ライフサイエンスコーパス: S. pyogenes

1 S. pyogenes bound purified fibulin-1 in a dose-dependent

2 S. pyogenes did not release HlpA during growth in vitro;

3 S. pyogenes dnaX encodes only the full-length tau, unlik

4 S. pyogenes expresses HSA-binding surface proteins, and

5 S. pyogenes grew from one or both swabs for 198 (37%) of

6 S. pyogenes IMPDH is a tetramer with its four subunits r

7 S. pyogenes MHC class II-bound peptide-specific CD4(+) T

8 S. pyogenes strains with this type of polymorphism cause

9 S. pyogenes-induced Th17 formation depended on TGF-beta1

10 C and 30 S. aureus, 15 S. pneumoniae, and 15 S. pyogenes isolates by disk diffusion (DD) methods.

11 was insertionally inactivated in an M type 2 S. pyogenes strain, T2MR.

12 e against challenge infections with M type 2 S. pyogenes.

13 In all, 1,800 Staphylococcus aureus, 259 S. pyogenes, 226 Streptococcus pneumoniae, 93 Enterococc

14 2 opsonized SOF-positive M type 2, 4, and 28 S. pyogenes in human blood but had no effect on SOF-nega

15 d but had no effect on SOF-negative M type 5 S. pyogenes.

16 M/emm type 6 S. pyogenes has intrinsic reduced susceptibility to fluo

17 Additionally, we analyzed M/emm type 6 S. pyogenes isolated during 1918-2003 from diverse locat

18 rated in erythromycin-resistant M/emm type 6 S. pyogenes, which raises concern for the emergence of m

19 ysis shows that in contrast to the type II-A S. pyogenes Cas9 that is widely used for genome engineer

20 Finally, we demonstrated that sloR, a S. pyogenes gene that closely resembles the Clostridium

21 show macrolide resistance (S. aureus A5177, S. pyogenes PIU2584, and S. pneumoniae 5649).

22 t SOF evokes bactericidal antibodies against S. pyogenes in humans, rabbits, and mice.

23 Biotin tagged whole antibodies against S. pyogenes were conjugated to Ptyr amine group via biot

24 gm shift from type-specific immunity against S. pyogenes to emm-cluster based immunity for this bacte

25 agent, compound 1 (MIC: 12-25 microM against S. pyogenes).

26 f the human adaptive immune response against S. pyogenes in both children and adults.

27 Thus, human immune responses against S. pyogenes consist of a robust Th1 cellular memory resp

28 We found that FH6-7/Fc alleviated S. pyogenes-induced sepsis in a transgenic mouse model e

29 istance to macrolides and tetracycline among S. pyogenes isolates in San Francisco County and shows t

30 se-dependent manner, suggesting a role as an S. pyogenes virulence factor.

31 examine this, we analyzed the behavior of an S. pyogenes mutant deficient in expression of the cytoly

32 nally, an allelic replacement analysis of an S. pyogenes strain with a naturally occurring insertion

33 ant to in vitro penetration by S. aureus and S. pyogenes and partially resistant to P. aeruginosa.

34 also prevented penetration by S. aureus and S. pyogenes; NeoForm was less effective in withstanding

35 ar adhesion and entry for B. burgdorferi and S. pyogenes.

36 tween S. dysgalactiae subsp. equisimilis and S. pyogenes alleles revealed a history of interspecies r

37 aureus was not found by culture or PCR, and S. pyogenes was not identified by any technique.

38 quences from two of these, S. pneumoniae and S. pyogenes.

39 topes contained in HIV, M. tuberculosis, and S. pyogenes.

