ライフサイエンスコーパス: GBS

1 GBS colonizes pregnant women worldwide, but prevalence a

2 GBS commonly colonizes the lower gastrointestinal and ge

3 GBS expressing pneumococcal NanA had increased invasion

4 GBS is likely an important cause of stillbirth, especial

5 GBS is most commonly used on crop plant genomes, and bec

6 GBS meningitis is an important risk factor for moderate

7 of the isolates (n = 172) identified all 10 GBS serotypes, most commonly types Ia (40% [69/172 isola

8 We included articles with >/=200 GBS colonized pregnant women that reported IAP coverage.

9 We identified 30 articles including 20328 GBS-colonized pregnant women for inclusion.

10 ak of severe invasive sequence type (ST) 283 GBS infections in adults epidemiologically linked to the

11 th existing methods, we developed GB-eaSy, a GBS bioinformatics workflow that incorporates widely use

12 ed, for the first time, M. pneumoniae from a GBS patient with antibodies against galactocerebroside (

13 tion as an alternative substrate to modify a GBS component in a manner that impairs growth kinetics.

14 Phenotypic screening of a GBS transposon insertion library identified a mutation w

15 All patients with GBS or a GBS variant who presented to the adult neurology departm

16 rtion library identified a mutation within a GBS-specific gene encoding a putative glycosyltransferas

17 ed, and we were unable to estimate NDI after GBS sepsis.

18 that the protective effect of MCPT4 against GBS dissemination and preterm labor can be attributed in

19 nvolved in proinflammatory responses against GBS, as well as the contribution of signaling modulators

20 Streptococcus agalactiae (GBS) is the leading cause worldwide of neonatal sepsis.

21 The risk of EOGBS among GBS-colonized pregnant women, from this first systematic

22 -friendly computer programs that can analyze GBS data on desktop computers.

23 We show that PMA, C. albicans and GBS use a related pathway for NET induction, whereas ion

24 tific bottlenecks in existing SNP arrays and GBS technologies and the strategies to develop targeted

25 and SELENBP1 was common to ZIKV, dengue, and GBS infection; ATF5, TNFAIP3, and BAMB1 were common to Z

26 e from outbreaks of Zika virus infection and GBS is that Zika virus infection is a trigger of GBS.

27 examined maternal and perinatal outcomes and GBS serotypes.

28 clarify the relation between HIV-status and GBS carriage.

29 que, we analyzed Zika virus surveillance and GBS data from Martinique in real time with a modeling fr

30 The primary outcomes were tolerability and GBS-specific antibody response (measured as geometric me

31 o determine the prevalence of HEV-associated GBS in a Belgian cohort, study the clinical spectrum of

32 but the clinical spectrum of HEV-associated GBS is not yet documented, and diagnosing acute HEV infe

33 tudy the clinical spectrum of HEV-associated GBS, and discuss difficulties in diagnosing acute HEV in

34 fectious temporal profile of ZIKV-associated GBS (ZIKV-GBS) has been described in clinical studies, w

35 We review all available GBS data worldwide, including maternal GBS colonization,

36 for which no reference genome is available, GBS-SNP-CROP is worth consideration by curators, researc

37 uses and offspring of pregnant women and (b) GBS in any population, and to describe the process and o

38 We aimed to assess the association between GBS maternal colonization and preterm birth in order to

39 ttle is known about the relationship between GBS and vaginal microbiota.

40 There was no relationship between GBS carriage and demographic characteristics, alpha-dive

41 Significant clustering by GBS status was noted on principal coordinates analysis,

42 notyping datasets like the ones generated by GBS; (ii) direct importation and conversion of Variant C

43 ntilation), and ability to walk (measured by GBS disability score).

44 onfidence interval [CI], 13 to 17%]) carried GBS; among 68 babies born to mothers with carriage, 26 (

45 Deletion of nonA did not change GBS-whole blood survival or brain microvascular cell inv

46 Present and future circulating GBS organisms and their genetic diversity may influence

47 s' gestation) and maternal GBS colonization (GBS isolation from vaginal, cervical, and/or rectal swab

48 tracycline resistance (89%) among colonizing GBS isolates.

49 I-V account for 98% of identified colonizing GBS isolates worldwide.

50 eonates could be an effective way to control GBS diseases.

