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1 ood mononuclear immune cells that respond to Coxsackievirus.
2 for some adenovirus (AdV) types and group B coxsackieviruses.
3 -fold more resistant to in vitro cleavage by Coxsackievirus 2A protease (2A(Pro)) than wild-type eIF4
4 man K562 cells were cleaved with recombinant Coxsackievirus 2A protease and the N- terminal domains p
8 ssay, neutralizing antibodies titers against coxsackievirus A16 (CA16), enterovirus 71 (EV71), PV I-I
9 e two serotypes Enterovirus A71 (EV-A71) and Coxsackievirus A16 (CV-A16) being responsible for the ma
10 inant virus types enterovirus 71 (EV-71) and coxsackievirus A16 (CV-A16) may account for the differen
13 causative agents are enterovirus 71 (EV71), coxsackievirus A16 (CVA16), and, most recently, coxsacki
14 common childhood illness primarily caused by coxsackievirus A16 (CVA16), for which there are no curre
15 interspersed phylogenetically with clades of coxsackievirus A16 and other EV species A serotypes.
16 s most typically caused by enterovirus 71 or coxsackievirus A16 and results in asymptomatic infection
18 poliovirus 2C(ATPase) interacts with VP3 of coxsackievirus A20, in the context of a chimeric virus.
21 ution of variants of the common-cold-causing coxsackievirus A21, an EV with tropism for the human int
24 everal serotypes of human adenovirus (HAdV), coxsackievirus A24, enterovirus 70, and herpes simplex-v
25 ent targets for designing anti-CVA6 vaccines.Coxsackievirus A6 (CVA6) causes hand, foot and mouth dis
29 viruses), and 292 (65%) of 448 patients with coxsackievirus A6 infection with available clinical data
32 ar with the severe variant of HFMD caused by coxsackievirus A6, include it in their differential diag
37 -B) in the family Picornaviridae consists of coxsackievirus A9; coxsackieviruses B1 to B6; echoviruse
38 ith different fiber shaft lengths and either coxsackievirus-Ad receptor (CAR)-interacting Ad serotype
39 t HD-RIGIE injections efficiently transduced coxsackievirus adenovirus receptor-expressing keratocyte
44 d5) involves fiber capsid protein binding to coxsackievirus-adenovirus receptor (CAR) at the cell sur
45 majority of adenovirus serotypes utilize the coxsackievirus-adenovirus receptor (CAR) for virus-host
46 We hypothesized that the expression of the coxsackievirus-adenovirus receptor (CAR), a viral recept
48 e variant of the extracellular domain of the coxsackievirus-adenovirus receptor (sCAR-Fc) was express
49 reatment with an engineered sCAR-Fc (soluble coxsackievirus-adenovirus receptor fused to the carboxyl
50 rabasal cells that express the high-affinity coxsackievirus-adenovirus receptor, CAR, whereas the pro
52 Ad) fiber protein mediates Ad binding to the coxsackievirus and Ad receptor (CAR) and is thus a major
53 have shown that although Ad2ts1 can bind the coxsackievirus and Ad receptor and undergo internalizati
54 hafted Ad vectors had no impact on knob-CAR (coxsackievirus and Ad receptor) interaction compared to
57 creening in Vero cells, which identified the coxsackievirus and adenovirus receptor (CAR) as a candid
58 onal assays, we identified and validated the coxsackievirus and adenovirus receptor (CAR) as a functi
59 While group B coxsackieviruses (CVB) use the coxsackievirus and adenovirus receptor (CAR) as the rece
60 ruses into target cells is expression of the coxsackievirus and adenovirus receptor (CAR) at the cell
68 we demonstrate that in the adult brain, the coxsackievirus and adenovirus receptor (CAR) is located
70 rity of adenovirus serotypes can bind to the coxsackievirus and adenovirus receptor (CAR) on human ce
72 In this study, a zebrafish homologue of the coxsackievirus and adenovirus receptor (CAR) protein was
75 novirus serotype 5 fiber protein engages the coxsackievirus and adenovirus receptor (CAR) to bind cel
77 this work, we investigated the roles of the coxsackievirus and adenovirus receptor (CAR), CD46, and
78 s many adenoviruses infect cells through the coxsackievirus and adenovirus receptor (CAR), group B ad
87 rosclerotic plaques we hypothesized that the coxsackievirus and adenovirus receptor (CXADR/CAR), alth
88 us virus with high concentrations of soluble coxsackievirus and adenovirus receptor (sCAR) were simil
90 presence of varied concentrations of soluble coxsackievirus and adenovirus receptor showed that the o
91 es), cardiac fibrosis, apoptosis, lower CAR (Coxsackievirus and adenovirus receptor) expression and C
92 tudy demonstrates that hiPSC-CMs express the coxsackievirus and adenovirus receptor, are susceptible
