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1               Ten patients developed IRIS (6 mycobacterial).
2 or phase separation in the function of these mycobacterial ABC transporters and their regulation via
3 ics and develop compounds with improved anti-mycobacterial activity.
4    This finding represents a new paradigm in mycobacterial adaptation to hypoxia.
5                                              Mycobacterial AdnAB is a heterodimeric helicase-nuclease
6 and CXC chemokines at baseline and following mycobacterial Ag or mitogen stimulation in individuals w
7                                         Upon mycobacterial Ag stimulation, S. stercoralis (+)LTB(+) i
8 s of CCL1, CCL2, CCL4, CCL11, and CXCL11 and mycobacterial Ag-stimulated levels of CCL1, CCL2, CCL11,
9 exhibit respiratory burst activity following mycobacterial-Ag or LPS stimulation and were less capabl
10  (absence of stimulation) and in response to mycobacterial-Ag stimulation than monocytes from S. ster
11 ly lower activation at baseline or following mycobacterial-Ag stimulation.
12 the basis for developing more effective anti-mycobacterial agents.
13 ae-abscessus complex (MCAC) are close to the mycobacterial ancestor and includes both human, animal a
14  in the elongation of the mannan backbone of mycobacterial and corynebacterial LM, further highlighti
15 hey are associated with an increased risk of mycobacterial and fungal infections.
16 rmore, conducting similarity searches in 101 mycobacterial and ~4500 other prokaryotic genomes, we as
17 hance immune clearance of refractory fungal, mycobacterial, and viral infections.
18                                              Mycobacterial antibody levels were not associated with d
19  G (IgG), serum markers of inflammation, and mycobacterial antibody levels.
20                However only MR1A can present mycobacterial antigen to MAIT cells.
21        Unconventional T cells that recognize mycobacterial antigens are of great interest as potentia
22 is associated with diminished recognition of mycobacterial antigens in T2D.
23 driver of IFNgamma production in response to mycobacterial antigens provides new insights into human
24 ponses endowed with long-term memory against mycobacterial antigens.
25 ch produce IFN-gamma normally in response to mycobacterial antigens.
26 (IPE) and squaramides (SQA) as inhibitors of mycobacterial ATP synthesis.
27 losis, providing a tool to better understand mycobacterial bioenergetics and develop compounds with i
28 in it was evaluated if 2-AI compounds affect mycobacterial bioenergetics.
29 hat, though residual chloramine may increase mycobacterial biomass in a DWDS, it may also decrease my
30                   Although the late steps of mycobacterial biotin synthesis, assembly of the heterocy
31 ntegrity, which was accompanied by a reduced mycobacterial burden in lung and spleen and a prolonged
32 tokines are biomarkers of disease extent and mycobacterial burden in pulmonary tuberculosis (PTB).
33                We find that the reduction in mycobacterial burden is dependent on macrophages and gra
34 cted zebrafish with aspirin markedly reduced mycobacterial burden.
35  their association with disease severity and mycobacterial burdens in PTB.
36    A growing body of evidence implicates the mycobacterial capsule, the outermost layer of the mycoba
37 size control are insufficient to explain the mycobacterial cell cycle.
38 tion and drug resistance leads ultimately to mycobacterial cell death.
39 ed that the TGD1 L45 loop interacts with the mycobacterial cell entry domain of TGD2.
40 tems to build a model of the dynamics of the mycobacterial cell envelope across space and time.
41 ction of MmpL transporters and regulation of mycobacterial cell envelope biogenesis.
42               Much of what we know about the mycobacterial cell envelope has been gleaned from model
43                                          The mycobacterial cell envelope is crucial to host-pathogen
44                                          The mycobacterial cell envelope is extremely hydrophobic, wh
45  These findings enhance our understanding of mycobacterial cell envelope structure and dynamics and h
46 t build the lipidated polysaccharides of the mycobacterial cell envelope, and are targets of anti-tub
47 acterial capsule, the outermost layer of the mycobacterial cell envelope, in modulation of the host i
48  formation occurs in the outer layers of the mycobacterial cell envelope.
49 sing measurements and stochastic modeling of mycobacterial cell size and cell-cycle timing in both sl
50         Growth was restored upon loss of the mycobacterial cell wall component phthiocerol dimycocero
51 N-2 are expressed on myeloid cells and sense mycobacterial cell wall glycolipids.
52  synthesis of essential mycolic acids in the mycobacterial cell wall, is the target for the frontline
53 n, localized in the periplasmic space of the mycobacterial cell wall, was shown to be an essential an
54 ttling a variety of lipids to strengthen the mycobacterial cell wall.