51 immune defenses are critical for controlling GBS dissemination and systemic infection.

52 a robust real-time PCR assay for determining GBS serotypes.

53 otential and lower probability of developing GBS following infection in Martinique, the total number

54 al cell-derived mast cell lysates diminished GBS adherence.

55 An effective GBS vaccine could reduce disease in the mother, the fetu

56 ously randomized (1:1:1:1) to receive either GBS vaccine at dosages of 0.5, 2.5, or 5.0 mug of each o

57 portant cytotoxin implicated in facilitating GBS invasion.

58 Across all five GBS analysis platforms, SNP calls showed unexpectedly lo

59 We compared the performance of five GBS pipelines using low-coverage Illumina sequence data

60 the percentage of infants with NDI following GBS meningitis.

61 For GBS, we included 36 items, of which more than half the r

62 Brazilian outbreak of ZIKV), admissions for GBS increased from a mean of 1.0 per month to 5.6 per mo

63 All patients fulfilled the criteria for GBS and had severe disease (defined as not being able to

64 e assessed at birth, day (D) 43, and D91 for GBS serotypes; 1 month postdose 3 (D127) for diphtheria;

65 ntified 16 genes conditionally essential for GBS survival in blood, of which 75% were members of the

66 e, the single most important risk factor for GBS neonatal disease.

67 ages revealed that PKD1 is indispensable for GBS-mediated activation of MAPKs and NF-kappaB and subse

68 ococcus (GBS) is the most common pathway for GBS disease in mother, fetus, and newborn.

69 o identify molecular mechanisms required for GBS to transition from a mucosal commensal lifestyle to

70 mples from nonpregnant women were tested for GBS, and amplicon-based sequencing targeting the 16S rib

71 We recorded prospective data from GBS meeting levels 1 or 2 of diagnostic certainty for th

72 of biomarkers associated with recovery from GBS.

73 ith an investigational CRM197-glycoconjugate GBS vaccine elicited higher GBS serotype-specific antibo

74 patients positive for ZIKV infection, 27 had GBS (18 demyelinating, 8 axonal, and 1 Miller Fisher syn

75 h carriage, 26 (38% [95% CI, 27 to 51%]) had GBS on their body surfaces, indicating vertical transmis

76 Patients misdiagnosed as having GBS were retrospectively excluded from the study.

77 7-glycoconjugate GBS vaccine elicited higher GBS serotype-specific antibody levels in infants until 9

78 Maternal vaccination led to higher GBS serotype-specific antibody concentrations in infants

79 of the protective response against type III GBS polysaccharide.

80 ve group B Streptococcus, capsular type III (GBS-III) bacteria resulted in augmented serum polysaccha

81 oglobulin (Ig) M antibodies were detected in GBS patients and healthy controls in 3% and 0% of adults

82 ing genomewide assessment of gene fitness in GBS.

83 Here we analyze NonA function in GBS pathogenesis, and through heterologous expression of

84 stent with this observation, the increase in GBS dissemination and preterm births observed in MCPT4-d

85 Mortality was significantly increased in GBS-associated NE vs NE alone (risk ratio, 2.07 [95% CI,

86 r, forced expression of pneumococcal NanA in GBS removed terminal sialic acid residues from the bacte

87 us expression of active pneumococcal NanA in GBS, potential costs of maintaining sialidase function.

88 dhesive properties linked to pathogenesis in GBS.

89 d us to unravel the role of M. pneumoniae in GBS in a case-control study.

90 hat PKD1 plays a critical regulatory role in GBS-induced proinflammatory reactions and sepsis, and in

91 vation together with antibiotic treatment in GBS-infected neonates could be an effective way to contr

92 Higher IFN-beta levels in vivo increase GBS killing by the host.

93 Additionally, increased GBS systemic infection and preterm births were observed

94 axis), maternal GBS disease, neonatal/infant GBS disease, and subsequent impairment, plus GBS-associa

95 The incidence of infant GBS disease remains high in some regions, particularly A

96 aimed to estimate NDI in survivors of infant GBS disease.

97 ms and their genetic diversity may influence GBS vaccine development.

98 estimates address data gaps to better inform GBS interventions including maternal immunization?

99 these patients presented with an infrequent GBS variant.

