ライフサイエンスコーパス: Mtb

1 Mtb does not encode any characterized cobalamin transpor

2 Mtb extract, but not SL-1, also stimulates non-nocicepti

3 Mtb organic extracts from mutants lacking SL-1 synthesis

4 Mtb protein tyrosine phosphatase B (mPTPB) is a virulenc

5 (Mtb) produces inflections in the host signaling networks

6 Mtb- specific antigens and live bacillus Calmette-Guerin

7 TNF-alpha is responsible for accelerated Mtb growth, and TNF-alpha neutralisation reverses augmen

8 se in TB, and inhibition of PD-1 accelerates Mtb growth via excessive TNF-alpha secretion.

9 we demonstrate in vivo activity in an acute Mtb infection model and provide further proof of DprE1 b

10 Infection with laboratory-adapted Mtb H37Rv resulted in granulomas that are characterized

11 and confer superior immunity against aerosol Mtb infection in the context of T2D.

12 = 0.56), based on an IFNgamma readout after Mtb antigen stimulation.

13 The compound shows activity against Mtb H37Rv residing in macrophages.

14 confers protective trained immunity against Mtb.

15 s of selenium nanoparticles (Se NPs) against Mtb and further introduce a novel nanomaterial-assisted

16 ion, provided substantial protection against Mtb infection, emphasizing the importance of delivery ro

17 to identify correlates of protection against Mtb infection.

18 id not confer significant protection against Mtb K.

19 tion correlates of immune protection against Mtb.

20 xamining how drug-resistance mutations alter Mtb physiology and differences in the immune response to

21 Although Mtb can synthesize vitamin B(12) (cobalamin) de novo, up

22 An Mtb mutant lacking SL-1, MtbDeltapks2, shows attenuated

23 Here, we show that an Mtb organic extract activates nociceptive neurons in vit

24 tegy manipulating antimicrobial immunity and Mtb clearance may potentially serve in more effective th

25 anti-Mtb LAM immunoglobulin M (IgM) and anti-Mtb LAM IgG respectively.

26 cient size generally provide for potent anti-Mtb activity of these dihydropyridomycins (minimum inhib

27 Moreover, the anti-Mtb LAM IgM bound sensor probes and the AuNP reagent sto

28 This indicates that their anti-Mtb activity does not critically depend on the inhibitio

29 monic (AuNP) labels functionalized with anti-Mtb LAM immunoglobulin M (IgM) and anti-Mtb LAM IgG resp

30 distinguishing between ATB and asymptomatic Mtb-infected latent individuals.

31 tinguish active TB disease from asymptomatic Mtb infection.

32 TNF-alpha neutralisation reverses augmented Mtb growth caused by anti-PD-1 treatment.

33 ving into lysosome-associated autophagosomal Mtb degradation linked to ROS-mitochondrial and PI3K/Akt

34 P-FAB based Mtb LAM sensor demonstrates its potential for an on-site

35 rates that the metabolic differences between Mtb-infected AMs and KCs lead to differences in the rest

36 Overall, this study provides a link between Mtb infection, epigenetics and host immune response, whi

37 stallography of four apo- and cofactor-bound Mtb-MenD structures, along with several spectroscopy ass

38 e exacerbation of HIV-1 infection induced by Mtb.

39 ption of human immune signaling molecules by Mtb remains elusive, limiting drug discovery.

40 uired for heme and hemoglobin utilization by Mtb.