94 beta, tumor-derived growth factor beta; CAR, coxsackievirus and adenovirus receptor; MLV, murine leuk
95 is the primary cellular receptor for group B coxsackieviruses and most adenovirus serotypes and plays
96 FP(A20) exhibited up to 50-fold increases in coxsackievirus- and-adenovirus-receptor-independent tran
97 binds with high affinity to the cell surface coxsackievirus-and-adenovirus receptor (CAR), and penton
98 egression to test for an association between coxsackievirus antibody titer and the presence or absenc
100 = .12), human bocavirus (aOR 9.1, P < .01), Coxsackieviruses (aOR 5.1, P = .09), rhinovirus A (aOR 3
102 ous observations suggesting that the group B coxsackieviruses are associated with the risk of type 1
108 al dissemination in released EMVs.IMPORTANCE Coxsackievirus B (CVB) can cause a number of life-threat
112 alized host factor that negatively regulates coxsackievirus B (CVB) replication through its control o
113 ental murine infections and in cell culture, coxsackievirus B (CVB) RNA can persist for weeks in the
114 eptors for poliovirus, human rhinovirus, and coxsackievirus B (CVB) serve to bind the viruses to targ
116 enteroviruses, including echovirus 11 (E11), coxsackievirus B (CVB), and enterovirus 71 (EV71), and t
121 rategies based on specific inhibitors of the coxsackievirus B proteinase 2A activity for acute and ch
128 icornaviridae consists of coxsackievirus A9; coxsackieviruses B1 to B6; echoviruses 1 to 7, 9, 11 to
130 fection with a suspected diabetogenic virus, Coxsackievirus B3 (CB3), NOD.Ncf1(m1J) mice remained res
131 of IL-12 and IFN-gamma on the development of Coxsackievirus B3 (CB3)-induced myocarditis, we examined
132 The first-described DAF-binding isolate, coxsackievirus B3 (CB3)-RD, was obtained during passage
133 ngth VP1 genes of poliovirus 1 (Polio 1) and coxsackievirus B3 (Cox B3) were cloned, and the encoded
135 d identified RIP3 as a positive regulator of coxsackievirus B3 (CVB) replication in intestinal epithe
136 ne was effective against poliovirus (PV) and coxsackievirus B3 (CVB3) and exhibited greater activity
140 B infection, we previously demonstrated that coxsackievirus B3 (CVB3) could infect neuronal progenito
141 larized human intestinal epithelial cells by coxsackievirus B3 (CVB3) depends on virus interaction wi
142 ar to humans, male BALB/c mice infected with coxsackievirus B3 (CVB3) develop more severe inflammatio
146 we describe the generation of a recombinant coxsackievirus B3 (CVB3) expressing the enhanced green f
150 eviously described a neonatal mouse model of coxsackievirus B3 (CVB3) infection and determined that p
154 ate immunity can determine susceptibility to coxsackievirus B3 (CVB3) infection, the present study ev
163 esent recent findings on the pathogenesis of coxsackievirus B3 (CVB3) myocarditis based on animal mod
165 l mouse model, we previously determined that coxsackievirus B3 (CVB3) preferentially targets prolifer
167 ed in pancreatic acinar cells, and show that coxsackievirus B3 (CVB3) requires autophagy for optimal
168 Previously, we described the ability of coxsackievirus B3 (CVB3) to infect proliferating neurona
170 We previously demonstrated the ability of coxsackievirus B3 (CVB3) to persist within the neonatal
173 xchanges between poliovirus type 1 (PV1) and coxsackievirus B3 (CVB3) utilizing an in vitro translati
175 ct of antibiotic treatment on infection with coxsackievirus B3 (CVB3), a picornavirus closely related
177 The IRESs of poliovirus, the cardiotropic coxsackievirus B3 (CVB3), and the hepatotropic hepatitis
179 1 reduced encephalomyocarditis virus (EMCV), coxsackievirus B3 (CVB3), poliovirus and enterovirus D68
180 spite this barrier, enteroviruses, including coxsackievirus B3 (CVB3), successfully penetrate the int
181 mice, IL-13 KO BALB/c mice developed severe coxsackievirus B3 (CVB3)-induced autoimmune myocarditis
182 In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice
195 oliovirus, foot-and-mouth disease virus, and coxsackievirus B3 and can lead to reduced cell surface e
197 l targeting of key residues, and screens for Coxsackievirus B3 fidelity variants, we isolated nine po
199 iants corresponding to Poliovirus type 1 and Coxsackievirus B3 have virtually the same structure, bas
202 the assay to monitor kinase signaling during coxsackievirus B3 infection of two different host-cell t
204 induced after intraperitoneal inoculation of coxsackievirus B3 into C57Bl/6 IRAK4-deficient mice and
