ライフサイエンスコーパス: GBS

1 GBS colonized 7%, 21%, and 23% of the infants at birth,

2 GBS contains almost double the number of TCSs compared t

3 GBS CPS III-TT conjugate vaccine significantly delayed a

4 GBS data are increasingly being used to genotype individ

5 GBS has many mechanisms to adapt and survive in its host

6 GBS infection increased levels of total and phosphorylat

7 GBS infections in neonates can cause severe complication

8 GBS possesses a capsule polysaccharide (CPS) with termin

9 GBS produce a pigmented, cytotoxic lipid, known as grana

10 GBS serotype-specific anti-capsular IgG was measured on

11 GBS Sia is known to bind inhibitory Sia-recognizing Ig s

12 GBS-SNP-CROP is a bioinformatics pipeline originally dev

13 ble to detect and successfully annotated 123 GBS loci (10.5%) under positive selection.

14 We describe a genomic analysis of 1345 GBS isolates from neonatal (age 0-89 days) invasive infe

15 Whole-genome sequencing of 15 GBS isolates from 11 laboratories revealed four unique d

16 ed the question of whether the new GII.13/21 GBS really has such a narrow glycan binding spectrum.

17 A total of 356 GBS cases were included, with 60% having LOGBS.

18 A GBS mutant deficient in CPS Sia was more efficiently kil

19 nt sera supports the case for licensure of a GBS polysaccharide-protein conjugate vaccine based on im

20 mber of SNPs (~1,250,000 in total) by adding GBS and 600 K SNP Chip.

21 Additionally, GBS is a bovine pathogen causing intramammary infections

22 than invasive disease, suggesting that adult GBS burden is considerably greater than previously recog

23 role of antibodies in the protection against GBS disease in infancy following maternal exposure to GB

24 rease of functional immune responses against GBS compared to the simple co-administration of GBS67, C

25 fb, the region targeted by the Xpert GBS and GBS LB assays.

26 ores at which the machine learning model and GBS identified patients who met the composite endpoint w

27 Recommendations for antepartum GBS detection include enriched culture with several opti

28 with undetectable baseline (pre-dose 1) anti-GBS levels reached this threshold post-dose 2.

29 with undetectable baseline (predose 1) anti-GBS levels, 90%-98% reached this threshold postdose 2.

30 Among women with undetectable baseline anti-GBS levels, post-dose 2 GMCs in previously GBS-vaccinate

31 Among women with undetectable baseline anti-GBS levels, postdose 2 GMCs in previously GBS-vaccinated

32 Women with undetectable pre-existing anti-GBS concentrations may benefit from a sufficiently space

33 of previously GBS-vaccinated women had anti-GBS concentrations exceeding an arbitrary threshold of 8

34 ously GBS-vaccinated women, 92%-98% had anti-GBS concentrations that exceeded an arbitrary threshold

35 Serotype-specific (Ia/Ib/III) anti-GBS antibodies were measured by multiplex immunoassay pr

36 Serotype-specific (Ia/Ib/III) anti-GBS antibodies were measured by multiplex immunoassay pr

37 monstrate both endogenous production of anti-GBS IgG in juvenile mice and vertical transfer of antibo

38 Women with undetectable preexisting anti-GBS concentrations may benefit from a sufficiently space

39 For each serotype, anti-GBS geometric mean concentrations (GMCs) 30/60 days post

40 For each serotype, anti-GBS geometric mean concentrations (GMCs) 30/60 days post

41 he Hologic Panther Fusion GBS, Luminex Aries GBS, and Cepheid Xpert GBS LB assays, to that of the sta

42 Invasive disease was defined as GBS isolated from a normally sterile site.

43 During pregnancy, ascending GBS infection from the vagina to the intrauterine space

44 The pathogenesis of ZIKV-associated GBS, a potentially life-threatening peripheral nerve dis

45 ance for the pathogenesis of ZIKV-associated GBS.

46 nt women aged 18-40 years and screened to be GBS III vaginal and rectal culture negative were randomi

47 In contrast to IFN-beta, GBS induced TNF-alpha independently of TLR7.

48 e course group, the adjusted OR for a better GBS disability score at 4 weeks was 0.70 (95%CI 0.16 to

49 Both GBS-SNP-CROP versions significantly outperform TASSEL-UN

50 main risk factors for infant colonization by GBS were simultaneous maternal colonization of the vagin

51 The molecular mechanisms used by GBS to survive and proliferate in blood are not well und

52 V-2 could be another viral infection causing GBS.

53 CC17 GBS crosses the intestinal barrier through M cells.

54 hich promote M cell differentiation and CC17 GBS invasiveness.