41 These findings support the use of clinical Mtb HN878 strain for infection in mice as an appropriate

42 correlation of genetic diversity of clinical Mtb isolates with clinically important phenotypes such a

43 Here we compare Mtb growth in mouse alveolar (AMs), peritoneal (PMs), an

44 -mediated clearance of bacteria.Conclusions: Mtb can persist in asymptomatic macaques for at least 7

45 rowth, some granulomas are unable to control Mtb growth, leading to bacteria and infected cells leavi

46 mice infected with an ULD or a conventional Mtb dose (50-100 CFU) that correlated with lung bacteria

47 The antitoxin, DarG(Mtb) , forms a cytosolic complex with DNA-repair protein

48 Rv0060 (DNA ADP-ribosyl glycohydrolase, DarG(Mtb) ), functions along with its cognate toxin Rv0059 (D

49 imultaneous deletion of both darT(Mtb) -darG(Mtb) does not alter viability of Mtb in vitro or in mice

50 We demonstrate that DarT(Mtb) -DarG(Mtb) form a functional TA pair and essentiality of darG(

51 Depletion of DarG(Mtb) alone is bactericidal, a phenotype that is rescued

52 functional TA pair and essentiality of darG(Mtb) is dependent on the presence of darT(Mtb) , but sim

53 Partial depletion of DarG(Mtb) triggers a DNA-damage response and sensitizes Mtb t

54 is essential for Mtb to survive partial DarG(Mtb) -depletion and leads to a hypermutable phenotype.

55 tb) , but simultaneous deletion of both darT(Mtb) -darG(Mtb) does not alter viability of Mtb in vitro

56 that assembles independently of either DarT(Mtb) or interaction with DNA.

57 rG(Mtb) is dependent on the presence of darT(Mtb) , but simultaneous deletion of both darT(Mtb) -darG

58 We demonstrate that DarT(Mtb) -DarG(Mtb) form a functional TA pair and essentiali

59 in Rv0059 (DNA ADP-ribosyl transferase, DarT(Mtb) ), to mediate reversible DNA ADP-ribosylation (Jank

60 Instead of the classical ATM-Chk2 DDR, Mtb gains survival advantage through ATM-Akt signaling c

61 of early alveolar macrophages and decreased Mtb control.

62 c experiments with clpC1- and clpP2-depleted Mtb cells suggested that the ClpC1P1P2 complex criticall

63 ork in concert with host immunity to disable Mtb.

64 Therefore, by using C10 to dissect Mtb persistence, we discovered that INH resistance is no

65 r after the loss of the MmpS6/MmpL6-encoding Mtb-specific deletion 1 region (TbD1).

66 powerful new tool that can rapidly evaluate Mtb drug resistance in a laboratory setting.

67 Pre-existing Mtb infection creates an immunological environment that

68 on, and we investigated whether pre-existing Mtb infection impacts the susceptibility of CD4+ T cells

69 and molecular insights into how pre-existing Mtb infection influences HIV-1 pathogenesis.

70 However, the impact of pre-existing Mtb infection on subsequent HIV infection has not been f

71 Experimentally Mtb-infected non-human primates (NHP) mirror the disease

72 Finally, Mtb-infected guinea pigs cough in a manner dependent on

73 hanistically, we demonstrate that, following Mtb infection, S100A8/A9 expression is required for upre

74 ral GSMNs networks have been constructed for Mtb and used to study the complex relationship between t

75 of the DNA-damage response is essential for Mtb to survive partial DarG(Mtb) -depletion and leads to

76 tify SR-B1 as the airway M cell receptor for Mtb.

77 SR-B1 is required for Mtb binding to and translocation across M cells in mouse

78 B (mPTPB) is a virulence factor required for Mtb survival in host macrophages.

79 emonstrate a previously undescribed role for Mtb EsxA in mucosal invasion and identify SR-B1 as the a

80 contrast to Pam(3)CSK(4) and FSL-1, we found Mtb LAM did not induce any of the classical PMN priming

81 r, both CD4(+) and CD8(+) T lymphocytes from Mtb infected, metformin treated animals maintained a mor

82 demonstrate that, unlike BCG or beta-glucan, Mtb reprograms HSCs via an IFN-I response that suppresse

83 HadD(Mtb) deletion triggered a marked change in Mtb keto-MA c

84 Importantly, HadD(Mtb) has a strong impact on Mtb virulence in the mouse m

85 The effects of the lack of HadD(Mtb) observed both in vitro and in vivo designate this p

86 letion mutant revealed the influence of HadD(Mtb) on the planktonic growth, colony morphology and bio

87 scovery of a third dehydratase protein, HadD(Mtb) (Rv0504c), whose gene is non-essential and sits ups

88 These data strongly suggest that HadD(Mtb) catalyzes the 3-hydroxyacyl dehydratation step of l

89 aries tested and get outside of the historic Mtb property space if we are to generate novel improved

90 3-ionized form using an arginine, Arg199, in Mtb.