40 he surface of Gram-positive bacteria such as S. pyogenes will enable professional phagocytes to elimi

41 y can be applied for specific agents such as S. pyogenes, or commercial multiplex NAATs for detection

42 All cluster-associated S. pyogenes isolates were genotype emm1 and were initial

43 The highly attenuated S. pyogenes mutant, SalY, was identified from a transpos

44 Genomic analyses of available S. pyogenes genomes revealed the presence of intact gene

45 Because S. pyogenes is known to release LTA and secrete at least

46 However, because S. pyogenes are only found in humans, how are new phages

47 c toxin B (SPE B) on the interaction between S. pyogenes strain NZ131 (serotype M49) and mammalian ce

48 en grown in sugar-limited Todd-Hewitt broth, S. pyogenes cells remained culturable for more than 1 ye

49 ds, the induction of caspase-1 activation by S. pyogenes did not require exogenous ATP or the P2X7R.

50 Two postpartum deaths caused by S. pyogenes occurred within 24 h; one was characterized

51 ft-tissue infection or bacteraemia caused by S. pyogenes, and it could have a protective role in muri

52 ovel vaccine to prevent infections caused by S. pyogenes.

53 crobiological diagnosis of empyema caused by S. pyogenes.

54 t to promote invasion of epithelial cells by S. pyogenes.

55 ut also for invasion of endothelial cells by S. pyogenes.

56 in that may function in host colonization by S. pyogenes.

57 When expressed by S. pyogenes, PFO, like SLO, had the ability to form func

58 SpyCEP expression by S. pyogenes hindered bacterial clearance from muscle, an

59 that fluoride causes decreased expression by S. pyogenes proteins used to respond to stress, virulenc

60 IFN-beta, which is significantly induced by S. pyogenes 23S rRNA in an Irf5-dependent manner.

61 required Myd88/Trif, whereas that induced by S. pyogenes was blocked by inhibition of NF-kappaB.

62 cells prevented nasopharyngeal infection by S. pyogenes, but not by Streptococcus pneumoniae, a bact

63 y-phase culture supernatant proteins made by S. pyogenes NZ131 rgg and NZ131 speB were separated by t

64 We hypothesize that SpyA is produced by S. pyogenes to disrupt cytoskeletal structures and promo

65 Binding of complement regulatory proteins by S. pyogenes has previously been attributed to the strept

66 ed proteomic analysis of protein released by S. pyogenes into the culture supernatant and observed de

67 , and NaCl may mimic relevant cues sensed by S. pyogenes during infection; and that identification of

68 y, we investigate hemoprotein utilization by S. pyogenes.

69 Moraxella catarrhalis, S. pyogenes, and culture-negative episodes were also sig

70 In this report, we characterize S. pyogenes DnaE polymerase and find that it is highly e

71 ellular expression of two well-characterized S. pyogenes virulence factors.

72 Finally, we assess comparative S. pyogenes and S. aureus Cas9 specificity using GUIDE-s

73 udy, we quantitatively analyzed and compared S. pyogenes proteins in the growth medium of a strain th

74 sing bioinformatics analysis of the complete S. pyogenes strain SF370 genome, we have identified a no

75 gest that under certain in vitro conditions, S. pyogenes cells can persist for greater than 1 year as

76 rtion of IgG-reactive proteins from cultured S. pyogenes are secreted.

77 ly larger amounts of the secreted cytotoxins S. pyogenes NADase (SPN) and streptolysin O (SLO).

78 ensors were also able to specifically detect S. pyogenes in 50% (v/v) human saliva, with good selecti

79 , illustrating the intrinsic ability of emm1 S. pyogenes to spread while retaining virulence.

80 we successfully delivered a plasmid encoding S. pyogenes Cas9 and sgRNA to the corneal epithelium by

81 binding to fibronectin (Fn) and facilitates S. pyogenes adherence and penetration into cells.

82 ae (Group B streptococci, GBS), E. faecalis, S. pyogenes, S. gordonii, and E. coli containing pDC123

83 transgenic mouse model expressing human FH (S. pyogenes binds FH in a human-specific manner).

84 e clinical settings, by a throat culture for S. pyogenes to increase the sensitivity of its detection

85 roxidase in S. pyogenes and is essential for S. pyogenes pathogenesis in several murine models that m

86 enized murine vaginal colonization model for S. pyogenes.

