ライフサイエンスコーパス: M. tuberculosis

1 M. tuberculosis expresses two respiratory terminal oxida

2 M. tuberculosis expressing PPE2 and PPE2-null mutants co

3 M. tuberculosis is known to have the ability to enter in

4 M. tuberculosis produces two classes of siderophore, lip

5 M. tuberculosis-specific CD4 T cells play a central role

6 M. tuberculosis-specific T cells are first activated in

7 t analysis of whole genome sequences of 1170 M. tuberculosis isolates together with their patient pro

8 solates, a transmission analysis revealed 18 M. tuberculosis isolates clustering within eight network

9 erform such an integrated analysis across 22 M. tuberculosis clinical isolates, representing ancient

10 this MRM-MS assay to selectively identify 40 M. tuberculosis peptides from 19 proteins that most comm

11 We identified at least one of the 40 M. tuberculosis peptides in 70 (95%) individuals with LT

12 For the targeted NGS approach, 46 M. tuberculosis-specific amplicon libraries had 99.6% (C

13 tection at 10(1) BCG cells/ml, with 31 to 59 M. tuberculosis complex reads.

14 of the transmission of resistant strains, 81 M. tuberculosis samples from Khyber Pakhtunkhwa province

15 tro and in vivo activities of the type III-A M. tuberculosis CRISPR system.

16 Moreover, a M. tuberculosis H37Rv deletion mutant in the Rv3134c-dos

17 Four replicate experiments achieved M. tuberculosis detection at 10(1) BCG cells/ml, with 31

18 eptible and drug-resistant latent and active M. tuberculosis infection.

19 IT cell activation and expansion early after M. tuberculosis challenge, these MAIT cells did not rest

20 rly MAIT cell activation and expansion after M. tuberculosis exposure, without attenuating M. tubercu

21 imum inhibitory concentration of 2B8 against M. tuberculosis correlated with a higher drug concentrat

22 amide has a different mode of action against M. tuberculosis compared to the two first-line antituber

23 le, PIPD1, as a potent lead compound against M. tuberculosis Herein, we show that PIPD1 and related a

24 play a critical role in host defense against M. tuberculosis infection.

25 munogenicity and protective efficacy against M. tuberculosis challenge.

26 rther validation of these inhibitors against M. tuberculosis-infected macrophages and animal models h

27 idence that suggests BCG may protect against M. tuberculosis infection as well as disease.

28 ice, conferred equivalent protection against M. tuberculosis infection in the lungs of Rag(-/-) mice

29 Protection against M. tuberculosis infection was strongly associated with B

30 f innate immune memory also protects against M. tuberculosis In this study, by using a murine model,

31 stricted T cells, which are reactive against M. tuberculosis, and underexplored as potential TB vacci

32 plicated in effective host responses against M. tuberculosis.

33 at 80, 85, and 95 degrees C inactivates all M. tuberculosis bacilli.

34 inhibited its DNA-binding activity and also M. tuberculosis growth in vitro and inside macrophages.

35 the construction and characterization of an M. tuberculosis sigE fadD26 unmarked double mutant fulfi

36 Through a loss-of-function screening of an M. tuberculosis transposon mutant library, we identified

37 Using an M. tuberculosis genomic dataset for the virulent Beijing

38 activity against planktonic M. abscessus and M. tuberculosis as well as against intracellular M. absc

39 et regions of MscL from Escherichia coli and M. tuberculosis and employ PELDOR/DEER distance and 3pES

40 eviously uncharacterized PPIs in E. coli and M. tuberculosis that both add components to known protei

41 this observation across antibody domains and M. tuberculosis specificities to define changes with the

42 Since both P. aeruginosa DsbB1 and M. tuberculosis VKOR complement an E. coli dsbB knockout

43 ounds tested against P. aeruginosa DsbB1 and M. tuberculosis VKOR using Escherichia coli cells.

44 ividuals with latent TB infection (LTBI) and M. tuberculosis-naive controls.

