ライフサイエンスコーパス: virulence

1 ice and confirmed that this trait is tied to virulence.

2 ed mycobacterial cytosolic translocation and virulence.

3 in GAG deacetylation, biofilm formation, and virulence.

4 orrying, given its high transmissibility and virulence.

5 owth, leading to host cell death and loss of virulence.

6 utations that decrease PE synthesis decrease virulence.

7 aute (AGO)/RNA-induced silencing complex for virulence.

8 may play an important role in determining HP virulence.

9 od in many species and are often involved in virulence.

10 s increasingly recognized as a key driver of virulence.

11 and there is evidence for ample variation in virulence.

12 n E3 ubiquitin ligase and promotes bacterial virulence.

13 ammasome, and this strain exhibited enhanced virulence.

14 es in the methylome, cellular physiology and virulence.

15 tal role in determining virus host range and virulence.

16 r gaining insights into bacterial growth and virulence.

17 ity, which is likely to affect phenotype and virulence.

18 ain, but multiple plc mutants showed reduced virulence.

19 ncy of the B. pseudomallei phospholipases in virulence.

20 ined the importance of CsrA for A. baumannii virulence.

21 htened V. parahaemolyticus' colonization and virulence.

22 ax, a HPr(-) EI(-) mutant was attenuated for virulence.

23 n and iron excess and is thereby crucial for virulence.

24 phenotypic markers for EAEC strains of high virulence.

25 Here, we studied its role in A. baumannii virulence.

26 but is important for adhesion, motility, and virulence.

27 hat arginine also directly impacts bacterial virulence.

28 hat T3SS1 repression is required for maximal virulence.

29 of upregulated regulatory genes in bacterial virulence.

30 is, biofilm formation, capsule synthesis and virulence.

31 tein secretion, a necessary prerequisite for virulence.

32 from OmpR repression of the key ToxR regulon virulence activator aphB, and ompR overexpression in wil

33 eactive oxygen species burst, while the full virulence activities of nuclear targeted PITG20303 and P

34 is grown on trimethoprim exhibited increased virulence against Caenorhabditis elegans.

35 of three compounds from 430D-F5 that reduce virulence and abate dermonecrosis: 3-oxo-olean-12-en-28-

36 Sequence-based characterization of virulence and antibiotic resistance may require testing

37 Many proteobacteria use AHL to coordinate virulence and biofilm formation in a cell density-depend

38 ae, resulting in the repeated convergence of virulence and carbapenem resistance in the United States

39 s are involved in regulating many aspects of virulence and chronic infection.

40 fense against pathogens, we investigated the virulence and colonization ability of the mutants.

41 or the transcription and translation of long virulence and conjugation operons in many Gram-negative

42 tem (TCS) is a global regulator of S. aureus virulence and critical for survival under environmental

43 This reduced acute virulence and enhanced biofilm formation, both of which

44 replication in vitro, it contributes to the virulence and growth of T. gondii in mice.

45 structuring protein and global repressor of virulence and horizontally-acquired genes in bacteria.

46 n shown to play important roles in bacterial virulence and in immune modulation through the transmiss

47 adpy19 parasites were strongly attenuated in virulence and induced protective immunity in mice.

48 Large-scale virulence and infectivity assays using insect and mouse

49 aureus strains and plays important roles in virulence and interbacterial competition.

50 ntal evidence for how admixture can modulate virulence and metabolism.

51 erence 1, is known to play a crucial role in virulence and pathogenesis of M. tuberculosis In our ear

52 ilm properties of FAs and their relations to virulence and quorum sensing, such as diffusible signal

53 Bacterial virulence and the spread of multidrug resistance have pr

54 MDV genetic diversity is important for viral virulence and transmissibility in susceptible animals.

55 diversity of type O FMDV could increase both virulence and transmissibility, thus leading to their do

56 implications for trade-offs between pathogen virulence and transmissibility.

57 litates sigma(70) binding to DNA to regulate virulence and virulence-enhancing genes.

58 jor phenotypes, including biofilm formation, virulence, and antibiotic tolerance.