87 based system as a standard typing scheme for S. pyogenes will facilitate the design of future studies

88 his protein, the hlpA genes were cloned from S. pyogenes, S. gordonii, S. mutans, and S. sobrinus, us

89 often highly related, but they differed from S. pyogenes, in that S. dysgalactiae subsp. equisimilis

90 strate that the multidomain protein Epf from S. pyogenes serotype M49 is a streptococcal adhesin.

91 nce analyses of larger regions of FnBPs from S. pyogenes and S. aureus reveal a repeating pattern of

92 his is the first methyltransferase gene from S. pyogenes to be cloned and to have its activity charac

93 o compare cytoplasmic proteins isolated from S. pyogenes wild-type strain NZ131 (serotype M49) to pro

94 sphoribosyltransferase activity of NadC from S. pyogenes allows the organism to sustain growth when Q

95 from those recognized by Cas9 proteins from S. pyogenes and S. thermophilus (SpCas9 and StCas9, resp

96 rated cellular and supernatant proteins from S. pyogenes cultures by high-resolution two-dimensional

97 regions of fibronectin-binding proteins from S. pyogenes, S. dysgalactiae, and S. equisimilis.

98 28-kDa streptococcal protease purified from S. pyogenes processed the 40-kDa mutant zymogen to a 28-

99 ial pathogen the group A Streptococcus (GAS; S. pyogenes) as a model organism, we review the types an

100 and virulence in group A Streptococcus (GAS; S. pyogenes), the precise role of the co-transcribing se

101 In S. pyogenes, mutS and mutL are organized on a polycistro

102 In S. pyogenes, Rgg influences the expression of several vi

103 an insertionally inactivated degP allele in S. pyogenes is similar to that reported for E. coli, wit

104 sly identified as cell surface associated in S. pyogenes.

105 sion, the elucidation of GAC biosynthesis in S. pyogenes reported here enhances our understanding of

106 tion by the Rgg2/3 quorum-sensing circuit in S. pyogenes.

107 Such genetic elements may be common in S. pyogenes since 6 of 13 completed genomes have related

108 Taken together, the CvfA-enolase complex in S. pyogenes is involved in the regulation of virulence g

109 e rgg mutant with an intact rgg gene copy in S. pyogenes NZ131 could restore SPE B production and con

110 Resistance to erythromycin in S. pyogenes can be as high as 48% in specific population

111 uitry governing virulence gene expression in S. pyogenes and its impact on pathogenesis.

112 to coregulate virulence factor expression in S. pyogenes.

113 pA, the gene which encodes trigger factor in S. pyogenes, produced mutant proteins deficient in PPIas

114 istence of a new global regulatory factor in S. pyogenes.

115 side cells, and the cellular role of GdpP in S. pyogenes has not been examined yet.

116 ociated with inactivation of the rgg gene in S. pyogenes strain NZ131 (serotype M49).

117 he first hemoprotein receptors identified in S. pyogenes; their possible role in iron capture is disc

118 he rgg gene was insertionally inactivated in S. pyogenes NZ131, which resulted in markedly decreased

119 standing of the function of the sal locus in S. pyogenes pathogenesis.

120 Thus, MMR in S. pyogenes SF370 is functional in exponentially growing

121 S, coordinate the transcriptional network in S. pyogenes.

122 eparate entries to a final common pathway in S. pyogenes virulence gene expression.

123 idase is the major glutathione peroxidase in S. pyogenes and is essential for S. pyogenes pathogenesi

124 acterized an intergenic VNTR polymorphism in S. pyogenes that affects toxin production and virulence.

125 gy and the function of VNTR polymorphisms in S. pyogenes.

126 e and lincosamide antibiotics are present in S. pyogenes strains in the United States.

127 itate further study of cellular processes in S. pyogenes.

128 ainst sHIP suggest a role for the protein in S. pyogenes pathogenesis.