55 ch 10%, 11%, and 13% were identified as CC17 GBS.

56 5% CI, 23%-56%) of infants colonized by CC17 GBS appeared colonized for the first time at D60 vs 18%

57 C(7) concentrations specifically favor CC17 GBS meningitis following mice oral infection.

58 Our findings provide an explanation for CC17 GBS responsibility in LOD in link with neonatal gastroin

59 ; P < .049) of infants colonized by non-CC17 GBS.

60 The high incidence of CC17 GBS in LOD is likely due to an enhanced post-delivery mo

61 days of life and are largely due to the CC17 GBS hypervirulent clone.

62 Maternal vaccination with whole-cell GBS induces production of GBS-specific IgG in dams that

63 of maternal immunization using a whole-cell GBS vaccine on the duration of intestinal colonization a

64 Low-coverage GBS produces data with a large number of missing or inco

65 Although COVID-GBS patients were more frequently admitted to intensive

66 tatory disorders were more frequent in COVID-GBS than non-COVID-GBS (OR = 27.59, 95% CI = 1.296-587)

67 re more frequent in COVID-GBS than non-COVID-GBS (OR = 27.59, 95% CI = 1.296-587) and COVID-non-GBS (

68 ed the association between naturally-derived GBS serotype-Ia and III IgG and risk reduction of IGbsD

69 r positivity, when PM CDM was used to detect GBS from ChromID, the sensitivity was 100%, with no true

70 aene-mediated hemolysis ex vivo and diminish GBS infection in vivo.

71 id response element (GRE) within each distal GBS.

72 Cloning each GBS into luciferase reporters revealed glucocorticoid-in

73 we selected patients whose modified Erasmus GBS Outcome Score at week 1 predicted a poor prognosis.

74 ve multicenter study in France, we evaluated GBS colonization in mother-baby pairs with 2 months of f

75 In our model, an experimental GBS infection was associated with changes in the miRNA p

76 ng vaccines could be harnessed to facilitate GBS vaccine development.

77 manganese transporter (mtsA) are crucial for GBS survival in whole blood and plasma, (ii) gene W903_1

78 shikimate pathway gene aroA is essential for GBS growth in whole blood and plasma, and (iv) deletion

79 chikungunya infection was a risk factor for GBS (odds ratio, 8.3; 95% confidence interval, 2.3-29.7;

80 e at least 1 of the 3 NAATs was positive for GBS in 155 specimens (31.0%).

81 Criteria included positivity for GBS colonization at antenatal screening or at delivery.

82 ndard of care culture method recommended for GBS screening using 500 vaginal-rectal swab specimens af

83 tified 85 and 41 genes that are required for GBS growth in whole blood and plasma, respectively.

84 ghted, including improving the screening for GBS colonization in pregnant women, offering intrapartum

85 In summary, the Panther Fusion GBS assay has clinical performance comparable to that of

86 on tests (NAATs), the Hologic Panther Fusion GBS, Luminex Aries GBS, and Cepheid Xpert GBS LB assays,

87 estigational trivalent CRM197-glycoconjugate GBS vaccine (targeting serotypes Ia/Ib/III), administere

88 f established in other host niches, however, GBS is highly pathogenic.

89 culture with several options for identifying GBS, some of which are time-consuming.

90 In GBS, more than 20 distinct two-component systems (TCSs)

91 G were 12.6 ug/mL (95% CI, 9.95 to 15.81) in GBS III-TT recipients, representing a 4-fold increase fr

92 etter outcomes after a second IVIg course in GBS with poor prognosis.

93 function and can be the target for damage in GBS, we characterized the interactions of ZIKV isolates

94 Racial differences in GBS disease rates have been previously documented with B

95 ed to characterize the racial disparities in GBS rates, and factors driving them.

96 marizes the GBS and host factors involved in GBS's state as both an asymptomatic colonizer and an inv

97 her a second IVIg course improves outcome in GBS.

98 uite of improvements to date, as realized in GBS-SNP-CROP v.4.0, with specific attention paid to a ne

99 ew discusses the structures of these TCSs in GBS as well as how selected systems regulate essential c

100 ding a fibrinogen-binding adhesin, increases GBS survival in whole blood.