100 ished data on the risk of NDI after invasive GBS disease in infants <90 days of age.

101 S) might provide protection against invasive GBS disease in infants.

102 d reduce vaccine protection against invasive GBS disease.

103 ute to increased susceptibility for invasive GBS disease in HIV-exposed uninfected infants.

104 desh has all of the ingredients for invasive GBS disease, including colonization of mothers by invasi

105 ated the global incidence of infant invasive GBS disease and the associated serotypes, updating previ

106 S colonization, (2) cases of infant invasive GBS disease, (3) deaths, and (4) disabilities.

107 The pooled incidence of invasive GBS disease in infants was 0.49 per 1000 live births (95

108 re 33000 (UR, 13000-52000) cases of invasive GBS disease in pregnant or postpartum women, and 57000 (

109 pus) and sought unpublished data on invasive GBS disease in women pregnant or within 42 days postpart

110 d sought unpublished data regarding invasive GBS disease in infants aged 0-89 days.

111 ection/stillbirth, and infants with invasive GBS disease presenting with neonatal encephalopathy.

112 h that observed among patients with invasive GBS infections in metropolitan Toronto.

113 sidered to be the main driver of serotype IV GBS expansion in North America.

114 Whole genome sequencing of 70 type IV GBS and subsequent phylogenetic analysis elucidated the

115 ithin the non-Lactobacillus-dominant CST IV, GBS positive status was significantly more prevalent in

116 e found that both live and antibiotic-killed GBS induce activation of PKD1 through a pathway that is

117 k-mediated death caused by antibiotic-killed GBS.

118 Lower GBS maternal colonization prevalence, with less serotype

119 less serotype III, may help to explain lower GBS disease incidence in regions such as Asia.

120 need to plan health-care resources to manage GBS patients.

121 Maternal GBS colonization was less common in women with low socio

122 Maternal GBS vaccines are in development.

123 rm birth (<37 weeks' gestation) and maternal GBS colonization (GBS isolation from vaginal, cervical,

124 al to inform interventions, such as maternal GBS vaccination.

125 Our adjusted estimate for maternal GBS colonization worldwide was 18% (95% confidence inter

126 livery should be included in future maternal GBS vaccine trials.

127 lable GBS data worldwide, including maternal GBS colonization, risk of neonatal disease (with/without

128 Most maternal GBS disease was detected at or after delivery.

129 lyses to derive pooled estimates of maternal GBS colonization prevalence at national and regional lev

130 s the denominator, the incidence of maternal GBS disease was 0.38 (95% confidence interval [CI], .28-

131 d of 11, estimates the incidence of maternal GBS disease worldwide.

132 ooled estimates of the incidence of maternal GBS disease.

133 ed data from investigator groups on maternal GBS colonization and neonatal outcomes.

134 Incidence data on maternal GBS disease in developing regions are lacking.

135 ntrapartum antibiotic prophylaxis), maternal GBS disease, neonatal/infant GBS disease, and subsequent

136 l model to estimate (1) exposure to maternal GBS colonization, (2) cases of infant invasive GBS disea

137 k ratio (RR) for preterm birth with maternal GBS colonization to be 1.21 (95% confidence interval [CI

138 at preterm birth is associated with maternal GBS colonization, especially where there is evidence of

139 ce bioinformatics pipeline that can maximize GBS data usage and perform high-density SNP genotyping i

140 proach integrating the results from multiple GBS bioinformatics pipelines may be the optimal strategy

141 ss the Netherlands participating in national GBS studies from May 5, 1986, through August 2, 2000.

142 s assessing the association between neonatal GBS disease and HIV-status of the mother and studies tha

143 e more than twice as likely to have neonatal GBS disease compared to unexposed neonates.

144 imes more likely to have late-onset neonatal GBS disease.

145 lic health interventions preventing neonatal GBS disease are urgently needed for the increasing group

146 o increase the accuracy and accessibility of GBS data analysis.

147 le, the seventh in a series on the burden of GBS disease, aims to estimate this risk and how it varie

148 e sixth in a series estimating the burden of GBS disease.

149 10th of 11 articles estimating the burden of GBS disease.

150 n 11-article series estimating the burden of GBS disease; here we aim to assess the proportion of GBS

151 ng: (1) Why estimate the worldwide burden of GBS disease?