91 D(Mtb) deletion triggered a marked change in Mtb keto-MA content and size distribution, deeply impact

92 n addition to validating the role of ClpB in Mtb's response to oxidants, we show that HtpG, a homolog

93 P2 protease subunits are well-established in Mtb, but the potential roles of the associated unfoldase

94 t clinical Rif(R) RNAP substitution found in Mtb infected patients (S456>L of the beta subunit).

95 tify the genes that support clpB function in Mtb.

96 Furthermore, in Mtb specific T cells, SIRT2 deacetylates NFkappaB-p65 at

97 Similar changes were identified in Mtb following antibiotic-treatment, and MDR-Mtb as mecha

98 Cell activation markers in Mtb-specific CD4+T cells distinguished ATB from LTBI and

99 imidazole are two top-scoring metabolites in Mtb-infected KCs and that acetylcholine is the top-scori

100 asis of various growth-essential proteins in Mtb, several of which contain intrinsically disordered r

101 oteins are targets for T-cell recognition in Mtb.

102 ce and an anticipatory metabolic response in Mtb.

103 and that acetylcholine is the top-scoring in Mtb-infected AMs.

104 d, decreased disease pathology and increased Mtb-specific protective immune responses.

105 Inhibition of PD-1 signalling increases Mtb growth, and augments cytokine secretion.

106 od from Mycobacterium tuberculosis-infected (Mtb-infected) individuals with and without HIV coinfecti

107 In the chronic stages of infection, Mtb infected metformin-treated animals had restored syst

108 d atropine (acetylcholine inhibitor) inhibit Mtb growth in AMs.

109 statin and mevastatin were unable to inhibit Mtb growth in THP-1 cells.

110 Interestingly, Mtb LAM did not abrogate priming responses elicited by P

111 d autophagy whereas imidazole directly kills Mtb by reducing cytochrome P450 activity.

112 t loss of TbD1 at the origin of the L2/L3/L4 Mtb lineages was a key driver for their global epidemic

113 ould discriminate active disease from latent Mtb infection (LTBI).

114 T cells derived from individuals with latent Mtb infection supported more efficient HIV-1 transcripti

115 g with ligands from bacterial pathogens like Mtb, may be important for early recognition of infected

116 avenous BCG prevents or substantially limits Mtb infection in highly susceptible rhesus macaques has

117 Infection with the LprE (Mtb) mutant also led to accumulation of autophagy-relate

118 d these mechanisms are among circulating MDR Mtb strains and what impact drug-resistance-conferring m

119 Mtb following antibiotic-treatment, and MDR-Mtb as mechanisms to circumvent antibiotic effects.

120 of ATM inhibitor enhances isoniazid mediated Mtb clearance in macrophages as well as in murine infect

121 Moreover, Mtb LAM did not elicit p38 MAPK phosphorylation or endoc

122 Reduced trafficking of this mutant Mtb strain to lysosomes correlated with enhanced intrace

123 iod but diverged for LTBI prevalence and new Mtb infections-outcomes for which definitive data are un

124 The recent discovery of a set of new Mtb inhibitory compounds that target Mtb-fumarase by bin

125 ls across the Mtb infection spectrum and non-Mtb-infected control individuals were analyzed for infla

126 Notably, Mtb infected CSE(-/-) macrophages show increased flux th

127 n of 3,724 distinct proteins covering 95% of Mtb protein-coding genes using artificial antigen-presen

128 human cohorts, demonstrating associations of Mtb bacteremia with progressive phenotypes of latent inf

129 were infected via inhalation with ~10 cfu of Mtb CDC1551, after which asymptomatic animals were eithe

130 o assess 3HP treatment-mediated clearance of Mtb infection in latently infected macaques.Methods: Six

131 dentify the epitopes targeted by clusters of Mtb-specific T cells, we carried out a screen of 3,724 d

132 A metabolomics comparison of Mtb-infected macrophages indicates that ornithine and im

133 istic lysosomal and Isoniazid destruction of Mtb.