55 ccharide lipoarabinomannan (LAM), present in mycobacterial cell walls, can provide results within min
56                      Instead, we showed that mycobacterial cell-cycle progression is regulated by an
57  as they occur in mycolic acids (MAs) in the mycobacterial cell.
58 an accumulation of protein substrates in the mycobacterial cell.
59 s have dual functions inside and outside the mycobacterial cell.
60                       Our data indicate that mycobacterial cells monitor biotin sufficiency through a
61 tein, Wag31, involved in polar elongation of mycobacterial cells.
62 erminant in facilitating polar elongation in mycobacterial cells.
63                        As in other bacteria, mycobacterial chromosomes are segregated by pair of prot
64 l, route significantly accelerates pulmonary mycobacterial clearance, limits lung pathology, and rest
65                 MPA, but not NET-A, subverts mycobacterial containment in vitro and downregulates pat
66 d lung segments.Conclusions: A lung-oriented mycobacterial controlled human infection model using liv
67 ion and antimicrobial gene expression by the mycobacterial cord factor that may contribute to mycobac
68                                              Mycobacterial cord factor trehalose-6,6-dimycolate (TDM)
69 ly delivered to granulomas and extracellular mycobacterial cords in vivo in an infected zebrafish mod
70  results suggest that a peptide derived from mycobacterial Cpn60.1 has a long-lasting anti-inflammato
71 gle raw sputum, which was then processed for mycobacterial culture and phenotypic drug susceptibility
72 pneumoniae urinary antigen detection, sputum mycobacterial culture and Xpert MTB/RIF, and nasopharyng
73                    IS samples were tested by mycobacterial culture and Xpert MTB/RIF.
74 d with microbiologically confirmed TB, using mycobacterial culture or Xpert MTB/RIF testing of sputum
75                                              Mycobacterial culture was done on 2 sputum samples, bloo
76 iagnostic tests, such as molecular assays or mycobacterial culture, in community and primary healthca
77 samples for polymerase-chain-reaction assay, mycobacterial culture, or both.
78 atheter cultures for BCG in patients in whom mycobacterial cultures were performed.
79 (i) = 4 muM), which also proved effective on mycobacterial cultures.
80 h the host membrane, resulting in attenuated mycobacterial cytosolic translocation and virulence.
81 uired for EsxA membrane permeabilization and mycobacterial cytosolic translocation and virulence.
82          Isoniazid- and moxifloxacin-induced mycobacterial death correlated with a transient increase
83 een energy metabolism and antibiotic-induced mycobacterial death is essential to develop potent drug
84 aluated by smear microscopy, BACTEC MGIT 960 Mycobacterial Detection System (MGIT) and Lowenstein-Jen
85 G-disA-OE) that overexpresses the endogenous mycobacterial diadenylate cyclase gene and releases high
86          RATIONALE: Pulmonary nontuberculous mycobacterial disease (PNTM) often affects white postmen
87        Human T-bet deficiency thus underlies mycobacterial disease by preventing the development of i
88                     We report a patient with mycobacterial disease due to inherited deficiency of the
89 lying deficits in IFNgamma responsiveness in mycobacterial disease syndrome resulting from a T168N mu
90  potential for host-directed therapy against mycobacterial disease targeting this nutrient and/or its
91 y contributes to Mendelian susceptibility to mycobacterial disease upon SPPL2a deficiency.
92 llular function, important for resistance to mycobacterial disease, has remained biochemically unchar
93 mpounds that modulate host immunity to limit mycobacterial disease, including the inexpensive, safe,
94  SPPL2a leads to Mendelian susceptibility to mycobacterial disease, which is attributed to a loss of
95 terferon gamma (IFN-gamma) immunity underlie mycobacterial disease.
96 um leprae causes leprosy and is unique among mycobacterial diseases in producing peripheral neuropath
97 vel therapies to combat a number of relevant mycobacterial diseases.
98 rial biomass in a DWDS, it may also decrease mycobacterial diversity.
99 -relevant stresses because it is part of the mycobacterial divisome and stabilizes the essential divi
100  conditions suggested it as a potential anti-mycobacterial drug target.
