for FMDV on CHO cells and revealed a novel, non-RGD-dependen

81 the B cell response are similar for all four FMDV serotypes tested following a homologous FMDV vaccin

82 CD8(+) T cells from FMDV serotype O-vaccinated A31(+) cattle recognized anti

83 Furthermore, FMDV yields were reduced in cells lacking Atg5, suggesti

84 were also tested on five recently generated FMDV datasets and the best model was able to achieve an

85 FMDV serotypes tested following a homologous FMDV vaccination regime.

86 and biochemical analyses, we have identified FMDV 3D(pol) mutations that affect polymerase fidelity.

87 Domain 3 in FMDV IRES is phylogenetically conserved and highly struc

88 presence of virus-specific CD8(+) T cells in FMDV-vaccinated and -infected cattle.

89 of RHA from the nucleus to the cytoplasm in FMDV-infected cells as infection progressed.

90 specific functional requirement for Ebp1 in FMDV IRES-directed translation that is independent of a

91 aimed to identify CD8(+) T cell epitopes in FMDV recognized by cattle vaccinated with inactivated FM

92 s that is stimulated by Beclin1; however, in FMDV-infected cells overexpressing Beclin1 this fusion o

93 and immunofluorescence staining to occur in FMDV-infected cells.

94 and confocal microscopy to actually occur in FMDV-infected cells.

95 l tertiary structure of the apical region in FMDV IRES domain 3.

96 Contrastingly, gene regulation in FMDV carriers suggested inhibition of T cell activation

97 of immunity to pathogens, but their role in FMDV infection of cattle is uncharacterized.

98 To study the role of the SGD sequence in FMDV receptor recognition and bovine virulence, we assem

99 of this mRT-PCR assay to identify viruses in FMDV-negative material not previously recognized by usin

100 t exposing moDC to IC containing inactivated FMDV resulted in significantly increased T cell stimulat

101 Current inactivated FMDV vaccines generate short-term, serotype-specific pro

102 l inoculation of three different inactivated FMDV serotypes (O, A, and Asia1 serotypes) a B cell resp

103 wing homologous and heterologous inactivated FMDV vaccination regimes.

104 t 2 (TI-2) antigenic response to inactivated FMDV capsid.IMPORTANCE We have demonstrated the developm

105 gnized by cattle vaccinated with inactivated FMDV serotype O.

106 e sample of choice for recovering infectious FMDV up to 400 days postinfection (dpi).

107 I and II IFNs act synergistically to inhibit FMDV replication in vitro and in vivo.

108 small interfering RNA constructs, inhibited FMDV replication.

109 When binding of intact FMDV particles (146 S; 8200 kDa) or pentameric FMDV coat

110 is an option to protect animals against many FMDV serotypes as soon as 24 h and for about 4 days post

111 Here, two marker FMDV vaccine candidates (A(24)LL3D(YR) and A(24)LL3B(PVK

112 conserved protein of 153 amino acids in most FMDVs examined to date.

113 ity to process P1 polyproteins from multiple FMDV serotypes.

114 wing sequential FMDV challenge with multiple FMDV serotypes.

115 production in bacteria.IMPORTANCE The mutant FMDV 3C protease L127P significantly increased yields of

116 Thus, neutralized FMDV concurrently loses its ability to infect susceptibl

117 otein P1D, comprising residues 795 to 803 of FMDV serotype O UKG/2001.

118 110 may allow for cell culture adaptation of FMDV by design, which may prove useful for vaccine manuf

119 gs resulting from cell culture adaptation of FMDV.

120 cattle were challenged by aerosolization of FMDV, using a method that resembles the natural route of

121 L127P) mutant produced crystalline arrays of FMDV-like particles in mammalian and bacterial cells, po

122 her understanding of this critical aspect of FMDV pathogenesis.

123 cally, it was demonstrated that clearance of FMDV from the nasopharyngeal mucosa was associated with

124 ity is essential for successful clearance of FMDV infection and should be considered for development

125 geal mucosa in association with clearance of FMDV.