134 ug-induced and phagolysosomal destruction of Mtb.

135 lth threat worldwide, and the development of Mtb vaccines could play a pivotal role in the prevention

136 While this lipid promotes the entry of Mtb into macrophages, which occurs via phagocytosis, its

137 Further, exposure of Mtb to H(2)S regulates genes involved in sulfur and copp

138 st lysosomal system is a defining feature of Mtb-infected macrophages and suggest that this altered l

139 Se/Man-Se NPs further promoted the fusion of Mtb into lysosomes for synergistic lysosomal and Isoniaz

140 Two groups of Mtb-exposed contacts of tuberculosis (TB) patients were

141 ndispensable for the extracellular growth of Mtb and for its survival in macrophages.

142 xyacyl-ACP dehydratases, HadAB and HadBC, of Mtb FAS-II complex required in-depth work.

143 Granulomas, the hallmark of Mtb infection, are complex structures that form in lungs

144 naphthoic acid (DHNA), binds to domain II of Mtb-MenD and inhibits its activity.

145 (3)CSK(4) We speculate that the inability of Mtb LAM to prime PMN may be due to differential localiza

146 at H(2)S reverses *NO-mediated inhibition of Mtb respiration.

147 resistance in cultured clinical isolates of Mtb and benchmark its performance with standard minimum

148 eight recently published metabolic models of Mtb-H37Rv to facilitate model choice.

149 profoundly alters the protective outcome of Mtb challenge in non-human primates (Macaca mulatta).

150 Phenotyping of Mtb hadD deletion mutant revealed the influence of HadD(

151 Cs lead to differences in the restriction of Mtb growth.

152 ts that DSBs inflicted by SecA2 secretome of Mtb provides survival niche through activation of ATM ki

153 NPs also induced autophagy sequestration of Mtb, evolving into lysosome-associated autophagosomal Mt

154 with aerosol exposure to the H37Rv strain of Mtb.

155 both drug-sensitive and resistant strains of Mtb and enhances the efficacy of front line anti-TB drug

156 insights into how drug-resistant strains of Mtb differentially impact immunometabolism.

157 shown that certain drug-resistant strains of Mtb modulate host metabolic reprogramming, and therefore

158 an unanticipated immune evasion strategy of Mtb in the BM that controls the magnitude and intrinsic

159 nal, structural, and bioinformatics study of Mtb enzymes initiating cholesterol catabolism and demons

160 d show Mpy-dependent antibiotic tolerance of Mtb in mouse lungs.

161 findings and show that in vivo treatment of Mtb-infected C57BL/6 mice with doramapimod, a p38 MAP-ki

162 (Mtb) -darG(Mtb) does not alter viability of Mtb in vitro or in mice.

163 ortion of memory T-cell subsets depending on Mtb infection status.

164 Siglec-1 expression depends on Mtb-induced production of type I interferon (IFN-I).

165 mportantly, HadD(Mtb) has a strong impact on Mtb virulence in the mouse model of infection.

166 B) strategy for mannosylated LAM (Man-LAM or Mtb LAM) detection down to attomolar concentrations.

167 tomatic for 7 months but harbored persistent Mtb infection, as shown by reactivation of latent infect

168 nce for 3HP-mediated clearance of persistent Mtb infection in human lungs has not been established.Ob

169 onal nanomaterials to promote phagolysosomal Mtb clearance remains a big challenge.