129 rify the function of HSA-binding proteins in S. pyogenes and underline the power of the quantitative

130 Macrolide and lincosamide resistance in S. pyogenes is mediated by several different genes.

131 ion of NadD confirmed its functional role in S. pyogenes, and its potential as an antibacterial targe

132 We investigated the role of SpyCEP in S. pyogenes necrotizing fasciitis and respiratory tract

133 or induced resistance to peroxide stress in S. pyogenes, genes for a novel mechanism of managing per

134 , and removal of read-through transcripts in S. pyogenes.

135 Here, we demonstrate that nuclease-inactive S. pyogenes CRISPR/Cas9 can bind RNA in a nucleic-acid-p

136 m by which Gram-positive bacteria, including S. pyogenes, coordinate multiple environmental cues, all

137 , and some Gram-positive pathogens including S. pyogenes use this cyclic nucleotide derivative as a s

138 gainst most streptococcal species, including S. pyogenes, S. agalactiae, S. dysgalactiae, S. equi, S.

139 hat M. catarrhalis can dramatically increase S. pyogenes adherence to human epithelial cells and that

140 ne of these inhibitors efficiently inhibited S. pyogenes NadD (sp.NadD) in vitro (50% inhibitory conc

141 a promoter-lacZ fusions were introduced into S. pyogenes via a bacteriophage-derived site-specific in

142 signaling protects the host against invasive S. pyogenes infection by restricting inflammation-driven

143 identified across four contemporary invasive S. pyogenes serotypes (M1, M3, M12 and M89).

144 pooled human immunoglobulin during invasive S. pyogenes infection, and demonstrate a potential route

145 t insights into the pathogenesis of invasive S. pyogenes infections.

146 ernatants prepared from cultures of invasive S. pyogenes strains of varying serotypes in the stationa

147 and the finding that patients with invasive S. pyogenes infection respond with antibody production a

148 ysis of samples from a patient with invasive S. pyogenes infection revealed dramatic differences in t

149 The utility of our model for investigating S. pyogenes factors contributing to mucosal carriage was

150 retion were induced by live, but not killed, S. pyogenes, and required expression of the pore-forming

151 d we evaluated the expression of other known S. pyogenes virulence factors.

152 tudy it is shown that AspA from serotype M28 S. pyogenes, when expressed on surrogate host Lactococcu

153 Since M49 S. pyogenes strains have been known to be associated wit

154 SPN and SLO in epidemic serotype M1 and M89 S. pyogenes strains is associated with rapid intercontin

155 0% S), and MIC(90)s ranged from 0.03 mug/ml (S. pyogenes/S. pneumoniae) to 1 mug/ml (Enterobacteriace

156 eutrophil extracellular traps, and modulates S. pyogenes virulence.

157 Both wild-type and mutant S. pyogenes bacteria were extremely sensitive to low pH.

158 ht of reports of hypervirulent SpeB-negative S. pyogenes variants present during invasive infections.

159 s required for survival of L. lactis but not S. pyogenes.

160 In conclusion, we have identified a novel S. pyogenes enzyme with 5'-nucleotidase activity and imm

161 ain SF370 genome, we have identified a novel S. pyogenes virulence factor, which we termed streptococ

162 Now S. pyogenes NAATs are being used with increasing frequen

163 mbinant SOF from M types 2, 4, 28, and 75 of S. pyogenes, indicating that the fibulin-1-binding domai

164 nsporter may be an example of the ability of S. pyogenes to adapt and evolve new survival strategies

165 of zinc homeostasis inhibits the ability of S. pyogenes to cause disease in a zinc-limited host mili

166 s rescued, demonstrating that the ability of S. pyogenes to utilize arginine was dispensable in the a

167 in the absence of FBP, Pi is an activator of S. pyogenes LDH, E. faecalis LDH1, and L. lactis LDH1 an

168 ered metabolism, the catabolic activities of S. pyogenes strain NZ131 (serotype M49) and an isogenic

169 fibulin-1 may be involved in the adhesion of S. pyogenes to extracellular matrices of the host.