126 This suggests that the clearing of FMDV infection is associated with an enhanced mucosal an

127 method, while applied here in the context of FMDV, is general and with slight modification can be use

128 of RNA helicase A (RHA) in the life cycle of FMDV.

129 rful and valuable tool for the dissection of FMDV populations within hosts.

130 VRP-GFP and challenged with a lethal dose of FMDV 24 h later were protected from death.

131 , it was of interest to analyze the entry of FMDV by cell-surface HS.

132 can identify already known viral epitopes of FMDV in the context of the viral capsid.

133 se results illustrate the rapid evolution of FMDV with alteration in receptor specificity and suggest

134 However, studies examining the function of FMDV 2C have been rather limited.

135 rus caffer) are the primary carrier hosts of FMDV in African savannah ecosystems, where the disease i

136 tein, resulting in IFN-induced inhibition of FMDV replication.

137 pig-adapted O Taiwan 97 (O Tw97) isolate of FMDV in swine.

138 el insights into the intricate mechanisms of FMDV persistence and contributes to further understandin

139 of 23 genomes (each of 8,200 nucleotides) of FMDV were recovered directly from epithelium tissue acqu

140 -term protection and the recent outbreaks of FMDV in formerly disease-free countries.

141 ary during the evolution and perpetuation of FMDV in nature.

142 The prevalence of FMDV persistence was similar in both groups (62% in vacc

143 Thus, the N-terminal region of FMDV 3D that acts as a nuclear localization signal (NLS)

144 lays an essential role in the replication of FMDV and potentially other picornaviruses through ribonu

145 se results further suggest that the route of FMDV entry into cells is a function solely of the viral

146 Given the demonstrated sensitivity of FMDV to IFN-alpha/beta, there was no productive or nonpr

147 ential epitopes on more than one serotype of FMDV, consistent with experimental results.

148 hly sensitive for detecting all serotypes of FMDV from experimentally infected animals, including the

149 -binding and cell culture-adapted strains of FMDV in vitro.

150 In this study, we used the structure of FMDV 3D(pol) in combination with previously reported res

151 now show is required for normal synthesis of FMDV RNA and proteins, is described in this report.

152 Treatment with 5D PPMO reduced the titers of FMDV strains representing five different serotypes by 2

153 ata demonstrate that contact transmission of FMDV O Tw97 in pigs mimics the fitness loss induced by t

154 This represents a change in the tropism of FMDV that could occur after the onset of the antibody re

155 ture will likely impact our understanding of FMDV infections, host range, and transmission.

156 Serological protection against one FMDV serotype does not confer interserotype protection.

157 RelA takes place in the absence of any other FMDV product.

158 alent peptides derived from all of the other FMDV serotypes.

159 Like other viral pathogens, FMDV recruits proteins encoded by host cell genes to acc

160 DV particles (146 S; 8200 kDa) or pentameric FMDV coat protein aggregates (12 S; 282 kDa) was detecte

161 l response in tissues maintaining persistent FMDV was downregulated, whereas upregulation of IFN-lamb

162 a interferon) in association with persistent FMDV.

163 Unlike other picornaviruses, FMDV-induced autophagosomes did not colocalize with the

164 y observed by others during plaque-to-plaque FMDV passage in vitro, suggesting that unknown mechanism

165 Although O1C3A-PLDGv FMDV and its parental virus (O1Cv) grew equally well in

166 nfected animals, including the porcinophilic FMDV strain O/TAW/97.

167 plication to rapidly and effectively prevent FMDV replication and dissemination.

168 expression of viral nonstructural proteins, FMDV induced autophagosomes very early during infection.

169 ignificantly increased yields of recombinant FMDV subunit antigens and produced virus-like particles

170 on 3C(L127P) increased yields of recombinant FMDV subunit proteins in mammalian and bacterial cells e

171 Recombinant FMDVs containing substitutions at 3D(pol) tryptophan res

172 RF7/3(5D) significantly and steadily reduced FMDV titers by up to 6 log10 units in swine and bovine c

173 c response upon contact with the replicating FMDV, suggesting that FMD vaccination induces the circul

174 have been identified on the capsid of a SAT2 FMDV.

