ライフサイエンスコーパス: pestis

1 uropean Black Death/bubonic plague (Yersinia pestis).

2 pulations confer heightened resistance to Y. pestis.

3 rfaH in Y. pseudotuberculosis but not in Y. pestis.

4 rticipate in broadening the host range of Y. pestis.

5 ague strains are basal to all known Yersinia pestis.

6 equences, of which the majority are Yersinia pestis.

7 eadly respiratory disease caused by Yersinia pestis.

8 ghtly controlled virulence determinant of Y. pestis.

9 Hfq in the closely related species Yersinia pestis.

10 ense in mice challenged intranasally with Y. pestis.

11 face protein of the deadly pathogen Yersinia pestis.

12 k to patients with laboratory evidence of Y. pestis.

13 lenged with inhaled lethal doses of Yersinia pestis.

14 CDC category A/B pathogens such as Yersinia pestis.

15 ened IL-1beta specifically in response to Y. pestis.

16 e or mutation provides protection against Y. pestis.

17 hoQ system, OmpR-EnvZ was the only one of Y. pestis' 23 other 2CSs required for production of bubonic

18 long-read nanopore sequencer (MinION) for Y. pestis (6.5 h) and B. anthracis (8.5 h) and sequenced st

19 Plague is initiated by Yersinia pestis, a highly virulent bacterial pathogen.

20 more, following intranasal infection with Y. pestis, A2AP-deficient mice exhibit no difference in sur

21 studied the interaction between the Yersinia pestis ABC heme importer (HmuUV) and its partner substra

22 ion limits initial growth but facilitates Y. pestis access to a protected replicative niche.

23 Y. pestis actively inhibits the innate immune system to gen

24 Yersinia pestis adopts a unique life stage in the digestive tract

25 uence of a singular introduction of Yersinia pestis, after which the disease established itself in Eu

26 Y. pestis Ail interacts with the regulatory factors Vn and

27 These findings demonstrate that Y. pestis Ail uses multiple extracellular loops to interact

28 F130, are required for the interaction of Y. pestis Ail with Vn, factor H and C4BP.

29 Here, we show that Y. pestis also inhibits release of granules in a T3SS-depen

30 ble in <4 h for B. anthracis and <6 h for Y. pestis and B. pseudomallei One exception was B. pseudoma

31 t Staphylococcus aureus, as well as Yersinia pestis and Bacillus anthracis, organisms of biodefense i

32 ame species, including 5 strains of Yersinia pestis and Bacillus anthracis.

33 r displayed 100% (n = 59) inclusivity for Y. pestis and consistent intraspecific signal transduction

34 irst global analysis of AI-2 signaling in Y. pestis and identifies potential roles for the system in

35 This response was not specific to Y. pestis and involved a reduced sensitivity to M2 polariza

36 0 nM between EGFP-labeled LcrV from Yersinia pestis and its cognate membrane-bound protein YopB inser

37 kines important to host responses against Y. pestis and many other infectious agents.

38 n the importance of neutrophils in AMI to Y. pestis and may provide a new correlate of protection for

39 atform for intranasal vaccination against Y. pestis and other infectious pathogens.

40 teins based on the roles of their aligned Y. pestis and S. enterica partners and showed that up to 73

41 igmentation locus-negative (pgm(-)) Yersinia pestis and that this phenotype maps to a 30-centimorgan

42 bacterial spread is key to understanding Y. pestis and the immune responses it encounters during inf

43 e protective F1 capsular antigen of Yersinia pestis and the LcrV protein required for secretion of vi

44 ication of new virulence factors in Yersinia pestis and understanding their molecular mechanisms duri

45 Studies in Y. pestis and Y. pseudotuberculosis have shown that YopM su

46 e in a strain-specific manner and only in Y. pestis and Y. pseudotuberculosis.