101 h anti-biofilm activity were shown to revert mycobacterial drug tolerance in an in vitro M. tuberculo
102 he basis for a novel class of broad-spectrum mycobacterial drugs.
103 rk for the development of Sdh-selective anti-mycobacterial drugs.
104 well-documented role for macrophages as anti-mycobacterial effector cells, badger macrophage (bdMphi)
105                            We speculate that mycobacterial EHs may have a narrow substrate specificit
106 ncentration determined to interfere with the mycobacterial electron transport chain.
107 n microscopy and x-ray crystal structures of mycobacterial EmbA-EmbB and EmbC-EmbC complexes in the p
108                                    Following mycobacterial entry into macrophages the ESX-1 type VII
109                                 However, the mycobacterial enzyme lacks this reverse activity, but th
110 und is a prodrug that is bioactivated by the mycobacterial enzyme MymA.
111              We report on the discovery of a mycobacterial enzyme, named here SucT, that adds succiny
112 s a heterodimer (EsxA:B) and are crucial for mycobacterial escape from phagosomes and cytosolic trans
113 a massive reservoir of genes for identifying mycobacterial essential functions, identifying potential
114                                          The mycobacterial F(1)-ATPase is most similar to the F(1)-AT
115 to advance this regulation as a new area for mycobacterial F-ATP synthase inhibitor development.
116       In silico screening identified a novel mycobacterial F-ATP synthase inhibitor disrupting epsilo
117 eraction of the N- and C-terminal domains of mycobacterial F-ATP synthase subunit epsilon is proposed
118 tion of large-scale image-based analyses for mycobacterial functional genomics, simultaneously establ
119                 We demonstrate that the core mycobacterial gene lpqI, encodes an authentic NagZ beta-
120  that the numerous proteins encoded by these mycobacterial genes dictate the immune pathogenesis of t
121 otypic profiling, we identify and categorize mycobacterial genes required for low iron fitness.
122                                  To identify mycobacterial genetic markers associated with increased
123 ns but also have provided numerous tools for mycobacterial genetics.
124  contains reactive oxygen species due to the mycobacterial genomes encoding a large number of dehydro
125               Comparison with other complete mycobacterial genomes indicate that the divergence of L8
126                        Surprisingly, neither mycobacterial genomic variants, lineage, nor dormancy st
127 ble TB, and that multiple factors, including mycobacterial genomic variation, would predict culturabl
128 uc and Hhy perform distinct functions during mycobacterial growth and survival.
129 antly enhanced the ability of INH to control mycobacterial growth ex vivo.
130 ctive immune responses and potently inhibits mycobacterial growth in a murine model of M. tb infectio
131                                              Mycobacterial growth in peripheral blood mononuclear cel
132 ibited myeloid differentiation and decreased mycobacterial growth in vitro.
133 ssion of Hb genes correlated positively with mycobacterial growth in whole blood from UK/Asian adults
134 m 172 patients) was also cultured by using a mycobacterial growth indicator tube (MGIT) and on Lowens
135  assay, broth microdilution (BMD) assay, and mycobacterial growth indicator tube (MGIT) assay.
136 ith Lowenstein-Jensen medium (LJ) and liquid mycobacterial growth indicator tube (MGIT) cultures.
137 ng increase in the time to positivity of the mycobacterial growth indicator tube (MGIT) liquid cultur
138 cystic fibrosis patients and compared to the mycobacterial growth indicator tube (MGIT) system and Mi
139 copic observation drug susceptibility assay, mycobacterial growth indicator tube, and by WGS on isola
140  flagged positive at 3 days of incubation in mycobacterial growth indicator tubes.
141              We present an optimised ex vivo mycobacterial growth inhibition assay (MGIA) to assess t
142                    We implemented an ex vivo mycobacterial growth inhibition assay (MGIA) to discrimi
143   As many of these systems are essential for mycobacterial growth or virulence, they provide opportun
144 rom baseline to Day 84 on a semiquantitative mycobacterial growth scale.
145 lyl reductase Rv2509 and outline its role in mycobacterial growth, highlighting its potential as a ne
146 ity of host cells within the lung to inhibit mycobacterial growth, including Bacille Calmette-Guerin
147 sion tomography-computed tomography imaging, mycobacterial growth, pathology and granuloma formation.
148 otein tyrosine phosphatase inhibition limits mycobacterial growth, suggesting a new strategy for host
149 division, suggesting specific impairments of mycobacterial growth.