175 otection can be induced following sequential FMDV challenge with multiple FMDV serotypes.

176 contrast, tissue culture adaptation of some FMDV serotypes results in the loss of viral virulence in

177 ation in RNA viruses and, more specifically, FMDV has been extensively examined during virus replicat

178 ed moDC were unable to efficiently stimulate FMDV-specific CD4(+) memory T cells, but exposing moDC t

179 ffaloes offers a unique opportunity to study FMDV persistence, as transmission from carrier ruminants

180 s not inhibited by wortmannin, implying that FMDV-induced autophagosome formation does not require th

181 We have recently shown that FMDV serotypes utilizing integrin receptors enter cells

182 These results suggest that FMDV induces autophagosomes during cell entry to facilit

183 These data suggest that FMDV persistence occurs in the germinal centers of lymph

184 n growth rates were up to 300% annually, the FMDV-like pathogen persisted in <25% of simulations rega

185 protein into mature capsid proteins, but the FMDV 3C protease is toxic to host cells.

186 Infection of moDC by the FMDV IC was productive and associated with high levels o

187 amples of complete genomic sequences for the FMDV SAT 2 topotype VII, which is thought to be endemic

188 Persistence probability was near 0 for the FMDV-like case under a wide range of parameter values an

189 action between RHA and the S fragment in the FMDV 5' nontranslated region.

190 accines requires cytosolic expression of the FMDV 3C protease to cleave the P1 polyprotein into matur

191 To identify less-toxic isoforms of the FMDV 3C protease, we screened 3C mutants for increased t

192 ork described here elucidates aspects of the FMDV carrier state in cattle which may facilitate identi

193 5' and 3' untranslated regions (UTRs) of the FMDV genome (strain A(24) Cruzeiro/Brazil/1955 [A(24)Cru

194 n of RHA did not require the activity of the FMDV leader protein.

195 ct structure, persistence probability of the FMDV-like pathogen was always <10%.

196 dy, we have investigated the kinetics of the FMDV-specific antibody-secreting cell (ASC) response fol

197 probability, even very early response to the FMDV-like pathogen in feral swine was unwarranted while

198 and epitope affinity were compared using the FMDV-recognizing VHH.

199 There were no sets of conditions where the FMDV-like pathogen persisted in every stochastic simulat

200 ine tract binding protein (PTB), whereas the FMDV IRES requires PTB and ITAF(45).

201 wed that 100% of animals inoculated with the FMDV A12 P1 deoptimized mutant (A12-P1 deopt) survived,

202 rminus and mediates the interaction with the FMDV IRES.

203 In addition, animals inoculated with the FMDV SAP mutant displayed a memory T cell response that

204 n distinct anatomic compartments critical to FMDV infection.

205 5-poIRF7/3(5D) 1 day before being exposed to FMDV were completely protected from viral replication an

206 so expressed CD32 but were nonsusceptible to FMDV immune complex (IC) infection, indicating a require

207 may explain why the early immune response to FMDV has evolved toward T cell independence in vivo.

208 A, and Asia1 serotypes) a B cell response to FMDV SAT1 and serotype C was induced.

209 ssue, further evidence of a TI-2 response to FMDV.

210 lete understanding of the immune response to FMDV.

211 a6 expression and enhanced susceptibility to FMDV infection for >/= 100 cell passages.

212 l line (LF-BK) that is highly susceptible to FMDV infection and then isolated clones that survived mu

213 icate that PPMOs have potential for treating FMDV infections and that they also represent useful tool

214 focal microscopy to analyze the entry of two FMDV serotypes (types A and O) after interaction with in

215 e clusters provided evidence that undetected FMDV infection had occurred.

216 imization of the P1 region rendered a viable FMDV progeny.

217 predict the probability of recovering viable FMDV by probang and culture, conditional on the animal's

218 ires the growth of large volumes of virulent FMDV in biocontainment-level facilities.