152 Data on the burden of GBS in Asian countries are lacking.

153 second in a series estimating the burden of GBS, aims to determine the prevalence and serotype distr

154 n order to inform estimates of the burden of GBS.

155 sed to transparently estimate this burden of GBS?

156 ongers were screened for enteric carriage of GBS.

157 ns to confirm the expected growth defects of GBS deficient in capsule or stringent response activatio

158 at arginine availability is a determinant of GBS cytotoxicity and that the pathway between stringent

159 the prevalence and serotype distribution of GBS colonizing pregnant women worldwide.

160 d nasal swabs, and (iii) the distribution of GBS serotypes.

161 ion and negative screening for etiologies of GBS.

162 work sheds further light on the evolution of GBS providing new insights on the recent emergence of se

163 e the clinical profiles and the frequency of GBS associated with ZIKV during the ZIKV outbreak in Mar

164 O property to directly inhibit the growth of GBS independent of host immunity.

165 This equates to a UK incidence of GBS-associated NE of 0.019 per 1000 live births.

166 lation-level data estimated the incidence of GBS-associated NE.

167 In infants of GBS vaccine recipients, GBS serotype-specific antibody g

168 the microbiota in promotion or inhibition of GBS colonization.

169 y RT-PCR should be part of the management of GBS cases.

170 cted persons, and the clinical management of GBS cases.

171 A deeper understanding of the mechanisms of GBS infections during pregnancy will facilitate the deve

172 infection in Martinique, the total number of GBS cases in Martinique would be substantially lower tha

173 tion, and the clinical course and outcome of GBS in patients treated with intravenous immunoglobulin

174 (2) What outcomes of GBS in pregnancy should be included?

175 derive pooled estimates of the percentage of GBS-associated stillbirths, regionally and worldwide for

176 loidy and repeat content, the performance of GBS analysis software can vary by target organism.

177 ng the outbreak, 30 had a proven presence of GBS, and 23 had a recent ZIKV infection.

178 to enhance the scope of global prevention of GBS disease.

179 Prevention of GBS infection in pregnancy is complex and is likely infl

180 Meta-analyses estimated the proportion of GBS disease in NE and mortality risk.

181 The consistent increased proportion of GBS disease in NE and significant increased risk of mort

182 ase; here we aim to assess the proportion of GBS in NE cases.

183 mics of the Zika virus epidemic, the risk of GBS in Zika virus-infected persons, and the clinical man

184 Given the severity of GBS, territories affected by Zika virus need to plan hea

185 All 18 studies followed up survivors of GBS meningitis; only 5 of these studies also followed up

186 these studies also followed up survivors of GBS sepsis and were too few to pool in a meta-analysis.

187 The timing of GBS disease suggests that a maternal vaccine given in th

188 ants and the amount of placental transfer of GBS serotype-specific antibodies from mothers to their i

189 e, (ii) the rate of vertical transmission of GBS, as determined by culturing ear, umbilicus, and nasa

190 is that Zika virus infection is a trigger of GBS.

191 congenital abnormalities and is a trigger of GBS.

192 ts in their workup of underlying triggers of GBS.

193 portant advancements in our understanding of GBS vaginal colonization, ascending infection, and prete

194 . chinensis), the reference-based version of GBS-SNP-CROP behaved similarly to TASSEL-GBS in terms of

195 bloodstream invasion, we performed Tn-seq on GBS strain A909 with human whole blood.

196 r rectal swabs; with separate subanalysis on GBS bacteriuria).

197 use either congenital brain abnormalities or GBS but agreed that the evidence was sufficient to recom

198 Compared to other GBS pipelines, GB-eaSy rapidly and accurately identified

199 GBS disease, and subsequent impairment, plus GBS-associated stillbirth, preterm birth, and neonatal e

200 duplicated genome, relatively little public GBS data and few dedicated tools.

201 l simplifies the preparation of high-quality GBS sequencing libraries.

202 gned for libraries of paired-end (PE) reads, GBS-SNP-CROP maximizes data usage by eliminating unneces

203 In infants of GBS vaccine recipients, GBS serotype-specific antibody geometric mean concentrat

204 etween HIV infection status and rectovaginal GBS carriage.

205 ssessed the association between rectovaginal GBS colonization and HIV status in women.