101 Concordance between maternal and infant GBS type was 96%.

102 From the International GBS Outcome Study, we selected patients whose modified E

103 idered the new gold standard for intrapartum GBS screening.

104 cine for protecting infants against invasive GBS disease (IGbsD) will likely need to be based on demo

105 For every invasive GBS infection, 3.7 non-invasive infections occurred.

106 oratory-based surveillance data for invasive GBS disease conducted through Active Bacterial Core surv

107 us (GBS) could protect infants from invasive GBS disease.

108 us (GBS) could protect infants from invasive GBS disease.

109 ts younger than 90 days and who had invasive GBS disease between 2009-2018.

110 spitalization where invasive or non-invasive GBS infections were identified among US adults in a defi

111 We summarise studies that have investigated GBS serum anticapsular or anti-protein antibodies, and s

112 l host-pathogen interactions that mediate LO GBS disease.

113 Passively acquired maternal GBS-specific antibodies protect newborns from early-onse

114 tification and determination of the maternal GBS colonization status, rapid nucleic acid amplificatio

115 performance comparable to that of the BD MAX GBS assay but provides a faster TAT, less HoT, and highe

116 ompared to results obtained using the BD MAX GBS assay on the BD MAX system.

117 DC enriched-culture method and to the BD MAX GBS assay.

118 nformation on the association of breast milk GBS serotype-specific capsular antibodies and risks for

119 t into granadaene and a strategy to mitigate GBS infection, which will be relevant to other toxic lip

120 entification of novel strategies to mitigate GBS virulence.

121 diated regulation of KLF9 involving multiple GBSs is depicted.

122 S isolates responsible for invasive neonatal GBS disease.

123 NeuMoDx GBS assay results were also compared to results obtained

124 The performance of the NeuMoDx GBS assay implemented on the NeuMoDx system compared fav

125 The NeuMoDx GBS assay results yielded a sensitivity of 96.9% (95% co

126 study was conducted to evaluate the NeuMoDx GBS assay, a real-time PCR test performed for vaginal/re

127 -6 years before enrollment (n = 53) or never GBS vaccinated (n = 27) received a single trivalent GBS

128 4-6 years before enrollment (n=53) or never GBS-vaccinated (n=27) received a single trivalent GBS va

129 structural evidence indicating that this new GBS recognizes a group of glycans with a common terminal

130 R = 27.59, 95% CI = 1.296-587) and COVID-non-GBS (OR = 7.875, 95% CI = 1.587-39.09) patients.

131 n exceeded postdose 1 GMCs in previously non-GBS-vaccinated women (>=7-fold).

132 exceeded post-dose 1 GMCs in previously non-GBS-vaccinated women (>=7-fold).

133 versus 36%-56% post-dose 1 in previously non-GBS-vaccinated women.

134 se 2 vs 36%-56% postdose 1 in previously non-GBS-vaccinated women.

135 atients diagnosed with GBS compared with non-GBS ZIKV-infected controls.

136 Notably, GBS induced a TLR7-dependent IFN-beta signal only in MPh

137 formed genome-wide screens to discover novel GBS genes required for bacterial survival in human whole

138 Using the new de novo GBS read simulator GBS-Pacecar, also introduced in this

139 The ability of GBS polysaccharide-protein conjugate vaccines currently

140 We hypothesized that the ability of GBS to elicit varying host responses in maternal decidua

141 glioside antibodies, and serum antibodies of GBS patients.

142 tion-based study outlines the full burden of GBS-associated hospitalization in adults and found incid

143 Serum concentrations of GBS III CPS-specific antibodies were determined using en

144 DM) digital imaging software in detection of GBS from LIM broth plated on ChromID Strepto B chromogen

145 Fusion and BD MAX systems, for detection of GBS in vaginal-rectal screening specimens.

146 For rapid detection of GBS, a three-site clinical study was conducted to evalua

147 ating all three methods for the detection of GBS, the sensitivities of NAAT, ChromID plus PM CDM at 4

148 he digital images and molecular detection of GBS.

149 nical variants and differential diagnoses of GBS.