170 ed with lung bacterial burdens and predicted Mtb infection outcomes across species, including risk of

171 Models found prevalent Mtb infection and migration to be more significant drive

172 eatures with human granulomas, and prolonged Mtb containment with unilateral pulmonary infection in s

173 However, how pulmonary Mtb infection causes cough remains undefined, and whethe

174 The emergence of Rif-resistant (Rif(R)) Mtb presents a need for new antibiotics.

175 at pharmacological inhibition of CBS reduces Mtb bacillary load in mice.

176 s an immunological environment that reflects Mtb infection status and influences the susceptibility o

177 at H(2)S is the effector molecule regulating Mtb survival in macrophages.

178 programming in the context of drug-resistant Mtb infection, previous literature examining how drug-re

179 ces in the immune response to drug-resistant Mtb provides significant insights into how drug-resistan

180 KCs restrict Mtb growth more efficiently than all other macrophages a

181 e or imidazole or the two together restricts Mtb growth.

182 riggers a DNA-damage response and sensitizes Mtb to drugs targeting DNA metabolism and respiration.

183 Ribonucleic acid sequencing, Mtb proteome arrays, and metabolic profiling were perfor

184 spectrometry establish that H(2)S stimulates Mtb respiration and bioenergetics predominantly via cyto

185 A powerful approach to study Mtb metabolism as a whole, rather than just individual e

186 In this work, we study Mtb metabolism of lactate and pyruvate combining classic

187 In summary, Mtb LAM activates PMN via TLR2/1, resulting in the produ

188 of new Mtb inhibitory compounds that target Mtb-fumarase by binding to a nonconserved allosteric sit

189 sion of other chaperones, demonstrating that Mtb's stress response network depends upon finely tuned

190 We hypothesized that Mtb infection creates an immunological environment that

191 Our results indicate that Mtb exploits host-derived H(2)S to promote growth and di

192 Here, we show that Mtb has an itaconate dissimilation pathway and that the

193 Here, we show that Mtb upregulates one of the key epigenetic modulators, NA

194 Here we show that Mtb-infected mice deficient in the H(2)S-producing enzym

195 We showed that Mtb-infected CSE(-/-) mice survive longer than WT mice,

196 of suppression of immunity and suggest that Mtb has its own transformation system resembling the hum

197 vironment changes as we age and suggest that Mtb may benefit from declining host defenses in the lung

198 nes a confluence of findings supporting that Mtb has restricted metabolism at acidic pH that results

199 The Mtb cell wall cording factor, trehalose 6,6'-dimycolate

200 The Mtb LAM is quantified in terms of absorption of light pa

201 ted from HIV-negative individuals across the Mtb infection spectrum and non-Mtb-infected control indi

202 o study the complex relationship between the Mtb genotype and its phenotype.

203 atification could be further improved by the Mtb Ag/BCG IFNgamma ratio (p < 0.0001 AUC = 0.91).

204 ociceptive neurons in vitro and identify the Mtb glycolipid sulfolipid-1 (SL-1) as the nociceptive mo

205 show that M cell transcytosis depends on the Mtb Type VII secretion machine and its major virulence f

206 es and non-IFN-gamma T cell responses to the Mtb-specific proteins ESAT6 and CFP10, immunologic evide

207 al compartments that share features with the Mtb intracellular compartment.

208 recruited and classified according to their Mtb infection status using the tuberculin skin test (TST

209 ere we show that deletion of TbD1 confers to Mtb a significant increase in resistance to oxidative st

210 A (SP-A) and surfactant protein D (SP-D) to Mtb.

211 We demonstrated that exposure to Mtb directs primary human CD34(+) cells to differentiate

212 d CFP10, immunologic evidence of exposure to Mtb.

213 ron axis in HSCs impairs trained immunity to Mtb infection.

214 evelopment of protective trained immunity to Mtb.