47 erences in virulence genes found in Yersinia pestis and Yersinia pseudotuberculosis compared to other

48 J-dependent cytotoxicity induced by Yersinia pestis and Yersinia pseudotuberculosis paradoxically lea

49 monella enterica serovar Typhi, and Yersinia pestis), and 3 protozoa (Leishmania spp., Plasmodium spp

50 ptibility by 50% to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to conventional met

51 n resistance in Bacillus anthracis, Yersinia pestis, and Francisella tularensis.

52 pathogen interactions of B. mallei, Yersinia pestis, and Salmonella enterica.

53 ogressive stages of the disease with anti-Y. pestis antibodies alone or in combination with the corti

54 y on the surface of many mammalian cells, Y. pestis appears to prefer interacting with certain types

55 tularensis, Bacillus anthracis, and Yersinia pestis are tier 1 select agents with the potential to ra

56 he most severe form of infection by Yersinia pestis, are needed, as past US Food and Drug Administrat

57 unded fears of the intentional release of Y. pestis as a biological weapon.

58 t steps in the evolution and emergence of Y. pestis as a flea-borne pathogen.

59 Deletion of Pla results in a decreased Y. pestis bacterial burden in the lung and failure to progr

60 cally documented pandemic caused by Yersinia pestis began as the Justinianic Plague in 541 within the

61 Y. pestis biofilm formation has been studied in the rat fle

62 cyclic diguanylate is essential for Yersinia pestis biofilm formation that is important for blockage-

63 9th century intestinal specimen and Yersinia pestis ("Black Death" plague) in a medieval tooth, which

64 that multiple and independent lineages of Y. pestis branched and expanded across Eurasia during the N

65 he bacteria Francisella tularensis, Yersinia pestis, Burkholderia mallei, and Brucella species.

66 epticemic infection by the KIM5 strain of Y. pestis but not to infection by the CO92 Deltapgm strain.

67 Wild-type Y. pestis, but not a Pla mutant (Deltapla), degrades FasL,

68 ved from the recognition of intracellular Y. pestis by host Toll-like receptor 7 (TLR7).

69 The 14th-18th century pandemic of Yersinia pestis caused devastating disease outbreaks in Europe fo

70 enomes from Southern Siberia suggest that Y. pestis caused some form of disease in humans prior to th

71 Yersinia pestis causes a rapid, lethal disease referred to as pla

72 Yersinia pestis causes bubonic plague, a fulminant disease where

73 Yersinia pestis causes bubonic, pneumonic, and septicemic plague,

74 Yersinia pestis causes bubonic, pneumonic, and septicemic plague.

75 Yersinia pestis causes the fatal respiratory disease pneumonic pl

76 endent caspase-1 activation pathway after Y. pestis challenge.

77 uantitate the internalization of virulent Y. pestis CO92 by macrophages and the subsequent activation

78 poprotein (Lpp) and MsbB attenuated Yersinia pestis CO92 in mouse and rat models of bubonic and pneum

79 haride function, reduced the virulence of Y. pestis CO92 in mouse models of bubonic and pneumonic pla

80 ltamsbB double mutant severely attenuated Y. pestis CO92 to evoke pneumonic plague in a mouse model w

81 ogen-activating protease (pla) genes from Y. pestis CO92.

82 cted with either F. tularensis SCHU S4 or Y. pestis CO92.

83 otection from a lethal challenge of Yersinia pestis CO92.

84 al regulator YfbA, which is essential for Y. pestis colonization and biofilm formation in cat fleas.

85 he noninflammatory environment needed for Y. pestis colonization and proliferation.