170 hould prove effective for future analyses of S. pyogenes mucosal colonization.

171 sed proteins to identify surface antigens of S. pyogenes.

172 e biochemical and kinetic characteristics of S. pyogenes IMPDH are similar to other bacterial IMPDH e

173 inhibitor ifs from a worldwide collection of S. pyogenes strains.

174 factors for the survival and colonization of S. pyogenes is well established, and many of these facto

175 plicated in non-suppurative complications of S. pyogenes, including glomerulonephritis and rheumatic

176 by how SAgs contribute to the life cycle of S. pyogenes remain poorly understood.

177 We constructed mutant derivatives of S. pyogenes that lack Fba, M1 protein, or both proteins

178 ity factor (SOF), a virulence determinant of S. pyogenes, reduced binding by approximately 50%, and a

179 However, dissemination of S. pyogenes to the lung was SpyCEP-dependent and was ass

180 the role of prophages in diversification of S. pyogenes and the close relationship between strain Ma

181 ay contribute to the phenotypic diversity of S. pyogenes.

182 ntly protected against the lethal effects of S. pyogenes.

183 Finally, examination of S. pyogenes following murine subcutaneous infection reve

184 SOF is also a virulence factor of S. pyogenes, but it has not been previously shown to eli

185 oxidase (NOXase) is a unique flavoprotein of S. pyogenes and other lactic acid bacteria which directl

186 Growth of S. pyogenes in blood was dependent on the presence of fi

187 ow the intracellular proteome homeostasis of S. pyogenes is influenced by the presence of human plasm

188 novel factors related to the invasiveness of S. pyogenes.

189 This study was a unique investigation of S. pyogenes factors required for successful invasive inf

190 vival of clinical and laboratory isolates of S. pyogenes and S. pneumoniae as both organisms are thou

191 Although all isolates of S. pyogenes possess the speB gene, not all of them produ

192 We surveyed 384 clinical isolates of S. pyogenes, isolated during 2002-2003, for susceptibili

193 tion, may be present in invasive isolates of S. pyogenes.

194 proximately half of the clinical isolates of S. pyogenes.

195 on that promoted opsonophagocytic killing of S. pyogenes in vitro and provided passive immunity in vi

196 Mrp4, Emm4 and Sof4 promoted the killing of S. pyogenes, but anti-SfbX serum had no effect.

197 t important for survival in a mouse model of S. pyogenes peritoneal infection.

198 resistant isolates from a recent outbreak of S. pyogenes infection in Pittsburgh and in the Lancefiel

199 ibution the toxin has to the pathogenesis of S. pyogenes and that both versions of SPN play an import

200 ulation is necessary for the pathogenesis of S. pyogenes.

201 for the in vivo survival and pathogenesis of S. pyogenes.

202 as titin and fibronectin, the giant pili of S. pyogenes evolved to abrogate mechanical extensibility

203 The putative Rgg polypeptide of S. pyogenes NZ131 consisted of 280 amino acids and had a

204 -moving outbreak highlights the potential of S. pyogenes to cause a range of diseases in the puerperi

205 comparing genomewide transcript profiles of S. pyogenes NZ131 and isogenic derivative NZ131 rgg duri

206 The encoded HlpA protein of S. pyogenes has 91 amino acids, a predicted molecular ma

207 The well-characterized Scl1 proteins of S. pyogenes show a dichotomous switch in ligand binding

208 important contribution to the regulation of S. pyogenes virulence factors.

209 We studied the resistance of S. pyogenes to erythromycin and clindamycin at an urban

210 re supernatants from multiple M serotypes of S. pyogenes isolates or a commercially available SLS pre

211 SLS contribute to the subcutaneous spread of S. pyogenes and to a fatal outcome of infection.

212 ophil recruitment during the early stages of S. pyogenes infection.