150 hen cover early recognition and diagnosis of GBS, admission to the intensive care unit, treatment ind

151 spring but does not decrease the duration of GBS intestinal colonization or reduce LO mortality follo

152 linical and laboratory-confirmed evidence of GBS infection from January 2014 through December 2016 fr

153 The relative frequency of GBS among ED patients was higher in COVID (0.15 per mill

154 The incidence of GBS can therefore increase during outbreaks of infectiou

155 Annual incidence of GBS-associated hospitalization was 73 per 100,000 adults

156 GBS acquisition, we assessed the kinetics of GBS GI colonization, progression to invasive disease, an

157 The likelihood of GBS interspecies transmission is largely unknown.

158 Diagnosis and management of GBS can be complicated as its clinical presentation and

159 uideline for the diagnosis and management of GBS.

160 pite its importance to all manifestations of GBS disease, studies towards understanding granadaene's

161 Using a mouse model of GBS-induced peritonitis, we show in this study that the

162 oth perinatal and postnatal murine models of GBS acquisition closely recapitulate the human disease s

163 studies demonstrated that the prevalence of GBS isolates containing deletions in the convenience sam

164 on with whole-cell GBS induces production of GBS-specific IgG in dams that is vertically transmitted

165 ude of the increase is less than the risk of GBS following influenza infection.

166 A possible small increased risk of GBS following influenza vaccination has been identified,

167 ression to invasive disease, and the role of GBS-specific IgG production in exposed offspring and juv

168 ion in future seroepidemiological studies of GBS disease.

169 We explored the potential transmission of GBS between cattle and people on dairy farms in Colombia

170 In addition, vertical transmission of GBS during or after birth results in life-threatening ne

171 ted in acute motor axonal neuropathy type of GBS and in FS, and less frequently in the acute inflamma

172 demyelinating polyneuropathy (AIDP) type of GBS or in central nervous system (CNS) diseases.

173 ch impregnate the fetus during pregnancy, on GBS neonatal infection in cellular and mouse models of h

174 eptococcus pneumoniae, and while research on GBS TCSs has been increasing in recent years, no compreh

175 (GBS) is the cause of early- and late-onset GBS disease in neonates and can present as septicemia, m

176 coccus agalactiae (group B streptococcus, or GBS) is a common cause of bacteremia and sepsis in newbo

177 nt colonization by CC17 at D60 than by other GBS (OR, 2.45; 95% CI, 1.02-5.88).

178 Furthermore, highly pathogenic GBS strains have acquired unique factors that enhance su

179 ernal immunization, a reduction in perinatal GBS disease might be possible.

180 sensitivity was 100%, with no true-positive GBS isolates missed by 48 h of incubation.

181 gression to invasive disease after postnatal GBS exposure in offspring.

182 urine models of both perinatal and postnatal GBS acquisition, we assessed the kinetics of GBS GI colo

183 n or reduce LO mortality following postnatal GBS exposure.

184 as a potential alternative method to prevent GBS disease in infants.

185 i-GBS levels, post-dose 2 GMCs in previously GBS-vaccinated women exceeded post-dose 1 GMCs in previo

186 ti-GBS levels, postdose 2 GMCs in previously GBS-vaccinated women exceeded postdose 1 GMCs in previou

187 s (GMCs) 30/60 days postdose 2 in previously GBS-vaccinated women were >=200-fold higher than baselin

188 (GMCs) 30/60 days post-dose 2 in previously GBS-vaccinated women were >=200-fold higher than baselin

189 92%-98% of previously GBS-vaccinated women had anti-GBS concentrations exceedi

190 90%-98% of previously GBS-vaccinated women with undetectable baseline (pre-dos

191 Of previously GBS-vaccinated women with undetectable baseline (predose

192 Of previously GBS-vaccinated women, 92%-98% had anti-GBS concentration

193 CBP/P300 silencing reduced proximal GBS activity, but negligibly affected KLF9 expression.

194 nt, interactions between distal and proximal GBSs and the TSS correlated with KLF9 induction.

195 While the proximal GBSs drove modest reporter induction by glucocorticoids,

196 of a global collection of recently recovered GBS isolates responsible for invasive neonatal GBS disea

197 ly delayed acquisition of vaginal and rectal GBS III colonization.

198 Using representative GBS isolates, we show that E2-P4 C(7) concentrations spe

199 t alter susceptibility to platelet-resistant GBS.

200 oring systems (the Glasgow-Blatchford score [GBS], admission Rockall score, and AIMS65).

201 Here we have used genotyping by sequencing (GBS) to determine the genetic variation and population s

202 of selection using genotyping by sequencing (GBS).