45 Iron is an essential metal and M. tuberculosis possesses two different systems to acqui

46 ot only play a role in phagosome rupture and M. tuberculosis cytosolic translocation but also functio

47 dependent streptococcal pathogens as well as M. tuberculosis with an IC(50) of 120-410 uM.

48 Upon assessing M. tuberculosis growth in several nitrogen sources, we f

49 ear cell-derived macrophages, and attenuated M. tuberculosis infection in mice.

50 . tuberculosis exposure, without attenuating M. tuberculosis growth, suggesting that MAIT cell enrich

51 rved mycobacterial tam genes be renamed bioC M. tuberculosis BioC presents a target for antituberculo

52 The molecular mechanism of inhibition by M. tuberculosis involves reduced phosphorylation of the

53 h analysis of nitrogen source utilisation by M. tuberculosis and reveals a flexible metabolic network

54 cing as a diagnostic tool for characterizing M. tuberculosis isolates, which will assist future epide

55 f whole-genome sequence data for 98 clinical M. tuberculosis isolates from a city in southern India.

56 d tolerance is a general feature of clinical M. tuberculosis isolates, we assessed macrophage-induced

57 ce determining region (RRDR), using clinical M. tuberculosis sequencing information.

58 is/simian immunodeficiency virus-coinfected (M. tuberculosis/SIV-coinfected) macaques to model M. tub

59 oxide (NALC-NaOH), chemicals that compromise M. tuberculosis viability and, consequently, the perform

60 ormed whole genome sequencing of consecutive M. tuberculosis isolates obtained during nine years from

61 In contrast, M. tuberculosis gyrase hydrolyzes ATP only slowly and is

62 subsequently mediate the failure to control M. tuberculosis infection in macrophages.

63 ent in the lung is not sufficient to control M. tuberculosis infection.

64 solving type I IFN responses and controlling M. tuberculosis infection.

65 of proinflammatory cytokines in controlling M. tuberculosis infection has been established, the effe

66 After coculture with coinfected DCs, M. tuberculosis Ag-specific CD4 T cells lost their abili

67 s spectrometry (MRM-MS) assays that detected M. tuberculosis peptides in serum extracellular vesicles

68 The pretreatment GeneXpert-determined M. tuberculosis load may be a useful predictor of neurol

69 Due to their role in detoxification, M. tuberculosis EH's have been identified as potential d

70 ility exists in ppe37 genes across different M. tuberculosis strains, with more than 60% of sequences

71 iscuss new approaches that will help dissect M. tuberculosis immune evasion mechanisms and devise str

72 Dormant M. tuberculosis induced quiescence in MSCs and promoted

73 as a long-term natural reservoir of dormant M. tuberculosis.

74 tion of Th1 cell input into the lungs during M. tuberculosis infection that is regulated by chemokine

75 utralize IL-10 in cynomolgus macaques during M. tuberculosis infection.

76 del of TB, induction of autophagy eliminated M. tuberculosis from MSCs, and consequently, the additio

77 Final validation employed M. tuberculosis-positive clinical samples (n = 20), reve

78 unique inflammatory signature, and enhanced M. tuberculosis phagocytosis and survival when compared

79 in tandem with other pathways to facilitate M. tuberculosis stress survival.

80 DPH oxidase-mediated ROS production to favor M. tuberculosis survival in macrophages.

81 N stimulated gene (ISG) expression following M. tuberculosis infection, cytosolic nucleic acid transf

82 alidated Illumina MiSeq sequencing assay for M. tuberculosis and phenotypic drug susceptibility testi

83 dividuals display substantial enrichment for M. tuberculosis-responsive CD4(+) T cells compared with

84 E functions as a lipase and is important for M. tuberculosis intracellular growth and in vivo infecti

85 first sequencing attempts on the iSeq100 for M. tuberculosis, the sequencing pool loading concentrati

86 rium marinum, a surrogate model organism for M. tuberculosis, and found that the esxBA-knockout strai

87 t in better defining a molecular pathway for M. tuberculosis pathogenesis and in expanding our apprec

88 applications, and set out best practices for M. tuberculosis WGS, including standards for bioinformat

89 ssed higher RNA levels of genes required for M. tuberculosis survival.