59 litates the spread of antibiotic resistance, virulence, and environmental persistence genes between n

60 e to the bacteriolytic activity of lysozyme, virulence, and host innate immune responses.

61 compare the in vitro growth characteristics, virulence, and host response of a wild-type and an atten

62 utations that increase PE synthesis increase virulence, and mutations that decrease PE synthesis decr

63 x plays an important role in influenza virus virulence, and the gene segments of influenza A(H5N8) vi

64 ae, ToxR is required for bile resistance and virulence, and ToxR is fully activated and protected fro

65 interbacterial competition, we observed our virulence-associated CdiA-CT domain to promote toxicity

66 preceded by one stop codon, or the 2stop+A4G virulence-associated combination were generated and char

67 bination occurring at distal sites harboring virulence-associated genes.

68 A primary virulence-associated trait of the opportunistic fungal p

69 subset of effectors, induced expression of a virulence-associated transcriptome in response to degrad

70 ant pathogen Pantoea ananatis lacks both the virulence-associated type III and type II secretion syst

71 s that target core determinants of bacterial virulence at the host-pathogen interface.

72 in our previous study, but the mechanisms of virulence attenuation are not fully understood.

73 ting the role of specific genetic changes in virulence attenuation is currently lacking.

74 e were not responsible for the difference in virulence between the two strains.

75 arge and previously unreported difference in virulence between two commonly used ZIKV strains, in two

76 contribute to bacterial host adaptation and virulence beyond the role of the Type I R-M systems agai

77 ce of riboregulation in controlling Shigella virulence, but they also have the potential to facilitat

78 himurium that plays a critical role in their virulence by changing the outer membrane permeability.

79 investigated the role of SpxA1 in growth and virulence by identifying genes regulated by SpxA1 in bro

80 ofilm-grown cells activate expression of the virulence cascade, including the toxin coregulated pilus

81 , hyphae, and biofilm development as well as virulence characteristics of diverse microbes.

82 and ROP18 induced more severe attenuation of virulence compared to single Deltagra12 or Deltarop18 mu

83 sses the host-immune system and an increased virulence compared to the low viral titer type.

84 igate the molecular basis for this increased virulence, comparing a virus from the 1990s and a contem

85 This enhanced virulence correlated with an increase in expression of t

86 The outer membrane is a key virulence determinant of gram-negative bacteria.

87 els has demonstrated QS-dependent control of virulence determinants and virulence in several human pa

88 infection, yet they lack expression of many virulence determinants associated with the pathogenicity

89 IL plasmid, KL51 capsule, and yersiniabactin virulence determinants.

90 ture resulted in up to a 10,000-fold drop in virulence during mouse infection, while compensatory dou

91 Plutella xylostella), thereby countering the virulence effect of Bacillus thuringiensis (Bt) toxins.

92 eport of triterpenoid acids with potent anti-virulence effects against S. aureus.

93 70) binding to DNA to regulate virulence and virulence-enhancing genes.

94 e.g., via drugs) affect disease dynamics and virulence evolution.

95 The Pseudomonas virulence factor (pvf) operon is essential for the biosy

96 mily, that we recently showed functions as a virulence factor alternating the host's immune response

97 protein, encoded by the emm gene, is a major virulence factor and vaccine candidate and forms the bas

98 r abscesses in humans worldwide and contains virulence factor capsular polysaccharides and lipopolysa

99 as a pleiotropic regulator of flotation and virulence factor elaboration in this strain.

100 The Mycobacterium tuberculosis virulence factor EsxA and its chaperone EsxB are secrete

101 challenging to study how pneumococci control virulence factor expression, because cues of natural env

102 microaerobic environments, which influences virulence factor expression.

103 xpansin proteins may be an under-appreciated virulence factor for many pathogen species.

104 se infection, identifying this receptor as a virulence factor for transmission.