203 arker approaches - genotyping-by-sequencing (GBS) and Diversity Array Technology (DArT) sequencing -

204 genotyped using a genotyping-by-sequencing (GBS) approach and sequence reads were analyzed for singl

205 Using a genotyping-by-sequencing (GBS) approach, a total of 19,353 SNPs were generated and

206 cterized using the genotyping-by-sequencing (GBS) approach.

207 hism (SNP) array and genotype-by-sequencing (GBS) data.

208 We employed genotyping-by-sequencing (GBS) to investigate how geographical isolation, habitat

209 Genotyping-by-Sequencing (GBS) was applied in a set of 53 diploid Prunus rootstock

210 through paired-end genotyping-by-sequencing (GBS), particularly in the absence of a reference genome.

211 00 SNP markers via genotyping-by-sequencing (GBS).

212 SNP) markers using Genotyping-By-Sequencing (GBS).

213 rkers obtained via genotyping-by-sequencing (GBS).

214 We used genotyping-by-sequencing-(GBS) derived markers to map recombinant inbred line (RIL

215 tion, geometric mean concentrations of serum GBS type III CPS-specific immunoglobulin G were 12.6 ug/

216 Using the new de novo GBS read simulator GBS-Pacecar, also introduced in this note, results show

217 a new, nonconventional glycan binding site (GBS) that binds Le(a) antigen.

218 mon glucocorticoid-induced GR binding sites (GBSs).

219 nism of the alloy is grain boundary sliding (GBS) accommodated by dislocation movement and static rec

220 ave demonstrated less group B streptococcal (GBS) invasive disease and gastrointestinal colonization

221 Group B Streptococci (GBS) are bacteria associated with preterm births, stillb

222 equent human pathogen group B Streptococcus (GBS) and other extracellular bacteria.

223 biofilm production in Group B Streptococcus (GBS) and Staphylococcus aureus.

224 Group B Streptococcus (GBS) can be found to colonize about 25% of all healthy,

225 f pregnant women with group B Streptococcus (GBS) can result in vertical transmission to neonates dur

226 Group B streptococcus (GBS) causes serious diseases in newborn infants, often r

227 immunization against group B streptococcus (GBS) could protect infants from invasive GBS disease.

228 immunization against Group B streptococcus (GBS) could protect infants from invasive GBS disease.

229 rates of early-onset Group B Streptococcus (GBS) disease (EOGBS) have declined since the implementat

230 the impact of infant group B streptococcus (GBS) disease in the United Kingdom.

231 Group B Streptococcus (GBS) frequently colonizes pregnant women and can cause s

232 covalently ligate the Group B Streptococcus (GBS) GBS67 protein antigen with the CpGODN TLR9 agonist.

233 urden of non-invasive Group B Streptococcus (GBS) infections in adults is unknown.

234 Group B streptococcus (GBS) is a beta-hemolytic gram-positive bacterium that co

235 Group B streptococcus (GBS) is a leading cause of young infant mortality and mo

236 GI) colonization with group B Streptococcus (GBS) is an important precursor to late-onset (LO) diseas

237 Group B Streptococcus (GBS) is an opportunistic bacterial pathogen that contrib

238 ococcus agalactiae or group B Streptococcus (GBS) is the cause of early- and late-onset GBS disease i

239 Group B Streptococcus (GBS) is the leading cause of invasive bacterial neonatal

240 Group B streptococcus (GBS) is the leading cause of neonatal invasive disease w

241 Group B Streptococcus (GBS) is the leading cause of neonatal sepsis and meningi

242 inoculation of either group B Streptococcus (GBS) or saline (n = 5/group).

243 Licensure of a Group B streptococcus (GBS) polysaccharide-protein conjugate vaccine for protec

244 the neonatal pathogen group B Streptococcus (GBS) to be remarkably resistant to platelet killing.

245 Group B Streptococcus (GBS), is a leading cause of neonatal death and an emergi

246 ichia coli (E. coli), Group B Streptococcus (GBS), Listeria monocytogenes, Haemophilus influenzae, S.

247 f acquisition of CC17 group B Streptococcus (GBS), the hypervirulent clone responsible for late-onset

248 al pathogens, such as group B Streptococcus (GBS).