219 The foot-and-mouth disease virus (FMDV) "carrier" state was defined by van Bekkum in 1959.

220 hallenged with foot-and-mouth disease virus (FMDV) 1 day later.

221 expression of foot-and-mouth disease virus (FMDV) 3C(pro) and that this requires the protease activi

222 region of the foot-and-mouth disease virus (FMDV) 3D polymerase contains the sequence MRKTKLAPT (res

223 The foot-and-mouth disease virus (FMDV) afflicts livestock in more than 80 countries, limi

224 xperiments for foot-and-mouth disease virus (FMDV) and African swine fever virus (ASFV).

225 ne recognizing foot-and-mouth disease virus (FMDV) and another recognizing the 16 kDa heat-shock prot

226 virus (EMCV), foot-and-mouth disease virus (FMDV) and other picornaviruses comprise five major domai

227 c diversity of foot-and-mouth disease virus (FMDV) arising over the course of infection of an individ

228 se (L(pro)) of foot-and-mouth disease virus (FMDV) blocks cap-dependent mRNA translation and that a g

229 onstrated that foot-and-mouth disease virus (FMDV) can utilize at least four members of the alpha(V)

230 Foot-and-mouth disease virus (FMDV) causes a fast-spreading disease that affects farm

231 nes.IMPORTANCE Foot-and-mouth disease virus (FMDV) causes a highly contagious acute vesicular disease

232 Foot-and-mouth disease virus (FMDV) causes a highly contagious acute vesicular disease

233 Foot-and-mouth disease virus (FMDV) causes a highly contagious infection in cloven-hoo

234 Foot-and-mouth disease virus (FMDV) causes an acute vesicular disease of farm animals.

235 y detection of foot-and-mouth disease virus (FMDV) from viruses that cause clinically similar disease

236 Two foot-and-mouth disease virus (FMDV) genome sequences have been determined for isolates

237 ld isolates of foot-and-mouth disease virus (FMDV) have a restricted cell tropism which is limited by

238 virus (PV) and foot-and-mouth disease virus (FMDV) in a variety of cells.

239 persistence of foot-and-mouth disease virus (FMDV) in micro-dissected compartments of the bovine naso

240 e picornavirus foot-and-mouth disease virus (FMDV) induces the formation of autophagosomes.

241 recovery from foot-and-mouth disease virus (FMDV) infection in calves was investigated by administer

242 of persistent foot-and-mouth disease virus (FMDV) infection was investigated in 46 cattle that were

243 Foot-and-mouth disease virus (FMDV) initiates infection by binding to integrin recepto

244 anner in which foot-and-mouth disease virus (FMDV) interacts with the innate and adaptive immune comp

245 se (L(pro)) of foot-and-mouth disease virus (FMDV) interferes with the innate immune response by bloc

246 pendent on the foot-and-mouth disease virus (FMDV) internal ribosome entry site (IRES) occurs at two

247 Foot-and-mouth disease virus (FMDV) is a highly contagious viral disease.

248 protein 3A of foot-and-mouth disease virus (FMDV) is a partially conserved protein of 153 amino acid

249 Foot-and-mouth disease virus (FMDV) is an important animal pathogen responsible for fo

250 se (L(pro)) of foot-and-mouth disease virus (FMDV) is involved in antagonizing the innate immune resp

251 ponses against foot-and-mouth disease virus (FMDV) is poorly understood.

252 ly inactivated foot-and-mouth disease virus (FMDV) is widely practiced to control FMD.