90 signed children who had negative results for M. tuberculosis infection according to the QuantiFERON-T

91 n spiked samples, the median C(T) values for M. tuberculosis, S. enterica, and EBV cfDNA were signifi

92 of preparing DNA for sequencing direct from M. tuberculosis-positive clinical samples (without cultu

93 We hypothesized that lipoarabinomannan from M. tuberculosis (Mtb LAM) would prime human PMN in a TLR

94 rties of the nitrogen metabolic network from M. tuberculosis, such as: (i) the lack of homeostatic co

95 nsasii is 86% identical to the ortholog from M. tuberculosis and catalytically active.

96 h sequence similarity to its orthologue from M. tuberculosis and generally high structural similarity

97 ividuals with LTBI, suggesting peptides from M. tuberculosis proteins involved in nitrogen metabolism

98 Conversely, deletion of ppe37 from M. tuberculosis results in a strain severely attenuated

99 e conserved in the orthologous proteins from M. tuberculosis Our findings support a role for EspE and

100 We analyzed whole blood samples from M. tuberculosis-infected South African adults who were r

101 uctures of hsNadE and NAD(+) synthetase from M. tuberculosis (tbNadE) with synthetase intermediate an

102 Furthermore, M. tuberculosis is able to inhibit IFNAR-mediated cell s

103 In this study, we evaluated global M. tuberculosis-induced gene expression in airway immune

104 ippine isolates within a phylogeny of global M. tuberculosis (n > 17,000), we established that they a

105 A high M. tuberculosis load predicted new neurological events a

106 ting Ag-specific T cells, we explored if HIV-M. tuberculosis-infected (coinfected) human DCs can dysr

107 Here, we show how M. tuberculosis causes caspase-1/NLRP3/gasdermin D-media

108 Here, we used this technology to evaluate if M. tuberculosis peptides can also be detected in individ

109 pK occur in clinical isolates, accumulate in M. tuberculosis-infected mice with further accumulation

110 regulation of MmpL11 transporter activity in M. tuberculosis and M. smegmatis.

111 nase is involved in ammonium assimilation in M. tuberculosis, in addition to its essential role in al

112 t for disrupting menaquinone biosynthesis in M. tuberculosis.

113 MMP-7, could reduce pulmonary cavitation in M. tuberculosis-infected C3HeB/FeJ mice.

114 se lipids contribute to biofilm formation in M. tuberculosis and M. smegmatis, and non-replicating pe

115 s may offer clues to glycolipid formation in M. tuberculosis.

116 e detection of wild and mutated rpoB gene in M. tuberculosis using an electrochemical DNA (E-DNA) sen

117 the targeted deletion of the pe/ppe genes in M. tuberculosis resulted in enhanced autophagy and impro

118 sed expression of glutamine pathway genes in M. tuberculosis-infected macrophages and blood transcrip

119 tic repertoire of epoxide hydrolase genes in M. tuberculosis.

120 olism of the cell wall and surface lipids in M. tuberculosis during growth and stasis, and speculate

121 easome contributes to nitrogen metabolism in M. tuberculosis, although this hypothesis had not been t

122 their divergence from wild-type (WT) mice in M. tuberculosis replication and neutrophilic inflammatio

123 identified five novel putative TA modules in M. tuberculosis.

124 Expression of VapC-mt11 in M. tuberculosis resulted in cleavage of only two tRNA is

125 ol bacterial burden and disease pathology in M. tuberculosis infection.

126 megmatis, and non-replicating persistence in M. tuberculosis.

127 hocyte activation, we report the presence in M. tuberculosis-infected subjects of HBHA-induced CD4(+)

128 in PolyP homeostasis play a critical role in M. tuberculosis physiology and virulence and are attract

129 the C. glutamicum gene NCgl2764 (Rv0224c in M. tuberculosis) abolished acetyltrehalose monocorynomyc

130 closely related than antitoxin sequences in M. tuberculosis Furthermore, the identification of addit

131 wth and responding to nitric oxide stress in M. tuberculosis, but its underlying mechanism is unclear

132 could represent an alternative substrate in M. tuberculosis.