105 Overall, virulence factor gene expression is also higher in vivo

106 The exotoxin TcsL is a major virulence factor in Paeniclostridium (Clostridium) sorde

107 s study, OSP24 is identified as an important virulence factor in systematic characterization of the 5

108 NA thermometer as a bona fide S. dysenteriae virulence factor in this bacterial pathogen.

109 ar pathogen harboring the surface-associated virulence factor InlB, which enables entry into certain

110 inhibitory factor (MIF) cytokine homolog, a virulence factor linked to severe disease.

111 The HIV-1 virulence factor Nef promotes high-titer viral replicati

112 The principal virulence factor of human pathogenic enterohemorrhagic E

113 immuno globulin gamma (IgG) interaction with virulence factor of S. aureus, staphylococcal protein A

114 Typhoid toxin is a virulence factor of Salmonella enterica serovar Typhi, t

115 leton and trafficking of the adhesin and key virulence factor PfEMP1 to the host cell surface.

116 s pneumoniae secrete a giant metalloprotease virulence factor responsible for cleaving host IgA1, yet

117 nfection are centered on core metabolism and virulence factor synthesis.

118 d thus indirectly stabilizes mRNA of a known virulence factor, delta-amastin surface antigen.

119 of the capsule operon, the main pneumococcal virulence factor, to be externally inducible (YES gate)

120 n germ-free mice to show that live bacterial virulence factor-driven immunogenicity can be uncoupled

121 annii pathogenesis, supporting its role as a virulence factor.

122 Tarp effector as a bona fide C. trachomatis virulence factor.

123 es (adhE, pflA, nrdDG) and a large number of virulence factors (lukSF, lukAB, nuc, gehB, norB, chs, s

124 positive bacteria leads to a rapid spread of virulence factors and antibiotic resistance.

125 l hydrocarbon receptor (AhR), which binds TB virulence factors and controls antibacterial responses.

126 h kinase, including phosphosites on parasite virulence factors and host erythrocyte proteins.

127 age nucleotide identity, 2) determination of virulence factors and undesirable genes, 3) determinatio

128 it autophagy, but the precise mechanisms and virulence factors are mostly unknown.

129 ential it is largely unclear which bacterial virulence factors are responsible for increased clinical

130 e mouse models of lung infection to identify virulence factors associated with severe bacteraemic pne

131 eria and evidence indicates that they act as virulence factors for host infection.

132 Putative virulence factors in K. aerogenes may account for these

133 We emphasize the virulence factors in xanthomonads, such as type III secr

134 To identify novel K. pneumoniae virulence factors needed to cause pneumonia, a high-thro

135 As important virulence factors of Mycobacterium tuberculosis, EsxA an

136 Toxin complex (Tc) toxins are virulence factors of pathogenic bacteria.

137 The virulence factors of this bacterium and their interactio

138 Among the multiple virulence factors produced by EAEC, the Pic serine prote

139 Quorum sensing (QS) controls biofilm and virulence factors production.

140 Some virulence factors serve to maintain the integrity of the

141 e results identify nsp1, nsp15, and nsp16 as virulence factors that contribute to the development of

142 Plasmodium parasites contain various virulence factors that modulate the host immune response

143 ected bone may recover the expression of key virulence factors through a rapid microevolution pathway

144 ctive antivirulence drug targets that attach virulence factors to the surface of Staphylococcus aureu

145 ression of hundreds of genes, including most virulence factors, in response to the availability of ke

146 eas TcdA and TcdB are considered the primary virulence factors, recent studies suggest that CDT incre

147 In addition, production of several virulence factors, such as BosR, RpoS, and OspC, was ele

148 In particular, bacteria use virulence factors, such as secreted toxins and effector

149 Bacterial virulence factors, such as the oncoprotein CagA, augment

150 To identify aphid virulence factors, we took advantage of the ability of t

151 ced by pathogenic bacteria function as major virulence factors, whereas when they are produced by non

152 ession of more than a dozen immunomodulatory virulence factors.

153 associated with strains expressing acquired virulence factors.

154 rns, such as the ones found for pneumococcal virulence factors.

155 ion pathway involving SigB regulation of key virulence factors.

156 one approach is the targeting of established virulence factors.