86 Finally, we find that at Y. pestis concentrations reflective of early-stage septicem

87 unctional outer membrane protein of Yersinia pestis, confers cell binding, Yop delivery and serum res

88 The pH 6 antigen (Psa) of Yersinia pestis consists of fimbriae that bind to two receptors:

89 Importantly, we find that Y. pestis containing combined deletions of YopJ and YopM in

90 Yersinia pestis continues to cause sporadic cases and outbreaks o

91 Ms) after challenge with a lethal dose of Y. pestis delivered as an aerosol, in 4 independent studies

92 e rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effecto

93 e second plague pandemic, caused by Yersinia pestis, devastated Europe and the nearby regions between

94 ction of F. tularensis, B. anthracis, and Y. pestis directly from patient blood samples was developed

95 nd water-borne enteric species from which Y. pestis diverged less than 6,400 y ago, exhibits signific

96 the existence of previously undocumented Y. pestis diversity during the sixth to eighth centuries, a

97 , Britain, Germany, France, and Spain for Y. pestis DNA and reconstructed eight genomes.

98 Here, we show that Y. pestis does not appreciably cleave A2AP in a Pla-depende

99 ty to the flea vectors of plague, whereas Y. pestis does not.

100 st severe form of disease caused by Yersinia pestis due to its ease of transmission, rapid progressio

101 g a comparable evolutionary trajectory of Y. pestis during both events.

102 in serum is critical for the survival of Y. pestis during the septicemic stage of plague infections.

103 t a step-wise evolutionary model in which Y. pestis emerged as a flea-borne clone, with each genetic

104 response to Y. pestis infection, and that Y. pestis entry into macrophages may involve the participat

105 The emergence of Y. pestis fits evolutionary theories that emphasize ecologi

106 entified has not been found in any extant Y. pestis foci sampled to date, and has its ancestry in str

107 opJ, yopM, and yopJ yopM mutants ofY ersinia pestis Following intravenous infection of mice, theY.

108 m BT organisms (Bacillus anthracis, Yersinia pestis, Francisella tularensis, Brucella spp., Burkholde

109 inct strains of Bacillus anthracis, Yersinia pestis, Francisella tularensis, Burkholderia mallei, Bur

110 ains from four pathogenic bacteria: Yersinia pestis, Francisella tularensis, Burkholderia pseudomalle

111 daptation that followed the divergence of Y. pestis from the closely related food- and waterborne ent

112 As Y. pestis further evolved, modern strains acquired a single

113 sd triple mutations was used to deliver a Y. pestis fusion protein, YopE amino acid 1 to 138-LcrV (Yo

114 s; however, it is not known at what point Y. pestis gained the ability to induce a fulminant pneumoni

115 genomic and historical data, we assembled Y. pestis genomes from nine individuals covering four Euras

116 Here we present five Y. pestis genomes from one of the last European outbreaks o

117 Here, we present six new European Y. pestis genomes spanning the Late Neolithic to the Bronze

118 ng this period and reconstruct 34 ancient Y. pestis genomes.

119 Yersinia pestis has caused at least three human plague pandemics.

120 Plague, caused by the bacterium Yersinia pestis, has killed millions in historic pandemics and co

121 Because Yersinia pestis HasA (HasA(yp)) presents a Gln at position 32, we

122 eport the oldest direct evidence of Yersinia pestis identified by ancient DNA in human teeth from Asi

123 mice that are cleaved and/or processed by Y. pestis in a Pla-dependent manner.

124 nfluenza A in lesser snow geese and Yersinia pestis in coyotes), we argue that with careful experimen

125 Five cases demonstrated evidence of Y. pestis in fetal or neonatal tissues.

126 regulates the entry and survival of Yersinia pestis in host macrophages is poorly understood.

127 apacity to modulate binding properties of Y. pestis in its hosts, in conjunction with other adhesins.

128 no significant reduction in virulence of Y. pestis in mice when it was administered i.n. but actuall

129 The discovery of molecular signatures of Y. pestis in prehistoric Eurasian individuals and two genom

130 PhiA1122::luxAB rapidly detects Y. pestis in pure culture and human serum by transducing a

131 , we report the first direct detection of Y. pestis in soil, which could be extremely useful in confi

132 re), sensitive, and specific detection of Y. pestis in such complex samples.