150 nly exception is a gyrase reconstituted from mycobacterial GyrA and B. subtilis GyrB, which exceeds t
151 rast, the specific insertions in E. coli and mycobacterial gyrase subunits appear to prevent efficien
152 ng that the activities of enzymes containing mycobacterial GyrB are limited by ATP hydrolysis.
153                                          The mycobacterial heparin-binding hemagglutinin (HBHA) is a
154 erminant in M. abscessus We demonstrate that mycobacterial HflX associates with the 50S ribosomal sub
155 acrolide-lincosamide resistance in which the mycobacterial HflX dissociates antibiotic-stalled riboso
156 acrolide-lincosamide antibiotics mediated by mycobacterial HflX, a conserved ribosome-associated GTPa
157   Mycobacteriophages are viruses that infect mycobacterial hosts including Mycobacterium tuberculosis
158                                Sequencing of mycobacterial hsp65 genes indicated that the chloraminat
159 by DNA hypermethylation of genes critical to mycobacterial immunity resulting in decreased mycobacter
160 ds are structurally related to the important mycobacterial immunogen cord factor.
161      Together, our findings demonstrate that mycobacterial infection alters the formation of erythroc
162                                              Mycobacterial infection and accompanying surface TLR act
163 lline metabolism for myeloid defense against mycobacterial infection and highlight the potential for
164  Il-1beta transcription in vivo during early mycobacterial infection and importantly highlight a host
165                 Recently, we have found that mycobacterial infection downregulated miR-148a-3p (now t
166 ron supplementation on the susceptibility to mycobacterial infection have been reported.
167                                              Mycobacterial infection in humans and zebrafish results
168                                 The sites of mycobacterial infection in the lungs of tuberculosis (TB
169 umans and livestock were screened for active mycobacterial infection, and opportunistic post-mortem e
170  In 3 patients with post-HCT IRIS related to mycobacterial infection, in vitro data demonstrate the e
171  mutations in LRRK2 confer susceptibility to mycobacterial infection, suggesting LRRK2 also controls
172 less infiltration of macrophages to sites of mycobacterial infection, thus impairing granuloma develo
173 ring the first few weeks following pulmonary mycobacterial infection, we found a drastic increase in
174 converged downstream pathways in response to mycobacterial infection, which was supported by data ind
175  complex granulomas that are the hallmark of mycobacterial infection.
176 l sites and are known to respond robustly to mycobacterial infection.
177 tion compromises protective host immunity to mycobacterial infection.
178 l dissemination characterize severe forms of mycobacterial infection.
179 ant component of vascular dysfunction during mycobacterial infection.
180  in the downregulation of immune response in mycobacterial infection.
181 s (e.g., interleukin-6 [IL-6] and IL-10), in mycobacterial infection.
182 5.10 and 4.65, respectively; both P = .001), mycobacterial infections (AIDS; P = .006), and viral inf
183  deficiency, which protects mice from severe mycobacterial infections, thereby laying the foundation
184 des a novel strategy for enhanced control of mycobacterial infections.
185 s a frequent and challenging complication of mycobacterial infections.
186 th efforts to develop new antimicrobials for mycobacterial infections.
187 e potential for the therapeutic treatment of mycobacterial infections.
188 s between host and pathogen lipids influence mycobacterial infectivity and suggests the use of statin
189          The upregulation of miR-148 reduced mycobacterial intracellular survival.
190 s and monocytes after ART initiation in IRIS/mycobacterial IRIS compared with non-IRIS patients.
191 row (BM) and spleen FDG uptake was higher in mycobacterial IRIS specifically.
192  BM and spleen metabolism is associated with mycobacterial IRIS, HIV viremia, and Glut-1 expression o
193 approximately 100 bacilli of 3 hypervirulent mycobacterial isolates (Mycobacterium tuberculosis strai
194 n the virulence properties of the sequential mycobacterial isolates.
195                             The diagnosis of Mycobacterial keratitis was made.
196  results reveal how the molecular shape of a mycobacterial lipid can modulate the biological response
197 hip drawn here, documented alteration in the mycobacterial lipidome during cellular infection and/or
198                 Interactions between PMN and mycobacterial lipids impact the activation state of thes
199  investigate protein interactions with other mycobacterial lipids.