157 at immune systems will likely cause enhanced virulence following emergence into secondary hosts with

158 B phospho-null mutants exhibited compromised virulence functions and were unable to suppress NPR1 acc

159 showed that SnRK2.8 was required for AvrPtoB virulence functions, including facilitating bacterial co

160 can be used as a tool to study T. marneffei virulence, furthering the understanding of the therapeut

161 EAEC virulence gene expression is controlled by the autoactiv

162 We found that DSFs repressed virulence gene expression of enteric pathogens by intera

163 arginine transport (DeltaartP) had decreased virulence gene expression.

164 an lead to highly selective dysregulation of virulence gene expression.

165 vealed previously unrecognized complexity of virulence gene regulation.

166 AtxA, the master virulence gene regulator of Bacillus anthracis, is a PRD

167 n amino acids and arginine biosynthesis) and virulence genes (eg, beta-toxin, delta-toxin) that defin

168 osa (P. aeruginosa), and the distribution of virulence genes (oprL, exoS, phzM, and toxA) and the ant

169 ps, sequence types (STs), H30, H30Rx, and 53 virulence genes (VGs).

170 lates bore more antimicrobial resistance and virulence genes and were less diverse than isolates from

171 ains, regular PCR cannot confirm whether the virulence genes are carried by adulterant or nonadultera

172 Major virulence genes carried by each of the top 7 STEC serogr

173 hanism enables a pathogen to express foreign virulence genes during infection without the need to evo

174 sequencing revealed differences in putative virulence genes encoding aggregative adherence fimbriae,

175 es that characterization of S. aureus CC and virulence genes helps to predict the likelihood of the o

176 to K. aerogenes isolates, including putative virulence genes involved in iron acquisition (n = 67), f

177 Although the virulence genes of S. suis have been extensively studied

178 The tested strains harbored the virulence genes phoA, hly, tsh, eaeA, sta, and lt with a

179 In this study, 38 ExPEC-associated virulence genes were added to the existing E. coli Virul

180 characterized for antimicrobial resistance, virulence genes, and diversity.

181 gene, which encodes the master regulator of virulence genes, has been previously implicated in regul

182 tional factor CpxR controlling expression of virulence genes, notably those within the locus of enter

183 two (MglA-SspA)-based strategies to activate virulence genes.

184 cting clinically relevant phenotypes such as virulence, host colonization, sporulation, biofilm forma

185 hat is revealed by the severe attenuation of virulence in a double mutant relative to the single indi

186 Brucella abortus, VtlR is required for full virulence in a mouse model of infection, and VtlR activa

187 ta; this deletion was accompanied by reduced virulence in a mouse model.

188 This strain displayed decreased virulence in a murine model of acute pneumonia compared

189 We propose that P. falciparum virulence in areas of seasonal malaria transmission is r

190 S that have been described to play a role in virulence in either the BCC or B. pseudomallei Since man

191 reductase (NR) promoter, NO production, and virulence in F. graminearum Our results reveal mechanist

192 oplasmic membrane and has been implicated in virulence in many bacterial pathogens.

193 ify two strain-specific determinants of ZIKV virulence in mice.

194 -mediated growth inhibition and have reduced virulence in mice.

195 ntrols anthranilate metabolism and bacterial virulence in P. aeruginosa.

196 in WT mice, whereas they are dispensable for virulence in S100a9 (-/-) mice, indicating the direct co

197 endent control of virulence determinants and virulence in several human pathogenic bacteria.

198 eral natural ASFV isolates showing decreased virulence in swine has been shown to be non-hemadsorbing

199 man immunoglobulins may affect C. neoformans virulence in vivo warrants further investigation.

200 the AdcR regulon genes are critical for GAS virulence in WT mice, whereas they are dispensable for v

201 ominant and no hitch-hiking, compensatory or virulence increasing mutations were detected showing tha

202 Virulence inhibitory activity in the RND-negative backgr

203 that plays critical roles in the control of virulence, interbacterial interactions, and biofilm form

204 enetic loci responsible for drug resistance, virulence, invasion, growth rate, and transmission.