133 iron(III)-yersiniabactin import in Yersinia pestis In this study, we compared the impact of ybtPQ on

134 s of C57BL/6 and SEG MPs exposed to Yersinia pestis in vitro were examined.

135 kine response, and a higher resistance to Y. pestis-induced apoptosis.

136 single-nucleotide polymorphisms modulate Y. pestis-induced cytokine responses.

137 host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as

138 g that a noncanonical mechanism occurs in Y. pestis-infected macrophages.

139 Y. pestis-infected Mefv(M680I/M680I) FMF knock-in mice exhi

140 erferon (IFN) signaling is induced during Y. pestis infection and contributes to neutrophil depletion

141 ntributes to type I IFN expression during Y. pestis infection and suggest that the TLR7-driven type I

142 Untreated Y. pestis infection during pregnancy is associated with a h

143 vivo; the role of A2AP during respiratory Y. pestis infection is not known either.

144 Our results suggest that the fate of Y. pestis infection of the lung is decided extremely early

145 al regimen, and 2) laboratory evidence of Y. pestis infection or an epidemiologic link to patients wi

146 s for NF-kappaB activation in response to Y. pestis infection, and that Y. pestis entry into macropha

147 e conclude that, throughout the course of Y. pestis infection, OmpR-EnvZ is required to counter toxic

148 odes (LNs), or buboes, characterize Yersinia pestis infection, yet how they form and function is unkn

149 ome activation, and host resistance after Y. pestis infection.

150 phasic inflammatory response to pulmonary Y. pestis infection.

151 for pneumonic plague during outbreaks of Y. pestis infections.

152 Here, we show that Y. pestis infects and replicates as a biofilm in the foregu

153 ptotic death pathway after infection with Y. pestis, influenced by Toll-like receptor 4-TIR-domain-co

154 cularly the N terminus of YscF from Yersinia pestis, influences host immune responses.

155 examine the effects of Ab opsonization on Y. pestis interactions with phagocytes in vitro and in vivo

156 repeated emergence of diverse lineages of Y pestis into human populations.

157 l-mediated defense against fully virulent Y. pestis Introducing a single point mutation into the acti

158 Here we show that in Yersinia pestis, irp2, a gene encoding the synthetase (HMWP2) for

159 Yersinia pestis is a Gram-negative bacterium that is the causativ

160 Yersinia pestis is a tier 1 agent due to its contagious pneumopat

161 Yersinia pestis is an arthropod-borne bacterial pathogen that evo

162 Bubonic plague results when Yersinia pestis is deposited in the skin via the bite of an infec

163 s frenzied inflammatory response to Yersinia pestis is poorly understood.

164 gests that maternal-fetal transmission of Y. pestis is possible, particularly in the absence of antim

165 Yersinia pestis is the causative agent of bubonic and pneumonic p

166 Yersinia pestis is the causative agent of bubonic, pneumonic, and

167 Yersinia pestis is the causative agent of plague.

168 The bacteria Yersinia pestis is the etiological agent of plague and has caused

169 The plague bacillus Yersinia pestis is unique among the pathogenic Enterobacteriaceae

170 Pneumonic plague, caused by Yersinia pestis, is a rapidly progressing contagious disease.

171 used by the Gram-negative bacterium Yersinia pestis, is favored by a robust early innate immune respo

172 deadliest form of disease caused by Yersinia pestis Key to the progression of infection is the activi

173 This study focuses on the Y. pestis KIM yapV gene and its product, recognized as an a

174 lethal doses (LD50) (2.4 x 10(4) CFU) of Y. pestis KIM6+(pCD1Ap) than chi10057(pYA3332) (40% surviva

175 ants of Y. pseudotuberculosis IP32953 and Y. pestis KIM6+.

