ライフサイエンスコーパス: virulence

1 binds to PsXEG1 to block its contribution to virulence.

2 tracellular traps, and modulates S. pyogenes virulence.

3 en critical in the ongoing evolution of MYXV virulence.

4 at the role of the T6SS is not restricted to virulence.

5 ost and their transmission at the expense of virulence.

6 ical for modulating parasite replication and virulence.

7 at protrude from bacteria and increase their virulence.

8 between them may confer host tissue-specific virulence.

9 ains multiple genetic variants, differing in virulence.

10 parasite Plasmodium chabaudi that differ in virulence.

11 and deletion of Sscp1 significantly reduced virulence.

12 to evaluate whether such compounds modulate virulence.

13 uctural elements that modulate stability and virulence.

14 es in attenuation proved to be important for virulence.

15 l gene expression; specifically, to modulate virulence.

16 incidentally adapted C. neoformans for human virulence.

17 host-imposed stresses, and is essential for virulence.

18 tion system (T2SS) that is required for full virulence.

19 motility and which is usually essential for virulence.

20 rium) inhibits T cell responses and mediates virulence.

21 FPI transcription and thus is essential for virulence.

22 ay, an activity required for this pathogen's virulence.

23 tness of P. gingivalis while diminishing its virulence.

24 ogical signals to activate S. flexneri 2457T virulence.

25 h rapid intercontinental spread and enhanced virulence.

26 agents by degrading biofilms and attenuating virulence.

27 g the importance of individual effectors for virulence.

28 n, alter global gene expression, and enhance virulence.

29 nase (FAK) complex, and FakA is required for virulence.

30 ns, which need iron for their metabolism and virulence.

31 ations for fundamental understanding of RVFV virulence.

32 in Avr2 (e.g. Avr2(R45H) ), but retain full virulence.

33 ), a recent isolate of increased house finch virulence.

34 the host protein functions as a mechanism of virulence.

35 ent mechanisms that would otherwise mitigate virulence.

36 nthomonas strain lacking raxX is impaired in virulence.

37 gene is not required for Esx-1 secretion or virulence.

38 d potential mechanism for this difference in virulence.

39 ic pathways may predispose isolates to human virulence.

40 (EPEC), an important human pathogen, both in virulence activating and non-activating conditions, we e

41 s, we provide a strong link between effector virulence activity and association with VPS52, and show

42 recognition is not based on monitoring Avr2 virulence activity, which includes suppression of immune

43 monstrated that PEG344 was required for full virulence after pulmonary challenge but, interestingly,

44 and Heterorhabditis bacteriophora for their virulence against different larval instars of Rhynchopho

45 Virulence alleles of AvrSr50 have arisen through DNA ins

46 tems (T2SSs) to secrete proteins involved in virulence and adaptation.

47 antigenic target (ESAT-6) is a known potent virulence and antigenic determinant.

48 nding collective microbial behavior, such as virulence and bioluminescence.

49 h their host and how these processes lead to virulence and disease seriously hampers the development

50 esults from the interaction between parasite virulence and genetically determined levels of host-plan

51 cantly from one clone to another in terms of virulence and host invasiveness, and that these differen

52 nfection depend on the interplay of pathogen virulence and host susceptibility.

53 functional studies suggest that a variety of virulence and immune evasive factors contribute to the s

54 We found that PumA is essential for virulence and inhibits NF-kappaB, a property transferabl

55 pability for aerosol transmission, affecting virulence and pathogenicity.

56 he obese/T2D host accounts for its increased virulence and persistence in this population is unknown.

57 t biofilm constituent critical for bacterial virulence and persistence.

58 ould potentially also transport farnesol for virulence and quorum sensing.

59 is not necessarily accompanied by increased virulence and suggest the presence of different mechanis

60 Mutation of PhoQ impaired the virulence and the ability to cause bacteremia of P. aeru

61 on of genetic factors required for survival, virulence and transmission in the most successful clones

62 dary metabolites (SMs) critical for defense, virulence, and communication.

63 e tumor subpopulation involved in metastatic virulence, and ongoing research seeks to characterize th

64 how that high VPS52 levels negatively impact virulence, and that aphids are able to reduce VPS52 leve

65 The interplay between antibiotic resistance, virulence, and the concerning international high-risk cl

66 determinant of R. equi is the surface bound virulence associated protein A (VapA).