253 Foot-and-mouth disease virus (FMDV) leader proteinase (L(pro)) cleaves itself from the

254 Foot-and-mouth disease virus (FMDV) mediates cell entry by attachment to an integrin r

255 Foot-and-mouth disease virus (FMDV) produces one of the most infectious of all livesto

256 ]) can inhibit foot-and-mouth disease virus (FMDV) replication in cell culture, and swine inoculated

257 ive to inhibit foot-and-mouth disease virus (FMDV) replication in swine, a similar approach had only

258 03 isolates of foot-and-mouth disease virus (FMDV) representing all seven serotypes and including the

259 Foot-and-mouth disease virus (FMDV) RNA-dependent RNA polymerase (RdRp) (3D(pol)) cata

260 e 2 (HRV2) and foot-and-mouth disease virus (FMDV) to control the translation of the matrix gene (M),

261 Foot-and-mouth disease virus (FMDV) utilizes different cell surface macromolecules to

262 The foot-and-mouth-disease virus (FMDV) utilizes non-canonical translation initiation for

263 ical data in a Foot and Mouth Disease Virus (FMDV) veterinary outbreak in England and a Klebsiella pn

264 ns recognizing foot-and-mouth disease virus (FMDV) were used for making biosensors, and azides were i

265 Foot-and-mouth disease virus (FMDV), as with other RNA viruses, recruits various host

266 pecies such as foot-and-mouth disease virus (FMDV), hemagglutinin (HA) and neuraminidase (NA) segment

267 Foot-and-mouth disease virus (FMDV), like other RNA viruses, exhibits high mutation ra

268 Foot-and-mouth disease virus (FMDV), particularly strains of the O and SAT serotypes,

269 Foot-and-mouth disease virus (FMDV), the causative agent of foot-and-mouth disease, is

270 Foot-and-mouth disease virus (FMDV), the causative agent of foot-and-mouth disease, is

271 tion enzyme of foot-and-mouth disease virus (FMDV), the RNA-dependent RNA polymerase, forms fibrils i

272 genic sites on foot-and-mouth disease virus (FMDV), which resulted in the identification of neutraliz

273 genic sites on foot-and-mouth disease virus (FMDV).

274 e picornavirus foot-and-mouth disease virus (FMDV).

275 the capsid of foot-and-mouth disease virus (FMDV).

276 iruses such as foot-and-mouth disease virus (FMDV).

277 day later with foot-and-mouth disease virus (FMDV).

278 site (IRES) of foot-and-mouth disease virus (FMDV).

279 ens, including foot-and-mouth disease virus (FMDV).

280 region (P1) of foot-and-mouth disease virus (FMDV).

281 K epidemics of Foot-and-Mouth Disease Virus (FMDV): the 2007 outbreak, and a subset of the large 2001

282 ly susceptible to most strains of FMD virus (FMDV) but are difficult and expensive to prepare and mai

283 over the biological relevance of FMD virus (FMDV) persistence.

284 en full genome sequences (FGS) of FMD virus (FMDV) were generated and analysed, including eight repre

285 ines, formulated with inactivated FMD virus (FMDV), are regularly used worldwide to control the disea

286 enhancer of IFN activity against FMD virus (FMDV).

287 to treat ongoing infections with FMD virus (FMDV).

288 Foot-and-mouth disease (FMD) virus (FMDV) circulates as multiple serotypes and strains in ma

289 enhanced mucosal antiviral response, whereas FMDV persistence is associated with suppression of the h

290 ent methods indicated that the date at which FMDV first infected livestock in the United Kingdom was

291 -kappaB suggests a global mechanism by which FMDV antagonizes the cellular innate immune and inflamma

292 h to IgG1 was clear in prescapular LN, while FMDV-specific ASC were detected in all lymphoid tissues

293 d5-pIFN-gamma and challenged all groups with FMDV 1 day later.

294 ficantly inhibited subsequent infection with FMDV as early as 6 h after treatment and for at least 12

295 During infection with FMDV, several host cell membrane rearrangements occur to

296 later by intradermolingual inoculation with FMDV.

297 D8(+) T cells responding to stimulation with FMDV-derived peptides revealed one putative CD8(+) T cel

298 mpletely protected against challenge with WT FMDV as early as 2 days postinoculation and for at least

299 evels detected in animals inoculated with WT FMDV that developed disease.

300 elA staining disappeared from wild-type (WT) FMDV-infected cells but not from double mutant virus-inf