206 rstand (i) the rate of maternal rectovaginal GBS carriage, (ii) the rate of vertical transmission of

207 men is associated with maternal rectovaginal GBS carriage, the single most important risk factor for

208 shed data from investigator groups reporting GBS-associated NE.

209 Here we aimed to review GBS screening policies and IAP implementation worldwide.

210 -specific contacts to a GR-binding sequence (GBS) half-site found embedded within the TRE motif.

211 Genotyping by sequencing (GBS) generates datasets that are challenging to handle b

212 In this study genotyping-by- sequencing (GBS) was used to construct the high-density linkage map.

213 xplored the use of Genotyping-By-Sequencing (GBS) in Iranian cannabis.

214 ughput genome wide genotyping-by-sequencing (GBS) method was used to generate 515,787 single nucleoti

215 different types of genotyping-by-sequencing (GBS) platforms have been developed in over 25 crop speci

216 Genotyping-by-sequencing (GBS), a method to identify genetic variants and quickly

217 e range, 56-71 years) and experienced severe GBS.

218 apacity is required for management of severe GBS cases.

219 ive activity of nearly all GR binding sites (GBSs) captured using chromatin immunoprecipitation (ChIP

220 Some GBS cases do not exhibit a high level of diagnostic cert

221 Survivors of infant group B streptococcal (GBS) disease are at risk of neurodevelopmental impairmen

222 however, the role of group B streptococcal (GBS) disease has not been reviewed.

223 ries on the burden of group B streptococcal (GBS) disease, aims to estimate the percentage of stillbi

224 ents most early-onset group B streptococcal (GBS) disease.

225 Group B streptococci (GBS) are one of the leading causes of life-threatening i

226 Infections such as group B Streptococcus (GBS) are an important cause of maternal sepsis, yet limi

227 Group B streptococcus (GBS) capsular serotypes are major determinants of virule

228 in the prevention of group B Streptococcus (GBS) disease with the introduction of intrapartum antibi

229 Group B streptococcus (GBS) infection is a leading cause of death among newborn

230 Group B Streptococcus (GBS) is an encapsulated, gram-positive pathogen that is

231 Group B Streptococcus (GBS) is an important perinatal pathogen, although previo

232 nal colonization with group B Streptococcus (GBS) is the most common pathway for GBS disease in mothe

233 tion structure of 102 group B Streptococcus (GBS) isolates prospectively sampled in 2014 from vaginal

234 s have suggested that group B Streptococcus (GBS) maternal rectovaginal colonization during pregnancy

235 l vaccination against group B Streptococcus (GBS) might provide protection against invasive GBS disea

236 Group B Streptococcus (GBS) or Streptococcus agalactiae are beta-hemolytic gram

237 Group B streptococcus (GBS) or Streptococcus agalactiae is a beta-hemolytic, Gr

238 Group B Streptococcus (GBS) remains a leading cause of neonatal sepsis in high-

239 ransfer specific to 8 group B Streptococcus (GBS) surface proteins among 81 HIV-uninfected and 83 HIV

240 inally colonized with group B Streptococcus (GBS), but the risk of EOGBS from vertical transmission h

241 ates of the burden of group B Streptococcus (GBS), including invasive disease in pregnant and postpar

242 ptococcus agalactiae (group B Streptococcus [GBS]) causes serious infections in neonates.

243 ptococcus agalactiae (group B Streptococcus [GBS]) has not been described as a foodborne pathogen.

244 ptococcus agalactiae (group B Streptococcus [GBS]) is an important neonatal pathogen and emerging cau

245 ptococcus agalactiae (group B streptococcus, GBS) causes neonatal disease and stillbirth, but its bur

246 ptococcus agalactiae (group B Streptococcus, GBS) is a leading cause of invasive bacterial infections

247 Of the sample of 34 patients with suspected GBS during the outbreak, 30 had a proven presence of GBS

248 urological disorder Guillain-Barre syndrome (GBS) and of microcephaly and other congenital brain abno

249 ted with a surge in Guillain-Barre syndrome (GBS) cases.