205 Its virulence is closely linked to the increase in rigidity

206 However, the mechanism by which virulence is regulated by PE synthesis is only partially

207 A potential way to reduce ZIKV virulence is to limit the action of the nonstructural pr

208 ndary metabolism (laeA) and the mechanism of virulence (lipA and meT) of A. flavus in the presence of

209 Several virulence lipids populate the outer cell wall of pathoge

210 limitations in using genetics to understand virulence lipids, we developed a chemical approach to tr

211 s predicting the presence or absence of this virulence marker.

212 he enzymatic activity of PPAD is not a major virulence mechanism during early stages of inflammatory

213 describe a virulence mechanism in which the bacterial pathogen Vibr

214 vations suggest that P. aeruginosa deploys a virulence mechanism to induce ribosome degradation and H

215 The virulence mechanisms associated with Staphylococcus aure

216 eutics, and begun to enable investigation of virulence mechanisms at the host-pathogen interface of M

217 cterial pathogens employ diverse fitness and virulence mechanisms to gain an advantage in competitive

218 Virulence mechanisms typically evolve through the contin

219 Here we use the Galleria mellonella insect virulence model to selectively isolate pathogenic bacter

220 ffects a broad range of phenotypes including virulence, motility and biofilm formation.

221 iosynthetic pathway, plays a key role in the virulence of A. baumannii.

222 odels confirmed that GGT is required for the virulence of A. baumannii.

223 sidue at P8 might be helpful to estimate the virulence of circulating and emerging strains.IMPORTANCE

224 tion system ExlB-ExlA is instrumental in the virulence of different Pseudomonas species, ranging from

225 emical environment, which profoundly impacts virulence of enteric pathogens.

226 and report that its depletion attenuates the virulence of Escherichia coli by reducing levels of LPS

227 small molecules, that modify the growth and virulence of individual species.

228 These findings suggest that the higher virulence of influenza A(H5N8) viruses from the 2016-17

229 nside macrophage is crucial for survival and virulence of M. tuberculosis ESAT-6, a 6-kDa-secreted pr

230 apparent contradiction of these results, the virulence of murine norovirus infection was unaffected b

231 the Clp system are essential for growth and virulence of mycobacteria, and their inhibitors show pro

232 In our study, we sought to explore the virulence of P. gingivalis (Pg) affecting glycogen synth

233 Until today, the virulence of RESTV for pigs has remained elusive, with u

234 as aeruginosa Colonization, persistence, and virulence of S. maltophilia were assessed in experimenta

235 is counterintuitive with the observed higher virulence of the 2016-17 outbreak viruses.

236 actors may contribute to the maintenance and virulence of the 2stop+A4G genotype in currently circula

237 not associated with a noticeable decrease in virulence of the ASFV Georgia isolate.

238 Long-chain fatty acids repress the virulence of the important enteric pathogens Salmonella

239 diation, IFS formation, host penetration and virulence of the pathogen.

240 critical role in driving in vivo fitness and virulence of the virus, through induction of key proinfl

241 G-Delta8DR) does not significantly alter the virulence of the virus.

242 inoculation, suggestive of enhanced pathogen virulence on soybean.

243 encode traits of key human interest, such as virulence or antibiotic resistance.

244 uenza viruses have not been tested for their virulence or organ tropism in ferrets.

245 Phasevarion switching alters virulence phenotypes and facilitates evasion of host imm

246 We developed a strategy to characterize virulence plasmids and applied it to analyze hundreds of

247 e generated a bb0345 mutant and assessed its virulence potential in immunocompetent mice.

248 terial isolates of S. aureus differ in their virulence potential it is largely unclear which bacteria

249 ly modulates pathogen function by inhibiting virulence programs essential for successful infection.

250 ty of the secreted chorismate mutase Cmu1, a virulence-promoting effector of the smut fungus Ustilago

251 Here we investigated the virulence properties and haemolytic activities of these

252 t canal infections and identified taxa whose virulence properties should be further explored.