133 xpands the known repertoire of TA systems in M. tuberculosis.

134 potential species-selective drug targets in M. tuberculosis.

135 with the main low-molecular-weight thiol in M. tuberculosis, mycothiol.

136 A significant role of VirS in M. tuberculosis survival in adverse conditions suggested

137 structures of three MetX proteins, including M. tuberculosis (MtMetX), Mycolicibacterium abscessus (M

138 Lower protection from BCG with increasing M. tuberculosis exposure and age can inform vaccine deve

139 This NaOH-induced M. tuberculosis viability loss was replicated in clinica

140 involved in the glutamine pathway influence M. tuberculosis-induced cytokines in a cohort of 500 ind

141 e migration and entry rate of Th1 cells into M. tuberculosis-infected lungs using competitive adoptiv

142 tidrug resistance gene MDR1 on intracellular M. tuberculosis survival during antituberculosis drug tr

143 The pathway of regulation involves M. tuberculosis infection of macrophages and suppression

144 Despite known M. tuberculosis sensitization determined by interferon-g

145 from 74 individuals presumed to have latent M. tuberculosis infection (LTBI) based on close contact

146 riptomic profiles of individuals with latent M. tuberculosis infection or tuberculosis.

147 parisons of the immune responses of latently M. tuberculosis-infected (LTBI) subjects to those of pat

148 cantly better than control cells at limiting M. tuberculosis replication.

149 A lower lung M. tuberculosis burden was apparent for all BTZ cohorts,

150 samples showed a significantly lower median M. tuberculosis C(T) These findings suggest that large-v

151 pectively, showed significantly lower median M. tuberculosis C(T) values than with the Streck blood c

152 induced under stressed conditions mimicking M. tuberculosis' intracellular niche.

153 berculosis/SIV-coinfected) macaques to model M. tuberculosis/HIV coinfection and study the impact of

154 CD11b(+) AMs phagocytosed significantly more M. tuberculosis, which expressed higher RNA levels of ge

155 Our findings demonstrated that multiple M. tuberculosis PE/PPE proteins are involved in inhibiti

156 cases among suspected patients with negative M. tuberculosis microbiological evidence.

157 mma release assay, 12/23 participants had no M. tuberculosis-specific CD4 T cells detectable by flow

158 tool successfully identified up to 90.9% of M. tuberculosis rpoB variants correctly, with sensitivit

159 Xs cumulatively contribute to the ability of M. tuberculosis to survive in nutrient-limiting, low-oxy

160 gh its effect on DCs, impairs the ability of M. tuberculosis-specific CD4 T cells to maintain a laten

161 subtilis GyrB, which exceeds the activity of M. tuberculosis gyrase and reaches the activity of the B

162 with other pathways linked to adaptation of M. tuberculosis to the host environment.

163 is the primary aspartate aminotransferase of M. tuberculosis, and mediates an essential but underreco

164 es an important baseline characterisation of M. tuberculosis genetic diversity for the Philippines, a

165 Early clearance of M. tuberculosis is associated with enhanced heterologous

166 lls lost their ability to enhance control of M. tuberculosis infection in infected macrophages.

167 We achieved the detection of 5 copies of M. tuberculosis genomic DNA (equaling 0.3 cell) in real

168 To date, cultivation of M. tuberculosis is the gold standard, which depends on i

169 he core components of the RNA degradosome of M. tuberculosis and to analyse their function in RNA met

170 1 ml typically yielded higher mean depths of M. tuberculosis genome coverage, with an overall range o

171 losis (ATB) currently relies on detection of M. tuberculosis (Mtb).