213 ased SpeB production in a clinical strain of S. pyogenes and relieved its growth phase dependency.

214 igo strain, and not the pharyngeal strain of S. pyogenes or the nonpathogenic S. gorgonii isolate, wa

215 re infected in thigh muscle with a strain of S. pyogenes that expresses a high level of SpyCEP, or wi

216 ized that adherence of an impetigo strain of S. pyogenes would be promoted by terminal differentiatio

217 aspA gene from two different M28 strains of S. pyogenes abrogated their abilities to form biofilms o

218 Hypervirulent strains of S. pyogenes have evolved a plethora of virulence factors

219 nteractions in attachment of skin strains of S. pyogenes to keratinocytes are unique and remain unide

220 lso differ for throat versus skin strains of S. pyogenes.

221 rence by isogenic M1(+) and M1(-) strains of S. pyogenes.

222 ontributes to the immune evasion strategy of S. pyogenes.

223 the efficacy of antibiotics in treatment of S. pyogenes infections.

224 term stationary-phase survival (>4 weeks) of S. pyogenes.

225 d but not methicillin-resistant S. aureus or S. pyogenes from cellulitis tissue specimens.

226 n with S. dysgalactiae subsp. equisimilis or S. pyogenes.

227 emm, scpA, sic, or cpa (genes encoding other S. pyogenes virulence factors).

228 ed a locus that is highly conserved in other S. pyogenes genomes and is homologous to an operon invol

229 2) For L. plantarum, S. pyogenes, and E. faecalis, the effects of Pi are dist

230 MPO directly killed H(2)O(2)-producing S. pyogenes but was ineffective against non-H(2)O(2)-pro

231 ss the need for a refined model of prolonged S. pyogenes asymptomatic mucosal colonization, we have a

232 tive form of the streptococcal CXC protease, S. pyogenes cell envelope proteinase, we developed a com

233 olysin, but not SIC, a protein that protects S. pyogenes from CAPs.

234 The polC gene from Streptococcus pyogenes (S. pyogenes, strain SF370) has been cloned and expressed

235 challenged by HRG, sHIP was found to rescue S. pyogenes bacteria.

236 demonstrated that the erythromycin-resistant S. pyogenes comprised multiple strains.

237 ern for the emergence of multidrug-resistant S. pyogenes.

238 s transcribed during cell growth in the same S. pyogenes strain.

239 s question, we discovered that all sequenced S. pyogenes strains possess the genes for the malic enzy

240 As with the previously sequenced S. pyogenes genomes, three unique prophages are a major

241 ed in a small subset of patients with severe S. pyogenes sepsis but not in patients with any other ca

242 st report to show natural induction of sigX, S. pyogenes remained nontransformable under laboratory c

243 The effector, SPN (S. pyogenes NAD-glycohydrolase), is capable of producing

244 mily ADP-ribosyltransferase designated SpyA (S. pyogenes ADP-ribosyltransferase).

245 AS; Streptococcus pyogenes) protease SpyCEP (S. pyogenes cell envelope protease) cleaves granulocyte

246 Confirmation that S. pyogenes Cas9 lacks the specificity to discriminate b

247 We demonstrated that S. pyogenes has an unusually high mRNA turnover rate, wi

248 We found that S. pyogenes M5-specific antibodies and sera from B. burg

249 We report here that S. pyogenes is able to bind to bovine submaxillary mucin

250 These findings justify the hypothesis that S. pyogenes infections are more important in the pathoge

251 These data indicate that S. pyogenes can interact with fibulin-1 and that SOF is

252 These results indicate that S. pyogenes has evolved multiple mechanisms for invasion

253 Consistent with the observation that S. pyogenes is responsible for a wider variety of human

254 In addition, we show that S. pyogenes demonstrates an inducible peroxide resistanc

255 These data suggest that S. pyogenes diversifies during survival in stationary ph

256 Taken together, these data suggest that S. pyogenes requires glutathione peroxidase to adapt to

257 Remarkably, these observations suggest that S. pyogenes uses SAgs to manipulate Vbeta-specific T cel

258 The S. pyogenes CAMP factor is specified by a 774-bp open re

259 The S. pyogenes M28_Spy1325 polypeptide (designated AspA) di

260 The S. pyogenes NAD(+) glycohydrolase (SPN) is a virulence f

261 The S. pyogenes tau binds PolC, but the interaction is not a

262 and Northern blot analyses to determine the S. pyogenes mRNA half-life of the transcriptome and to u