206 inistration on the development of autoimmune coxsackievirus B3 myocarditis and dilated cardiomyopathy
208 have previously engineered more than a dozen coxsackievirus B3 polymerase mutations that significantl
213 zed the structure of 5' UTR genomic RNA from coxsackievirus B3 using selective 2'-hydroxyl acylation
214 BL/6 endothelial cells with a nonmyocarditic coxsackievirus B3 variant, H310A1, which is a poor induc
215 ated that infection by another picornavirus (coxsackievirus B3) causes SRp20 to relocalize from the n
217 f Aichi virus, bovine kobuvirus, poliovirus, coxsackievirus B3, and human rhinovirus 14 all copurify
218 exposure to heat or bleach, but poliovirus, coxsackievirus B3, and reovirus can be stabilized by bac
219 on is enhanced in cells infected with the EV coxsackievirus B3, but the related poliovirus has no sig
220 om the binding site of DAF on the surface of coxsackievirus B3, indicating that there are independent
221 this study, we analyzed the role of PAR-1 in coxsackievirus B3-induced (CVB3-induced) myocarditis and
222 re profiled in both human myocarditis and in Coxsackievirus B3-injected mice, comparing myocarditis-s
229 A59, Theiler's encephalomyelitis virus, and Coxsackievirus B3] in mice with autoantibodies to a cent
233 tion in nonobese diabetic (NOD) mice through coxsackievirus B4 (CVB4) infection requires a preexistin
234 This study of the pancreatropic enterovirus Coxsackievirus B4 (CVB4) shows that although infection a
238 ve analysis of global gene expression during coxsackievirus B4-induced acute and chronic pancreatitis
239 -cell biology, we investigated the impact of coxsackievirus B5 (CVB5) infection on the cellular expre
240 itive-sense single-stranded RNA human virus, coxsackievirus B5, by applying both qPCR- and culture-ba
241 beacons (MBs) for the real-time detection of coxsackievirus B6 replication in living Buffalo green mo
242 uced into BGMK cell monolayers infected with coxsackievirus B6, a discernible fluorescence was observ
244 Newborn pups were extremely vulnerable to coxsackievirus CNS infection, and this susceptibility de
245 ovirus (E) 6 (7.6%), E14 (7.6%), E11 (7.4%), coxsackievirus (CV) B3 (7.4%), E25 (5.6%), CVB5 (4.9%),
256 type-specific antibodies against the group B coxsackieviruses (CVBs), which have been linked to diabe
257 ended this phenotype to Zika virus; however, coxsackievirus did not similarly produce noninfectious p
258 Despite replicating to very high titers, coxsackieviruses do not elicit strong CD8 T-cell respons
267 espect, IKK-induced cardiomyopathy resembled Coxsackievirus-induced myocarditis, during which the NF-
268 be used to model the pathogenic processes of coxsackievirus-induced viral myocarditis and to screen a
271 extreme susceptibility of newborn infants to coxsackievirus infection and viral tropism for the CNS,
273 and adenovirus receptor, are susceptible to coxsackievirus infection, and can be used to predict ant
274 of the microbiota was sufficient to decrease coxsackievirus infection, while poliovirus infection was
278 hermore, a sex bias for severe sequelae from coxsackievirus infections has been observed in humans.
279 Neonates are particularly susceptible to coxsackievirus infections of the central nervous system
281 s as an antiviral factor during infection by coxsackievirus or human rhinovirus, suggesting a common
282 he RNA template sequence, the origin of VPg (coxsackievirus or poliovirus), the origin of 3D polymera
283 or poliovirus), the origin of 3D polymerase (coxsackievirus or poliovirus), the presence and origin o
284 by picornaviruses, such as human rhinovirus, coxsackievirus, poliovirus, foot-and-mouth disease virus
292 pathogens for humans, including poliovirus, coxsackievirus, rhinovirus, as well as newly emerging gl
293 ally important pathogens such as poliovirus, coxsackievirus, rhinovirus, enterovirus 71 and foot-and-
294 ypes of cardiomyocytes, we demonstrated that coxsackievirus RNAs harboring 5' deletions ranging from
296 experiments use intraperitoneal injection of coxsackievirus to infect mice, bypassing the intestine.
297 study, we created a library of 135 barcoded coxsackieviruses to examine viral population diversity a
298 pro) proteins from diverse enteroviruses and coxsackieviruses to interfere with type I IFN induction
299 ribe an "Open sesame!" strategy developed by coxsackieviruses to invade the organism through the inte
300 encapsidation of poliovirus and of C-cluster coxsackieviruses, which are prototypes of enteroviruses,