172 The detection of M. tuberculosis peptides in serum extracellular vesicles

173 Detection of M. tuberculosis was associated with mortality (adjusted

174 rther understanding of how this diversity of M. tuberculosis isolates affects disease and treatment o

175 ring infection, which limits the exposure of M. tuberculosis to sublethal concentrations of antimicro

176 58 genes were shared with essential genes of M. tuberculosis and M. marinum, respectively.

177 )propionamide (3bMP1) inhibits the growth of M. tuberculosis, and resistance to this compound is conf

178 ersible frameshift mutations in the 7C HT of M. tuberculosis glpK occur in clinical isolates, accumul

179 eal both the reduction and the impairment of M. tuberculosis-specific CD4 T cells, although the cellu

180 to identify genes required for infection of M. tuberculosis H37Rv in C57BL/6 mice.

181 ble mice infected with a clinical isolate of M. tuberculosis resembles that of active human TB diseas

182 Clinical isolates of M. tuberculosis differed in their ability to activate in

183 Clinical isolates of M. tuberculosis from both Egypt and Saudi Arabia were su

184 ensively drug-resistant clinical isolates of M. tuberculosis, suggesting that PIPD1's mode of action

185 MDR1 improves antibiotic-mediated killing of M. tuberculosis.

186 Different immune landscapes of M. tuberculosis granulomas depending on the time after i

187 this study, the limit of detection (LOD) of M. tuberculosis H37Rv in all spiked animal samples were

188 We found the majority of M. tuberculosis isolates were the CAS/Delhi strain-type

189 to that observed in other in vitro models of M. tuberculosis tolerance.

190 We recently showed that a sigE mutant of M. tuberculosis was more attenuated and more efficacious

191 The results highlight the dynamic nature of M. tuberculosis infection, population structure and resi

192 a central role in determining the outcome of M. tuberculosis infection.

193 rucial role in virulence and pathogenesis of M. tuberculosis In our earlier study, we demonstrated th

194 for the basic physiology and pathogenesis of M. tuberculosis.

195 Our study confirms the presence of M. tuberculosis infection in cattle in India, sequencing

196 o be associated with decreased prevalence of M. tuberculosis infection in adults.

197 Coinfection of DCs reduced proliferation of M. tuberculosis Ag-specific CD4 T cells without affectin

198 study, we found that a secretory protein of M. tuberculosis PPE2 disrupted the assembly of NADPH oxi

199 letion of LprE (Mtb) results in reduction of M. tuberculosis virulence in human and mouse macrophages

200 yte-derived macrophages to study the role of M. tuberculosis in regulation of MDR1 and drug resistanc

201 In summary, direct-from-sample sequencing of M. tuberculosis genomes was facilitated by a low-cost th

202 igma70-family primary sigma factor sigmaA of M. tuberculosis containing the conserved region 4 (sigma

203 innate immune protection in early stages of M. tuberculosis infection in the lung.

204 a from 97 US immigrants at various stages of M. tuberculosis infection, we showed protective in vitro

205 riminatory power between different states of M. tuberculosis infection and disease.

206 ariations among recently isolated strains of M. tuberculosis in two closely related countries with di

207 ffective against highly resistant strains of M. tuberculosis, but uptake has been slow globally.

208 r retrospective (and prospective) studies of M. tuberculosis genetic epidemiology.

209 erential associations between sublineages of M. tuberculosis and patient profiles, including ages, et

210 ficantly inhibited intracellular survival of M. tuberculosis in human macrophages.

211 s ppe37 exhibits HIA as efficient as that of M. tuberculosis, achieving robust growth with <0.2 uM he

212 f untreated controls, NALC-NaOH treatment of M. tuberculosis reduced the MBLA-detectable bacillary lo

213 age is crucial for survival and virulence of M. tuberculosis ESAT-6, a 6-kDa-secreted protein of regi

214 notyping and drug-susceptibility analyses on M. tuberculosis from sputum.

215 effect of P2C/5-OP-RU-induced MAIT cells on M. tuberculosis control.