249 ptococcus agalactiae (group B Streptococcus [GBS]) from several geographic locations in the United St

250 ptococcus agalactiae (group B Streptococcus [GBS]) is an important cause of invasive infection in new

251 l host factors also exist that either subdue GBS upon vaginal colonization or alternatively permit in

252 Guillain-Barre syndrome (GBS) and Fisher syndrome (FS) are acute autoimmune neuro

253 We diagnosed 11 Guillain-Barre syndrome (GBS) cases among 71,904 COVID patients attended at 61 Sp

254 24 cases developed Guillain-Barre syndrome (GBS) during the 2014 chikungunya outbreak in the French

255 ies in Zika-induced Guillain-Barre syndrome (GBS) has not yet been investigated.

256 Guillain-Barre syndrome (GBS) is a rare, but potentially fatal, immune-mediated d

257 l abnormalities and Guillain-Barre syndrome (GBS).

258 (3) vaccine-induced Guillain-Barre syndrome (GBS); (4) vaccine-induced autoimmune diseases; (5) safet

259 hibitory Siglec-9 on their surface, and that GBS can engage this receptor in a Sia-dependent manner t

260 We conclude that GBS Sia has dual roles in counteracting platelet antimic

261 composite endpoint with an AUC of 0.90, the GBS with an AUC of 0.87 (P = .004), the Rockall score wi

262 The primary endpoint, the GBS disability scale at 4 weeks, was assessed with multi

263 ite endpoint with AUC values of 0.88 for the GBS (P = .001), 0.73 for Rockall score (P < .001), and 0

264 Our findings provide new insight into the GBS-host interactions in human blood.

265 This review summarizes the GBS and host factors involved in GBS's state as both an

266 er RNA (eRNA) production from three of these GBSs in BEAS-2B cells.

267 This GBS dataset was used to identify candidate SNPs under se

268 se in infancy following maternal exposure to GBS colonization.

269 ing both perinatal and postnatal exposure to GBS, with 21% and 27%, respectively, developing invasive

270 rve to reduce fetal and neonatal exposure to GBS.

271 reversed platelet suppression in response to GBS infection.

272 family protein, contributes significantly to GBS survival in whole blood, (iii) the shikimate pathway

273 owing infection, both of which could trigger GBS-associated pregnancy complications.

274 eviously vaccinated with 1 dose of trivalent GBS vaccine 4-6 years before enrollment (n = 53) or neve

275 iously vaccinated with one dose of trivalent GBS vaccine 4-6 years before enrollment (n=53) or never

276 A second trivalent GBS vaccine dose administered 4-6 years post-dose 1 was

277 A second trivalent GBS vaccine dose administered 4-6 years postdose 1 was i

278 cinated (n = 27) received a single trivalent GBS vaccine injection.

279 accinated (n=27) received a single trivalent GBS vaccine injection.

280 Two GBSs mapped to the 5'-proximal region relative to KLF9 t

281 Additionally, we used GBS data from the 270 field clones from which the labora

282 irst comprehensive GWAS study on olive using GBS.

283 among targeted trees was uncovered utilizing GBS (Genotyping by Sequencing) platform.

284 For time to first acquisition of vaginal GBS III, vaccine efficacy was 36% (95% confidence interv

285 Here, using a highly virulent GBS strain and transposon-directed insertion site sequen

286 Although the mechanisms by which GBS traffics from the lower genital tract to vulnerable

287 capitulate the human disease state, in which GBS colonizes the intestine and causes LO disease.

288 h the machine learning model versus 12% with GBS (P < .001).

289 Among 1076 adults with GBS infection, median age was 52 years, 51% were male, a

290 o define an immune correlate associated with GBS disease risk reduction on the basis of studies of na

291 ters to DENV and to ZIKV are associated with GBS during ZIKV infection.

292 tection of pups from a lethal challenge with GBS.

293 Intestinal colonization with GBS induces an endogenous IgG response within 20 days of

294 NV2 in ZIKV-infected patients diagnosed with GBS compared with non-GBS ZIKV-infected controls.

295 al cells (dT-HESCs) following infection with GBS strains from septic neonates or colonized mothers.

296 n the acute-phase sera of some patients with GBS suggested the carbohydrate-carbohydrate interaction

297 high levels of Cxcl2 after stimulation with GBS or other bacteria.

298 on GBS, Luminex Aries GBS, and Cepheid Xpert GBS LB assays, to that of the standard of care culture m

299 n gene cfb, the region targeted by the Xpert GBS and GBS LB assays.

300 zed during verification studies of the Xpert GBS assay in 12 laboratories between 2012 and 2018.