263 two-cassette system expressing pieces of the S. pyogenes Cas9 (SpCas9) protein which splice together

264 the highly recombinatorial FCT region of the S. pyogenes genome is under strong selection for change

265 pt that can detect intergenic regions of the S. pyogenes genome.

266 ed the ExPortal, a unique microdomain of the S. pyogenes membrane, specialized for protein secretion

267 rain found that between 3.7 and 28.5% of the S. pyogenes transcripts were differentially expressed, d

268 d partial inhibition of C3 deposition on the S. pyogenes surface.

269 ts with mutually permissive NGGRRT PAMs, the S. pyogenes Cas9 and S. aureus Cas9 yield indels at comp

270 between a known effector of the pathway, the S. pyogenes NAD(+) glycohydrolase (SPN), and a second se

271 Here, we report that the S. pyogenes cell surface protein Fba can mediate binding

272 We show here that the S. pyogenes DnaE polymerase also functions with the beta

273 similar and unique features compared to the S. pyogenes enzyme.

274 nto structure-function relationships in this S. pyogenes virulence factor.

275 f SLPI and lysozyme would be advantageous to S. pyogenes in establishing colonization on mucosal surf

276 ontrol protein modules 6 and 7) that bind to S. pyogenes, linked to the Fc region of IgG (FH6-7/Fc).

277 ther, these data show that ME contributes to S. pyogenes' carbon source repertory, that malate utiliz

278 contribute to the binding of hemoproteins to S. pyogenes.

279 tion of Tn5-based transposome mutagenesis to S. pyogenes with initial screening for reduced expressio

280 ate that caspase-1 activation in response to S. pyogenes infection requires NF-kappaB and the virulen

281 e for pro-IL-1beta induction, in response to S. pyogenes infection.

282 both SPN and SLO contribute significantly to S. pyogenes pathogenesis in these virulence assays.

283 subsp. equisimilis isolates were similar to S. pyogenes isolates, in that strains of the same emm ty

284 r1)-deficient mice are highly susceptible to S. pyogenes infection.

285 a-lactam antibiotics, commonly used to treat S. pyogenes infections, do not readily permeate mammalia

286 In contrast to wild-type S. pyogenes, the SLS- mutant was associated with the rob

287 lerated compared to infection with wild-type S. pyogenes.

288 rmed that the cluster was caused by a unique S. pyogenes clone.

289 When S. pyogenes was identified in samples from the epidemic

290 tt and Robin Patel of the Mayo Clinic, where S. pyogenes NAATs have been used for well over a decade

291 ests a novel mechanism of virulence by which S. pyogenes uses its metabolism to modulate innate immun

292 Under experimental conditions in which S. pyogenes is grown in THY medium, the strength of the

293 contributes to the virulence associated with S. pyogenes; however, little is known about its regulati

294 design rules and paired S. aureus Cas9 with S. pyogenes Cas9 to achieve dual targeting in a high fra

295 l infection following a nasal challenge with S. pyogenes M serotype 14.

296 rum IgG, prevented pharyngeal infection with S. pyogenes, and promoted survival.

297 n may be a specific feature of patients with S. pyogenes-induced shock.

298 Our current results with S. pyogenes Glu-AdT support this characterization of Glu

299 recombinant S5nA acted synergistically with S. pyogenes nuclease A to generate macrophage-toxic deox

300 For many years, S. pyogenes testing algorithms used a rapid and specific