216 he depletion of CD4(+) and CD8(+) T cells on M. tuberculosis-induced BAL cell gene expression in LTBI

217 BCG, but not virulent wild-type M. bovis or M. tuberculosis.

218 the survival of phagocytosed M. smegmatis or M. tuberculosis D. discoideum cells lacking the putative

219 Unlike most other organisms M. tuberculosis has six putative genes for epoxide hydro

220 g an 18 h generation time equal to log phase M. tuberculosis, with latency period modeled as a contin

221 ages 1-3, representing the other predominant M. tuberculosis strains responsible for tuberculosis glo

222 ontribute to the pathogenesis of progressive M. tuberculosis infection.

223 This condition promotes M. tuberculosis survival and potentially enhances the em

224 predominant host cell during early pulmonary M. tuberculosis infection and, therefore, represent attr

225 In the absence of MbcA, MbcT triggers rapid M. tuberculosis cell death, which reduces mycobacterial

226 Deletion of PPE51 rendered M. tuberculosis cells unable to replicate on propionamid

227 Drug resistant M. tuberculosis is an emerging threat for TB control, ma

228 against rifampicin- and isoniazid-resistant M. tuberculosis strains with MIC values of 9.46 and 9.90

229 challenge, these MAIT cells did not restrict M. tuberculosis bacterial load.

230 NA) modulate macrophage function to restrict M. tuberculosis replication in addition to their direct

231 acterium tuberculosis RNA polymerase (RNAP), M. tuberculosis ECF sigma factor sigma(L), and promoter

232 on for loss of tRNA(Lys43-UUU) by the second M. tuberculosis lysine tRNA, tRNA(Lys19-CUU), ribosome s

233 that constitutive ESX-5 secretion sensitizes M. tuberculosis to an immune response that still occurs

234 n 60% of sequences from completely sequenced M. tuberculosis genomes having mutations that result in

235 (BMDMs) were infected with laboratory strain M. tuberculosis H37Rv or clinical isolates from various

236 cells enter the lung parenchyma and suppress M. tuberculosis growth, while CX3CR1(+) KLRG1(+) Th1 cel

237 ly be exploited by small molecules to target M. tuberculosis.

238 controlled (latent) versus uncontrolled (TB) M. tuberculosis infection.

239 l, our study supports the novel concept that M. tuberculosis evolved to inhibit autocrine type I IFN

240 These observations demonstrate that M. tuberculosis has a fully-functioning CRISPR interfere

241 Furthermore, we demonstrate that M. tuberculosis isolates that induce low levels of IL-1b

242 Therefore, it is essential that M. tuberculosis immune evasion-related pathogen virulenc

243 Thus, we have established that M. tuberculosis gains dormancy in MSCs, which serve as a

244 Therefore, we provide evidence that M. tuberculosis strains manipulate host-pathogen interac

245 We report a novel finding that M. tuberculosis up-regulates MDR1 during infection, whic

246 The findings that M. tuberculosis PPE2 protein is involved in the modulati

247 We hypothesized that M. tuberculosis-specific inflammatory responses used to

248 It is known that M. tuberculosis recruit holotransferrin at the surface o

249 Herein we show that M. tuberculosis and Mycobacterium bovis BCG are able to

250 681 patients with pulmonary TB and show that M. tuberculosis isolates from cases with mild disease co

251 These results suggest that M. tuberculosis enters a quiescent state during latency,

252 These studies suggest that M. tuberculosis probably targets the ESAT-6 protein to i

253 vivo efficacy of polyclonal IgG against the M. tuberculosis capsular polysaccharide arabinomannan (A

254 t in vitro bactericidal activity against the M. tuberculosis strain mc(2)6230 and also against a pane

255 Although the M. tuberculosis "Manila" ancient lineage 1 strain-type i

256 d (coinfected) human DCs can dysregulate the M. tuberculosis-specific CD4 T cell phenotype and functi

257 we first identified the RNA targets for the M. tuberculosis VapC-mt11 (VapC11, Rv1561) toxin in vitr

258 report that the rate of new mutations in the M. tuberculosis genome decline dramatically after two ye