176 In vivo, Y. pestis lacking OmpR-EnvZ did not induce an early immune

177 th genomes shows the diversification of a Y. pestis lineage into multiple genetically distinct clades

178 We find the origins of the Yersinia pestis lineage to be at least two times older than previ

179 We conclude that the Y pestis lineages that caused the Plague of Justinian and

180 viously identified the causative agent as Y. pestis, little is known about the bacterium's spread, di

181 Thus, by degrading FasL, Y. pestis manipulates host cell death pathways to facilitat

182 cell-mediated defense against Pla-mutant Y. pestis Moreover, the efficacy of T cell-mediated protect

183 produce disease, the causal agent (Yersinia pestis) must rapidly sense and respond to rapid variatio

184 ere the agent of flea-borne plague, Yersinia pestis, must replicate to produce a transmissible infect

185 A Yersinia pestis mutant synthesizing an adjuvant form of lipid A (

186 e throughout human history, such as Yersinia pestis, Mycobacterium tuberculosis, and Mycobacterium le

187 acteria in the footpad revealed increased Y. pestis-neutrophil interactions and increased neutrophil

188 izing Ab had a dramatic effect in vivo on Y. pestis-neutrophil interactions in the dermis and dLN ver

189 we sequenced and analysed draft genomes of Y pestis obtained from two individuals who died in the fir

190 indings demonstrate that self-adjuvanting Y. pestis OMVs provide a novel plague vaccine candidate and

191 agents such as Bacillus anthracis, Yersinia pestis, or Burkholderia pseudomallei Conventional suscep

192 shown with recombinant Escherichia coli, Y. pestis, or purified passenger domains.

193 a functional ureD was sufficient to make Y. pestis orally toxic to fleas.

194 Thus, Y. pestis-orchestrated LN remodeling promoted its dissemina

195 The Y. pestis outer membrane Pla protease is essential for the

196 Using the Yersinia pestis outer transmembrane beta-barrel Ail as a model, w

197 flammatory responses and enables enhanced Y. pestis outgrowth in the lungs.

198 embrane remodeling is a hallmark of Yersinia pestis pathogenesis.

199 adly used in many fields, including Yersinia pestis pathogenesis.

200 ith host sensing of YscF, consistent with Y. pestis pathogenesis.

201 nents, and provide a handle for targeting Y. pestis pathogenesis.

202 h could be extremely useful in confirming Y. pestis persistence in the ground.

203 E by annotating two newly sequenced Yersinia pestis phage genomes.

204 olytomy similar to others seen across the Y. pestis phylogeny, associated with the Second and Third P

205 a single putatively extinct clade in the Y. pestis phylogeny.

206 of Bacillus anthracis (anthrax) or Yersinia pestis (plague) would prompt a public health emergency.

207 a pestis This study demonstrated that the Y. pestis plasminogen activator Pla, a protease that promot

208 fection with either wild-type or Deltapla Y. pestis, Prdx6-deficient mice exhibit no differences in b

209 gests that both Y. pseudotuberculosis and Y. pestis produce an oligosaccharide core with a single O-a

210 n to the 2' position of lipid A, in Yersinia pestis produced bisphosphoryl hexa-acylated lipid A at 3

211 on of a single protein, e.g., YscF (Yersinia pestis), PscF (Pseudomonas aeruginosa), PrgI (Salmonella

212 , it afforded complete protection against Y. pestis pulmonary infection.

213 ptional profiling experiments to identify Y. pestis quorum sensing regulated functions.

214 that oversynthesized the LcrV antigen of Y. pestis, raised the amounts of LcrV enclosed in OMVs by t

215 Y. pestis recently evolved from the gastrointestinal pathog

216 n, we found that infection with wild-type Y. pestis reduces the abundance of extracellular Prdx6 in t

217 this antibody-mediated immunity (AMI) to Y. pestis remain poorly understood.