67 re available regarding their resistance- and virulence-associated gene expression profiles.

68 sian or Southeast Asian isolates alone, with virulence-associated genes being among those over-repres

69 s harboring engineered deletions of specific virulence-associated genes induce solid protection again

70 Identification of these virulence-associated PKs provides new insights into T. b

71 e matches a known synthetic inhibitor of the virulence-associated pyochelin siderophore system in Pse

72 andida albicans have long been implicated in virulence at the mucosal surface, including contribution

73 phenotypic marker to screen for spontaneous virulence-attenuating mutations in L. monocytogenes Sixt

74 9V) or a premature stop codon causing strong virulence attenuation in mice.

75 taneous infection model, suggesting that the virulence attributes of these isolates are adapted to ca

76 for virulence evolution, with an increase in virulence being achieved apparently entirely by overcomi

77 otility, biofilm formation, and acute insect virulence, but not in mucoidy.

78 ssential cellular roles and are required for virulence by certain bacteria.

79 This demonstrates how pathogen virulence can be achieved through numbers and aggregatio

80 ly moderately pathogenic to mammalian hosts, virulence can still increase.

81 n in vivo in a variety of tissues and showed virulence comparable to that of wild-type and marker-res

82 The control of virulence (CovRS) two-component system has a major role

83 e expression that includes components of the virulence-critical ESX-1 secretion system.

84 , the loss of CpsY in GAS does not result in virulence defects in murine models of infection, suggest

85 RVFV virulence depends on the interferon antagonist non-struc

86 The likely more deeply studied P. aeruginosa virulence determinant is the type III secretion system (

87 Previous studies determined that the major virulence determinant of R. equi is the surface bound vi

88 dle ear infection demonstrated that VP1 is a virulence determinant.

89 ited than macaques for the identification of virulence determinants or the evaluation of therapeutics

90 microbes, functional amyloids are often key virulence determinants, yet the structural basis for the

91 ema denticola (TDE) and one of its principal virulence determinants.

92 ence factors, PASTA kinases are critical for virulence due to their roles in regulating bacterial phy

93 e diversity of cells through the delivery of virulence effectors into the cell cytoplasm via a type I

94 of this highly conserved family of bacterial virulence effectors target different host protein substr

95 s complex, multifactorial, and influenced by virulence effects of CovR, HvgA, and capsule.

96 oebal chemotherapy by potentially abrogating virulence-enhancing properties of bacterial endosymbiont

97 To understand virulence evolution in Pgt, we identified the protein li

98 nants responsible for this canonical case of virulence evolution remain to be determined.IMPORTANCE T

99 This suggests either that virulence evolution was defined by amino acid changes ot

100 unity acts as a powerful selective force for virulence evolution, with an increase in virulence being

101 Candida albicans excretes E,E-farnesol as a virulence factor and quorum sensing molecule that preven

102 P. gingivalis colonization and expression of virulence factor are therefore attractive approaches for

103 The virus-encoded NSs protein acts as a virulence factor by impairing host cell transcription.

104 appaB pathway was identified as the key UPEC virulence factor causing a significant increase (P < 0.0

105 rus (IAV) nonstructural protein 1 (NS1) is a virulence factor essential for counteracting the innate

106 nt system has a major role in regulating GAS virulence factor expression.

107 nt on the surface-exposed, membrane-embedded virulence factor IcsA, which recruits the host actin reg

108 ion system 5 (T6SS-5), which is an essential virulence factor in both species.

109 c-like serine/threonine protein kinase, is a virulence factor in Mycobacterium tuberculosis, required

110 ualifies ClpG as a potential persistence and virulence factor in P. aeruginosa.

111 us influenzae protein F (PF) is an important virulence factor interacting with laminin, an extracellu

112 cus aureus protein A, an important S. aureus virulence factor involved in immune evasion and biofilm

113 ies by 18- to 210-fold, including the silent virulence factor malleilactone.