259 are well-conserved among the members of the M. tuberculosis complex, which cause tuberculosis in ani

260 humans, our data support the key role of the M. tuberculosis surface glycan AM and suggest the import

261 we assessed the relative conservation of the M. tuberculosis TA systems and found that most TA orthol

262 More than half of the M. tuberculosis TA systems belong to the VapBC (virulenc

263 pathogenicity precluded in vivo studies, the M. tuberculosis Tam also replaced E. coli BioC both in v

264 Transwell experiments demonstrated that the M. tuberculosis-mediated inhibition of type I IFN signal

265 ubversion of host immune responses using the M. tuberculosis CDC1551 LprE (LprE (Mtb) ) mutant (MtbDe

266 uggesting that they may confer advantages to M. tuberculosis by modulating its interactions with host

267 eve pulmonary delivery daily over 10 days to M. tuberculosis infected mice for FG2 HSA nanoparticles

268 cting the initial response to re-exposure to M. tuberculosis in the human lung.

269 mmune landscape associated with AwM prior to M. tuberculosis exposure and whether such AwM play a cri

270 In reference to M. tuberculosis culture, CRP had a sensitivity of 78% (9

271 e the intracerebral inflammatory response to M. tuberculosis and improve TBM clinical outcomes.

272 ry nutrient, but its role in the response to M. tuberculosis is unknown.

273 oteins in regulating macrophage responses to M. tuberculosis In this study, we demonstrate that TRIM1

274 ing how BCG alters early immune responses to M. tuberculosis provides new avenues to improve upon the

275 ormin-derived host metabolic-fitness towards M. tuberculosis infection.

276 a major role in Mycobacterium tuberculosis ( M. tuberculosis or Mtb) pathogenesis as they occur in my

277 Mycobacterium tuberculosis (M. tuberculosis) has coevolved with humans for millennia

278 et drug tolerant Mycobacterium tuberculosis (M. tuberculosis), responsible, in part, for the lengthy

279 sistent pathogen Mycobacterium tuberculosis (M. tuberculosis).

280 tment could reflect a mechanism to fine-tune M. tuberculosis membrane properties to its advantage.

281 regulon, formed less biofilm than wild type M. tuberculosis, a phenotype reverted upon reintroductio

282 esponse to phosphate limitation by wild-type M. tuberculosis The esx-5 RegX3 binding site deletion (D

283 option for the accurate detection of viable M. tuberculosis and treatment response monitoring.

284 tive in macrophages infected with a virulent M. tuberculosis mutant encoding a deletion in pncA.

285 mycobacterial drug tolerance in an in vitro M. tuberculosis biofilm model.

286 PBS) or albumin/PBS solutions in an in vitro M. tuberculosis-infected macrophage model.

287 Unlike macrophages, where M. tuberculosis resides in early-phagosomal compartments

288 While M. tuberculosis-reactive antibody levels are heterogeneo

289 Our data indicate that while M. tuberculosis requires ESX-5 for virulence, it tightly

290 e enrolled adults 18 to 50 years of age with M. tuberculosis infection (defined by positive results o

291 antly increased by coinfection compared with M. tuberculosis single infection.

292 BCG complemented with M. tuberculosis ppe37 exhibits HIA as efficient as that

293 at TLR2 knockout (TLR2KO) mice infected with M. tuberculosis HN878 exhibit increased bacterial burden

294 Among adults infected with M. tuberculosis, vaccination with M72/AS01(E) elicited a

295 driven immunopathology during infection with M. tuberculosis HN878 infection, likely by curtailing CX

296 Infection with M. tuberculosis, by contrast, was most likely in individ

297 inform treatment strategies in patients with M. tuberculosis/HIV coinfection.

298 R transgenic mice at 2 wk postinfection with M. tuberculosis and progressively decreased at later tim

299 eral blood mononuclear cells stimulated with M. tuberculosis displayed decreased cytokine (ie, interl

300 ays, particularly following stimulation with M. tuberculosis, and upregulation of genes involved in p