218 Yersinia pestis remains endemic in Africa, Asia, and the Americas

219 Early after inhalation, Yersinia pestis replicates to high numbers in the airways in the

220 Immunization against a concomitant lethal Y. pestis respiratory challenge was correlated with tempora

221 Inhalation of the bacterium Yersinia pestis results in primary pneumonic plague.

222 ge of Myd88(-/-) mice with wild-type (WT) Y. pestis results in significant loss of pro- and anti-infl

223 complex, fluctuating environment in which Y. pestis senses nutrient depletion via OmpR-EnvZ.

224 , lungs of mice challenged with wild-type Y. pestis show reduced levels of FasL and activated caspase

225 terest - pre-modern bubonic plague (Yersinia pestis), smallpox (Variola virus) and cholera (Vibrio ch

226 eened DNA extracts for the presence of the Y pestis-specific pla gene on the pPCP1 plasmid using prim

227 e relevant protein markers encoded by the Y. pestis-specific plasmids pFra (murine toxin) and pPla (p

228 recent 19(th) century pandemic, in which Y. pestis spread worldwide [5] and became endemic in severa

229 al. (2014) explore the mechanism by which Y. pestis spreads and thus leads to this striking lymphaden

230 Through deep sequencing analysis of the Y. pestis sRNA-ome, we found 63 previously unidentified put

231 utaneously infected with a fully virulent Y. pestis strain and treated at progressive stages of the d

232 nic approach, we created 5,088 mutants of Y. pestis strain CO92 and screened them in a mouse model of

233 mmunization with the EV76 live attenuated Y. pestis strain rapidly induced the expression of hemopexi

234 cell-mediated protection against various Y. pestis strains displayed an inverse relationship with th

235 d them with a database of genomes from 131 Y pestis strains from the second and third pandemics, and

236 A phylogenic tree including 36 Y. pestis strains highlighted an association between the ge

237 nce for the presence of multiple distinct Y. pestis strains in Europe.

238 onstructed draft genomes of the infectious Y pestis strains, compared them with a database of genomes

239 All Y. pestis strains, including those phylogenetically closest

240 red to that after infection with Deltapla Y. pestis, suggesting that Pla cleaves Prdx6 in the pulmona

241 he LPS membrane, and collectively promote Y. pestis survival in human serum, antibiotic resistance, a

242 of Pla suffices to render fully virulent Y. pestis susceptible to primed T cells.

243 nvestigated the role and function of this Y. pestis system in fleas.

244 atory responses through TLRs by the Yersinia pestis T3S needle protein, YscF, the Salmonella enterica

245 s binding sites in both P. aeruginosa and Y. pestis T3SS promoters prevent activation by ExsA and Lcr

246 U/ml for B. anthracis, and 4.5 CFU/ml for Y. pestis The sensitivity was 100% at the LOD for all three

247 Pathogenic Yersinia, including Y. pestis, the agent of plague in humans, and Y. pseudotube

248 oducts are functional receptors for Yersinia pestis, the agent of plague, as shown by overexpression

249 y YopM is required for virulence of Yersinia pestis, the agent of plague.

250 thropod-borne transmission route of Yersinia pestis, the bacterial agent of plague, is a recent evolu

251 Yersinia pestis, the bacterium that causes plague, is a highly pa

252 Yersina pestis, the bubonic plague bacterium, is coated with a p

253 is no FDA-approved vaccine against Yersinia pestis, the causative agent of bubonic and pneumonic pla

254 Yersinia pestis, the causative agent of plague, binds host cells

255 Yersinia pestis, the causative agent of plague, expresses the pla

256 nguish DNA amplicons generated from Yersinia pestis, the causative agent of plague, from the closely

257 For transmission to new hosts, Yersinia pestis, the causative agent of plague, replicates as bio

258 al gene prediction in the bacterium Yersinia pestis, the causative agent of plague.

259 a candidate recombinant antigen for Yersinia pestis, the causative agent of plague.