200 tment, significantly reduced lung and spleen mycobacterial loads compared to antibiotic treatment alo
201                                              Mycobacterial MCM thus joins enzymes in the glyoxylate s
202               We defined a critical role for mycobacterial membrane phenolic glycolipid (PGL) in engi
203        Integral membrane transporters of the Mycobacterial Membrane Protein Large (MmpL) family and t
204 e cytoplasm to the periplasmic space via the mycobacterial membrane protein large (MmpL) family of pr
205                                          The mycobacterial membrane protein large (MmpL) proteins are
206                                          The mycobacterial membrane protein large (MmpL) proteins tra
207                                              Mycobacterial membrane protein Large 3 (MmpL3) is essent
208                                              Mycobacterial membrane protein Large 3 (MmpL3), an essen
209 rophore redundancy within the non-pathogenic mycobacterial model organism M. smegmatis (Msmeg), to id
210                               One quarter of mycobacterial mRNAs are leaderless, beginning with a 5'-
211 ection and DNA sequencing of PIPD1-resistant mycobacterial mutants revealed the presence of single-nu
212 or-unrestricted and recognize CD1b-presented mycobacterial mycolates.
213 ed patients with disseminated nontuberculous mycobacterial (NTM) disease.
214  of 3 patients with suspected nontuberculous mycobacterial (NTM) infection after receiving tattoos at
215                  The defining feature of the mycobacterial outer membrane (OM) is the presence of myc
216 portant roles in the synthesis and export of mycobacterial outer membrane lipids.
217 osate determined the low permeability of the mycobacterial outer membrane, and the PE/PPE proteins ap
218 h Mtb20S shed light on their selectivity for mycobacterial over human proteasomes.
219 ary metabolic pathways and associated P450s, mycobacterial P450s seem to play a role in utilization o
220 of importance for our basic understanding of mycobacterial pathogenesis and innate immune sensing.
221 irulence factor that plays a crucial role in mycobacterial pathogenesis in the context of innate immu
222 l to illuminate poorly understood aspects of mycobacterial pathogenesis, particularly the host membra
223 ) and causes blunted interferon responses to mycobacterial pathogens and cytosolic nucleic acid agoni
224 found to be active against Gram-positive and mycobacterial pathogens.
225 tol-phosphate biosynthesis in the context of mycobacterial pathogens.
226 ore and applied this property to investigate mycobacterial peptidoglycan synthesis and remodeling wit
227 alveolar lavage and tissues were sampled for mycobacterial persistence, pathology, and immune correla
228 bacterial cord factor that may contribute to mycobacterial persistence.
229 y, became bactericidal, killed drug-tolerant mycobacterial persisters, and rapidly cleared M. tubercu
230 est, associated with increased maturation of mycobacterial phagosomes, indicating that extended PtdIn
231 id transporters that are important for basic mycobacterial physiology and Mycobacterium tuberculosis
232 ylation is important for maintenance of both mycobacterial physiology and redox poise, an axis that i
233 hus providing a defined role for this USP in mycobacterial physiology and stress responses.
234                                              Mycobacterial Pol1 is a bifunctional enzyme composed of
235           Distinctive structural features of mycobacterial Pol1 POL include a manganese binding site
236 hanism by which aggregates are sorted to the mycobacterial pole is not known.
237  likely a bottleneck step at the majority of mycobacterial promoters.
238 tion; (ii) survival capacity; and (iii) anti-mycobacterial properties.
239 ormed semi-quantitative mass-spectrometry of mycobacterial protein aggregates in wild-type, hspX-dele
240                           The FHA-containing mycobacterial protein GarA is a central element of a pho
241 ntiated beta-lactam antibiotics by affecting mycobacterial protein secretion and lipid export.
242 ective highlights chemical tools specific to mycobacterial proteins and the cell lipid envelope that
243 recedented insights into the function of the mycobacterial proteome and lipidome.
244 ry isolates met criteria for non-tuberculous mycobacterial pulmonary disease (NTM-PD).
245 overed a DsbA-like mycoredoxin that promotes mycobacterial resistance to oxidative stress and reacts
246 oxidase-encoding genes cydAB, Q203 inhibited mycobacterial respiration completely, became bactericida
247 em, and identify filamentation as a defining mycobacterial response to histidine starvation.