250 Guillain-Barre syndrome (GBS) has been reported to be associated with Zika virus

251 Guillain-Barre syndrome (GBS) is an immune-mediated peripheral neuropathy.

252 Clinically, Guillain-Barre syndrome (GBS) predominated among regions affected by the ZIKV epi

253 cedent infection in Guillain-Barre syndrome (GBS), but the clinical spectrum of HEV-associated GBS is

254 s hospitalized with Guillain-Barre syndrome (GBS), meningoencephalitis, or transverse myelitis.

255 me in patients with Guillain-Barre syndrome (GBS).

256 ications (including Guillain-Barre syndrome [GBS]) with ZIKV infection.

257 gate the contribution of chymase to systemic GBS infection and rates of preterm birth.

258 of GBS-SNP-CROP behaved similarly to TASSEL-GBS in terms of the number of SNPs called but had an imp

259 sed risk of mortality provides evidence that GBS infection contributes to NE.

260 Our conservative estimates suggest that GBS is a leading contributor to adverse maternal and new

261 The GBS PSIII epitope is made by six sugars.

262 led in cohort 1 (40 randomly assigned to the GBS 20 mug group and 40 randomly assigned to the placebo

263 te numbers of preterm births attributable to GBS.

264 illion preterm births may be attributable to GBS.

265 a CST and alpha-diversity are not related to GBS status.

266 sin-like cleavage specificity in response to GBS.

267 acquired immunoglobulin G (IgG) responses to GBS capsular polysaccharides (CPS) and pilus proteins in

268 Proinflammatory responses to GBS mediated through host innate immune receptors play a

269 D (PKD)1 in the proinflammatory responses to GBS.

270 the kinetics of transplacentally transferred GBS serotype-specific capsular antibodies in the infants

271 d 7 ventilators would be sufficient to treat GBS cases.

272 unogenicity of a CRM197-conjugated trivalent GBS vaccine in non-pregnant and pregnant women, and anti

273 centre study of an investigational trivalent GBS vaccine in healthy non-pregnant women (cohort 1), an

274 ed transcriptome sequencing (RNA-seq) on two GBS strains grown under stringent response or control co

275 We assessed maternal recto-vaginal GBS colonization (7,967 women), stillbirth and neonatal

276 , yellow fever, Japanese encephalitis virus, GBS, and control datasets.

277 d in MCPT4-deficient mice was abolished when GBS was deficient in expression of the fibronectin-bindi

278 , HIV infection and undernutrition, but when GBS-colonized, they were more probably colonized by the

279 ositive for ZIKV infection (6%) died (1 with GBS and 1 with encephalitis), 18 (51%) had chronic pain,

280 e enrolled, including 29 patients (73%) with GBS (90% Brighton level 1 certainty), 7 (18%) with encep

281 Preterm birth was associated with GBS bacteriuria in cohort studies (RR, 1.98 [95% CI, 1.4

282 re found to be significantly associated with GBS carriage by linear discriminant analysis.

283 tify the total burden of NDI associated with GBS disease, and inform program priorities.

284 he percentage of stillbirths associated with GBS disease.

285 HEV infection was frequently associated with GBS in our cohort.

286 HIV exposure of neonates is associated with GBS neonatal disease.

287 The proportion of NE associated with GBS was 0.58% (95% confidence interval [CI], 0.18%-.98%)

288 city, 4 taxa were positively associated with GBS, and 6 were negatively associated.

289 5% CI, 2%-6%) in Africa were associated with GBS.

290 und in 4% of adults and 25% of children with GBS (p = 0.001).

291 ly >/=28 weeks' gestation or >/=1000 g, with GBS isolated from a sterile site) as a percentage of tot

292 levels were determined in 174 patients with GBS (mean [SD] age, 49.6 [20.1] years; 99 males [56.9%])

293 mples derived from a cohort of patients with GBS admitted to hospitals across the Netherlands partici

294 Patients with GBS may develop hypoalbuminemia after treatment with IVI

295 All patients with GBS or a GBS variant who presented to the adult neurolog

296 treatment response to IVIG in patients with GBS.

297 F; and NAMPT and PMAlP1 were common to ZIKV, GBS, and WNF.

298 Mechanisms for ZIKV-GBS and other neurological syndromes have been hypothesi

299 emporal profile of ZIKV-associated GBS (ZIKV-GBS) has been described in clinical studies, which may s

300 ST283 is a zoonotic GBS clone associated with farmed freshwater fish, capabl