260 is essential in the pathogenesis of Yersinia pestis, the causative agent of plague.

261 In Yersinia pestis, the deadly agent that causes plague, the protein

262 Yersinia pestis, the etiologic agent of plague, is a bacterium as

263 covery and genome reconstruction of Yersinia pestis, the etiological agent of plague, in Neolithic fa

264 possible scenario for the early spread of Y. pestis: the pathogen may have entered Europe from Centra

265 ith 5 x 10(3) CFU (50 LD(50)) of virulent Y. pestis This protection was significantly superior to tha

266 man disease caused by the bacterium Yersinia pestis This study demonstrated that the Y. pestis plasmi

267 The discovery that Y. pestis thwarts T cell defense by promoting fibrinolysis

268 most ancestral, deeply rooted strains of Y. pestis to cause pneumonic plague, indicating that Y. pes

269 The ability of Y. pestis to create this early noninflammatory environment

270 c basis of the evolutionary adaptation of Y. pestis to flea-borne transmission.

271 roy immune cells in humans, thus enabling Y. pestis to reproduce in the bloodstream and be transmitte

272 vector prior to transmission may preadapt Y. pestis to resist the initial encounter with the mammalia

273 s, suggesting an evolutionary adaption of Y. pestis to specific local animal hosts or reservoirs.

274 These findings reveal adaptations of Y. pestis to the dermis and how these adaptations can defin

275 m for interrogating such couplings: Yersinia pestis transmission exerts intense selective pressure dr

276 Y. pestis type III secretion system effectors YopJ and YopM

277 that LcrV, the needle cap protein of the Y. pestis type III secretion system, binds to the N-formylp

278 tects neutrophils from destruction by the Y. pestis type III secretion system.

279 Previous work established that Y. pestis uses the T3SS to inhibit neutrophil respiratory b

280 rine/threonine kinase YopO (YpkA in Yersinia pestis), uses monomeric actin as bait to recruit and pho

281 The causative agent of plague, Yersinia pestis, uses a type III secretion system to selectively

282 en activator protease (Pla) is a critical Y. pestis virulence factor that is important for early bact

283 nt pyrin interacts less avidly with Yersinia pestis virulence factor YopM than with wild-type human p

284 esponses are believed to be suppressed by Y. pestis virulence factors in order to prevent clearance,

285 t cell surface expression of Ail produces Y. pestis virulence phenotypes in E. coli, including resist

286 , including novel multimeric forms of the Y. pestis virulence plasmid, pPCP1, MinION reads were error

287 These findings indicate that Y. pestis was capable of causing pneumonic plague before it

288 In addition, Y. pestis was identified directly from positive blood cultu

289 , ureD mutation early in the evolution of Y. pestis was likely subject to strong positive selection b

290 o cause pneumonic plague, indicating that Y. pestis was primed to infect the lungs at a very early st

291 d to the LcrV virulence factor from Yersinia pestis were characterised for their Fab affinity against

292 ludes serious pathogens such as the Yersinia pestis, which causes plague, Yersinia pseudotuberculosis

293 robust titers of antibodies against LcrV, Y. pestis whole-cell lysate (YPL), and F1 antigen and more

294 wed increased association of Ab-opsonized Y. pestis with neutrophils in the dermis in a mouse model o

295 ytes in vitro and in vivo Opsonization of Y. pestis with polyclonal antiserum modestly increased phag

296 immune environment leading to survival of Y. pestis within the eukaryotic host.

297 However, some non-pestis Yersinia strains and Enterobacteriaceae did elici

298 Thus, we conclude that Y. pestis YopJ and YopM can both exert a tight control of h

299 l as the causative agent of plague, Yersinia pestis (Yp).

300 of IgG response to whole-cell lysates of Y. pestis (YpL) and subunit LcrV similar to those seen with

301 ases: Burkholderia mallei BmaI1 and Yersinia pestis YspI.