248 his observation, we infer the existence of a mycobacterial restriction-modification system, and ident
249 mportant pleiotropic roles of the enzymes in mycobacterial RNA metabolism highlighting their potentia
250           Initiation of transcription by the Mycobacterial RNA polymerase (RNAP) has previously been
251 to 4-thiouridine-labelled RNA, we mapped the mycobacterial RNA-bound proteome and identified degrados
252 etic insights to the division of labor among mycobacterial RNases H by deleting the rnhA, rnhB, rnhC
253      Here we present crystal structures of 9 mycobacterial SDRs in which the insertion buries the NAD
254 A2 mutant, we identified a new player in the mycobacterial SecA2 pathway that we named SatS for SecA2
255 t of these functions, we annotated Rv2672 as mycobacterial secreted hydrolase 1 (Msh1).
256  in recognition, transport or utilization of mycobacterial siderophores, we identify novel putative l
257 al relevance of such identifications vary by mycobacterial species and geographical location.
258 to characterize essential genes in different mycobacterial species both in vitro and in vivo.
259 ls is a critical process for the survival of mycobacterial species in many environmental niches.
260         Overall, these studies indicate that mycobacterial species may regulate their overall membran
261  class of deaminases, predominantly found in mycobacterial species that act on the commercially impor
262 ion; (ii) in principle can be applied to any mycobacterial species to identify endogenous bacterial p
263 compounds exhibit promising activity against mycobacterial species, including Mycobacterium tuberculo
264 streptococcal species and arabinogalactan of mycobacterial species.
265 uctases (FDORs) and is widely distributed in mycobacterial species.
266 he unique lipid and metabolite repertoire of mycobacterial species.
267 er organisms, but is highly conserved across mycobacterial species.
268 ifferences unique to PD caused by a specific mycobacterial species.
269 substrate specificity and catalysis in a new mycobacterial species.
270 e is exclusively targeted for hibernation by mycobacterial-specific protein Y (Mpy), which binds to t
271 idered host detrimental since it facilitates mycobacterial spread.
272                                     However, mycobacterial sputum bacillary load and clinical charact
273 amma interferon (MIG) (CXCL9) in response to mycobacterial stimulation and decreased production of IF
274 were no differences in cytokine responses to mycobacterial stimuli, but compared to converters, persi
275                        Cryptic minor variant mycobacterial subpopulations exist below the resolving c
276          Lysosomal alterations are caused by mycobacterial surface components, notably the cell wall-
277 and transports trehalose monomycolate to the mycobacterial surface.
278 emonstrate that 2-phospho-L-ascorbic reduces mycobacterial survival in macrophage infections, hence c
279 id M. tuberculosis cell death, which reduces mycobacterial survival in macrophages and prolongs the s
280 containing glycoconjugates in eukaryotic and mycobacterial systems.
281                       Since the discovery of mycobacterial T7SSs about 15 y ago, genetic, structural,
282 lucidation of the structure and mechanism of mycobacterial T7SSs in protein secretion.
283 e data, we propose that the highly conserved mycobacterial tam genes be renamed bioC M. tuberculosis
284                 We measured the systemic and mycobacterial (TB) antigen-stimulated levels of type 1,
285 ting and processing large volumes of CSF for mycobacterial testing are important for optimal diagnost
286 ome is an attractive adjunct to current anti-mycobacterial therapy that warrants further investigatio
287 d a 2.76 A-resolution crystal structure of a mycobacterial transcription initiation complex (TIC) wit
288  regulation of the highly medically-relevant mycobacterial transcription machinery and define HelD as
289                                              Mycobacterial type VII secretion systems consist of five
290 des, we solved the crystal structures of the mycobacterial upstream (phosphorylation-dependent) compl
291                                   While live mycobacterial vaccines show promising efficacy, HIV co-i
292 esis, such as Ri03, affect streptococcal and mycobacterial viability and can serve as lead compounds
293 undance of mycolic acids (MAs), essential to mycobacterial viability, and of other species-specific l
294 y required for oxidative phosphorylation and mycobacterial viability.
295 ate synthase (PIPS), an essential enzyme for mycobacterial viability.
296                Cell envelope lipids are also mycobacterial virulence factors that influence the host
297        In addition, cell envelope lipids are mycobacterial virulence factors.
298            In addition, cell wall lipids are mycobacterial virulence factors.
299 H37Rv M tuberculosis strain as reference for mycobacterial virulence.
300 ared clinical characteristics, and performed mycobacterial whole-genome sequencing, dormancy phenotyp

 
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