215 However, exposure of PMN to Mtb LAM did elicit pro- and anti-inflammatory cytokine p

216 etformin promotes natural host resistance to Mtb infection by maintaining immune cell metabolic homeo

217 ously associated with the immune response to Mtb and demonstrates the power of high-throughput analys

218 sights into the early protective response to Mtb infection and possible avenues to interfere with Mtb

219 The proinflammatory immune response to Mtb infection in untreated guinea pigs was associated wi

220 F-alpha, and IFN-gamma levels in response to Mtb infection.

221 computational model, MultiGran, that tracks Mtb infection within multiple granulomas in an entire lu

222 olic flux profiles indicate that BDQ-treated Mtb is dependent on glycolysis for ATP production, opera

223 sotopomer analysis, we show that BDQ-treated Mtb redirects central carbon metabolism to induce a meta

224 that lipoarabinomannan from M. tuberculosis (Mtb LAM) would prime human PMN in a TLR2-dependent manne

225 ntly relies on detection of M. tuberculosis (Mtb).

226 Mycobacterium tuberculosis (Mtb) and human immunodeficiency virus (HIV) coinfection

227 to ribosomes in Mycobacterium tuberculosis (Mtb) and show Mpy-dependent antibiotic tolerance of Mtb

228 ly infected with Mycobacterium tuberculosis (Mtb) and to group them according to their specificity.

229 Mycobacterium tuberculosis (Mtb) can enter the body through multiple routes, includi

230 robial-resistant Mycobacterium tuberculosis (Mtb) causes over 200,000 deaths each year.

231 Mycobacterium tuberculosis (Mtb) continues to be a major health threat worldwide, an

232 lted in improved Mycobacterium tuberculosis (Mtb) control during chronic but not acute TB.

233 The viability of Mycobacterium tuberculosis (Mtb) depends on energy generated by its respiratory chai

234 termined whether Mycobacterium tuberculosis (Mtb) directly regulates myeloid commitment.

235 stance, with new Mycobacterium tuberculosis (Mtb) drugs having the highest priority.

236 r persistence of Mycobacterium tuberculosis (Mtb) during asymptomatic latent tuberculosis infection (

237 Mycobacterium tuberculosis (Mtb) employs plethora of mechanisms to hijack the host d

238 sis (TB) are the Mycobacterium tuberculosis (Mtb) escape from phagolysosomal destruction and limited

239 s expressing the Mycobacterium tuberculosis (Mtb) ESX-1 secretion system (BCG::RD1 and BCG::RD1 ESAT-

240 e human pathogen Mycobacterium tuberculosis (Mtb) harbors a well-orchestrated Clp (caseinolytic prote

241 "hypervirulent" Mycobacterium tuberculosis (Mtb) HN878 induces human-like granulomas composed of bac

242 e in controlling Mycobacterium tuberculosis (Mtb) infection and disease progression.

243 TB) is caused by Mycobacterium tuberculosis (Mtb) infection and is a major public health problem.

244 egies to prevent Mycobacterium tuberculosis (Mtb) infection are urgently required.

245 Mycobacterium tuberculosis (Mtb) infection causes tuberculosis (TB), a disease chara

246 Murine models of Mycobacterium tuberculosis (Mtb) infection demonstrate progression of M1-like (proin

247 Mycobacterium tuberculosis (Mtb) infection is among top ten causes of death worldwid

248 a consequence of Mycobacterium tuberculosis (Mtb) infection, contributes to TB pathogenesis, and when

249 85A expressed by Mycobacterium tuberculosis (Mtb) is a bacterial surface protein that is commonly use

250 Mycobacterium tuberculosis (Mtb) is an obligate human pathogen and the causative age

251 dissemination of Mycobacterium tuberculosis (Mtb) is critical to the pathogenesis of progressive tube

252 adaptability of Mycobacterium tuberculosis (Mtb) is still unresolved.

253 Mycobacterium tuberculosis (Mtb) is the leading cause of death from infection worldw

254 ound in clinical Mycobacterium tuberculosis (Mtb) isolates phenocopy lepA deletion to varying degrees

255 (TB), caused by Mycobacterium tuberculosis (Mtb) latently infects approximately one-fourth of the wo

256 role of H(2)S in Mycobacterium tuberculosis (Mtb) pathogenesis.