253 ver, surface expression of the P. falciparum virulence protein PfEMP-1 was significantly reduced in i

254 at perceive the presence of pathogen-derived virulence proteins (effectors) to induce immune response

255 type III secretion systems (T3SS) to inject virulence proteins into host cells.

256 large and diverse family of autotransporter virulence proteins, suggesting sequence patterns that fa

257 mechanical stimuli are required for optimal virulence regulation and colonization of the host intest

258 role of OmpR in V. cholerae biology outside virulence regulation remained unknown.

259 r of Bacillus anthracis, is a PRD-Containing Virulence Regulator (PCVR) as indicated by the crystal s

260 nsor (CovRS) two-component system is a major virulence regulator of GAS that has been extensively stu

261 es both the protease Lon and the DNA-binding virulence regulator PhoP.

262 icated that V. cholerae OmpR functioned as a virulence regulator through repression of the LysR-famil

263 In this study, we found that another key virulence regulator, ToxR, was important for V. cholerae

264 The control of virulence regulator/sensor (CovRS) two-component system

265 hat they are important for the regulation of virulence-related genes that control biofilm formation,

266 ons, which can significantly increase cancer virulence, renders tumors sensitive to aKG esters by tar

267 Such fitness trade-offs include reduced virulence, resensitization to antibiotics, and colonizat

268 g a correlation between MuV fusogenicity and virulence, sequence information on the amino acid residu

269 d RNAP holoenzyme (RNAPsigma(70)), forming a virulence-specialized polymerase.

270 ue mechanism for Ft pathogenesis involving a virulence-specialized RNAP that employs two (MglA-SspA)-

271 and colons of all mice infected with a high-virulence strain of C. difficile; however, significant d

272 onary but not systemic infection with a high-virulence strain of C. neoformans significantly induced

273 tuberculosis immune evasion-related pathogen virulence strategies are considered to maximize the effe

274 ly lyse cells is essential for understanding virulence strategies of several pathogenic bacteria, and

275 Here, we describe two virulence strategies that converge to promote the abilit

276 etect and counteract these pathogen-specific virulence strategies.

277 s to determine how fungal morphology impacts virulence strategies.

278 he plasma membrane of host cells is a common virulence strategy for bacterial pathogens such as methi

279 ding on the nature of the alteration and the virulence strategy of the pathogen.

280 ulness of microbes and the interplay between virulence systems and host cell resources to evolve an i

281 hree proteins (FliPQR in flagella, SctRST in virulence systems).

282 llei Since many of these TCS are involved in virulence, TCS are potential novel therapeutic targets,

283 nsible for more crucial abilities, including virulence, than currently thought.

284 ify two strain-specific determinants of ZIKV virulence that are evident in only Ifnar1 (-/-) mice but

285 h strain, leading to predictions of relative virulence that are validated in a mouse infection model.

286 findings support a role for EspE and EspF in virulence that is independent of the EsxA and EsxB subst

287 ay crucial roles in bacterial physiology and virulence, the mechanisms governing their quality contro

288 expression in wild-type cells also repressed virulence through aphB We further show that ompR express

289 Isolates were also tested for virulence to 20 near-isogenic lines that differ for leaf

290 cus aureus relies on quorum sensing to exert virulence to establish and maintain infection.

291 GI.1 Lot 001-09NV appears to be similar in virulence to previous passages of NV strain 8fIIa.

292 ions of P. triticina are highly variable for virulence to resistance genes in wheat and adapt quickly

293 , while compensatory double mutants restored virulence to WT levels.

294 mobile genetic elements (MGEs), which encode virulence, toxin, antimicrobial resistance, and other me

295 phenotypes such as antibiotic resistance or virulence traits.

296 exhibits phenotypic variation between insect virulence (V) and the mutualistic (M) support of nematod

297 Virulence was restored by expressing atxA from an altern

298 Despite an increased growth rate, virulence was still dependent on the mevalonate pathway

299 Expression of exl1 correlates with pathogen virulence, where symptoms are reduced in a Deltaexl1 mut

300 microbial resistance, CRISPR/Cas systems and virulence with phage susceptibility in Acinetobacter bau