257 mice can control Mycobacterium tuberculosis (Mtb) replication, they have exacerbated inflammation and

258 Mycobacterium tuberculosis (Mtb) strains are classified into different phylogenetic

259 of ligands from Mycobacterium tuberculosis (Mtb) to MAIT cells.

260 interruption of Mycobacterium tuberculosis (Mtb) transmission, 2) sustained resolution of LTBI and T

261 hanisms by which Mycobacterium tuberculosis (Mtb) worsens HIV-1 pathogenesis remain scarce.

262 ive agent of TB, Mycobacterium tuberculosis (Mtb), and therefore metabolic pathways have recently re-

263 une responses to Mycobacterium tuberculosis (Mtb), as adjunctive treatment given with antitubercular

264 isease caused by Mycobacterium tuberculosis (Mtb), manifests with a persistent cough as both a primar

265 is infected with Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB).

266 Mycobacterium tuberculosis (Mtb), the causative infectious agent of tuberculosis (TB

267 In the pathogen Mycobacterium tuberculosis (Mtb), the protective effect of chaperones extends to sur

268 cterial pathogen Mycobacterium tuberculosis (Mtb), three contain antitoxins essential for bacterial v

269 ess responses in Mycobacterium tuberculosis (Mtb)-infected host cells.

270 is expressed in Mycobacterium tuberculosis (Mtb)-infected lung tissue but is absent in areas of immu

271 ally elevated in Mycobacterium tuberculosis (Mtb)-infected macrophages.

272 al. find that a Mycobacterium tuberculosis (Mtb)-specific lipid, SL-1, stimulates human nociceptive

273 rs cell death in Mycobacterium tuberculosis (Mtb).

274 by the bacterium Mycobacterium tuberculosis (Mtb).

275 with aerosolized Mycobacterium tuberculosis (Mtb).

276 ssion of InhA in Mycobacterium tuberculosis (Mtb).

277 e human pathogen Mycobacterium tuberculosis (Mtb).

278 icity factors of Mycobacterium tuberculosis (Mtb).

279 g populations of Mycobacterium tuberculosis (Mtb).

280 fections such as Mycobacterium tuberculosis (Mtb).

281 on detection of Mycobacterium tuberculosis (Mtb).

282 by the pathogen Mycobacterium tuberculosis (Mtb).

283 ical isolates of Mycobacterium tuberculosis (Mtb).

284 ors of ThyX from Mycobacterium tuberculosis (Mtb).

285 co-infected with Mycobacterium tuberculosis (Mtb)/simian immunodeficiency virus (SIV) suggests that c

286 r tenfold more hits than screening wild-type Mtb alone, with chemical-genetic interactions providing

287 emonstrating that Sor inhibits the wild-type Mtb RNAP by a similar mechanism as Rif: by preventing th

288 TAX1BP1, mediates clearance of ubiquitylated Mtb and targets bacteria to LC3-positive phagophores.

289 inant analyses to validate an approach using Mtb-specific CD4+T-cell activation markers in blood to d

290 of light membranes from Pam(3)CSK(4) versus Mtb LAM-stimulated cells demonstrated differential patte

291 The virulent Mtb strain, Rv caused double strand breaks (DSBs), where

292 tion, macaques were challenged with virulent Mtb.

293 Similarly, in vitro Mtb infection of macrophages resulted in reduced colony

294 causes cough remains undefined, and whether Mtb produces a neuron-activating, cough-inducing molecul

295 population is estimated to be infected with Mtb, accounting for ~1.3 million deaths in 2017.

296 idence of active TB following infection with Mtb and were subsequently either treated with 3HP (n = 7

297 Notably, in vivo infection with Mtb led to sustained DSBs and ATM activation during chro

298 ction and possible avenues to interfere with Mtb infection, including vitamin B5 supplementation.Anal

299 bserved that Hsp20 is poorly expressed in WT Mtb and that its expression is greatly induced upon depl

300 ated lysosomal rewiring compared with the WT Mtb in both in vitro and in vivo infections.