114 he M protein is the major surface-associated virulence factor of group A Streptococcus (GAS) and an a

115 The viral protein R (Vpr) is an accessory virulence factor of HIV-1 that facilitates infection in

116 Typhoid toxin, a unique virulence factor of Salmonella Typhi (the cause of typho

117 onstructural protein, termed NSs, is a major virulence factor of SBV, and it is known to promote the

118 Pyocyanin is a virulence factor produced as a secondary metabolite by t

119 scriptional regulators coordinately silences virulence factor production is proposed.

120 rature-associated differential modulation of virulence factor production was linked to the phosphoryl

121 lation between the genomic sequence type and virulence factor profiles based on prevalence of the iso

122 The bacterial virulence factor PSMalpha, but not alpha-toxin or delta-

123 In an effort to disentangle hypha-associated virulence factor regulation from morphological transitio

124 e proteins have evaded selection in previous virulence factor screens in animals.

125 nowledge, the first characterized, bona fide virulence factor secreted by Acinetobacter species.

126 y essential homeostatic processes as well as virulence factor secretion and the elimination of drugs.

127 ates interconnectivity between inhibition of virulence factor synthesis and growth.

128 e activity of 112 virulence-linked genes and virulence factor synthesis pathways that produce 17 uniq

129 l (PQS) compound is a secreted P. aeruginosa virulence factor that contributes to the pathogenicity o

130 ococcal pyrogenic exotoxin B (SpeB) is a key virulence factor that is produced abundantly during infe

131 with a mutation in the gamma134.5 protein, a virulence factor, stimulates dendritic cell (DC) maturat

132 urface-expressed M1 protein, a classical GAS virulence factor, was required for high-level histone re

133 lactopyranose (UDP-Galp) and is an important virulence factor.

134 nisms, suggesting that pGP3 is a key in vivo virulence factor.

135 e compounds were able to reduce QS-regulated virulence factors (elastase, rhamnolipid, and pyocyanin)

136 The GAS CpsY regulon includes known virulence factors (mntE, speB, spd, nga [spn], prtS [Spy

137 they are also involved in the production of virulence factors and conferring resistance to various a

138 lycoside hydrolase 12 (GH12) proteins act as virulence factors and pathogen-associated molecular patt

139 tween clinical and environmental isolates in virulence factors and stress response genes.

140 Although several virulence factors and their roles in pathogenesis are we

141 This method of regulation suggests that virulence factors are only utilized in early infection t

142 t encode 80 genes, including novel and known virulence factors associated with adherence and autoaggr

143 y, B. pertussis maintained the production of virulence factors at 24 degrees C, whereas B. bronchisep

144 cular microbiome on host damage and pathogen virulence factors during infection.

145 covered here may facilitate targeting of GAS virulence factors for disease management.

146 Type IV pili (Tfp), which are key virulence factors in many bacterial pathogens, define a

147 of the multilaminate cell wall and essential virulence factors in pathogenic species.

148 porting the consideration of these traits as virulence factors in this system.

149 Quorum sensing controlled virulence factors include secreted toxins responsible fo

150 oduction of several well-known P. gingivalis virulence factors including fimbrial proteins and gingip

151 tisomes of gram-negative pathogens to export virulence factors into host cells.

152 tems that breach immune barriers and deliver virulence factors into mammalian cells.

153 finding that numerous skin strain-associated virulence factors make slight but significant contributi

154 Among the virulence factors of B. anthracis is the S-layer-associa

155 ment of nonantibiotic agents that target the virulence factors of bacterial pathogens is one way to b

156 By examining secreted virulence factors of Staphylococcus aureus, we determine

157 Many pathogens deliver virulence factors or effectors into host cells in order

158 tor (agr) operon to coordinate expression of virulence factors required for invasive infection.

159 electron transport chain and cannot produce virulence factors such as leukocidins, hemolysins, or th

160 ally important pathogen with an abundance of virulence factors that are necessary for survival within

161 sms of drug resistance are well studied, the virulence factors that govern Acinetobacter pathogenesis

162 ureus is an AD-associated pathogen producing virulence factors that induce skin barrier disruption in

163 in the inability of P. aeruginosa to produce virulence factors that kill S. aureus These data could p

164 Our approaches reveal key virulence factors that respond to restricted oxygen avai

165 toxin or though regulating the stability of virulence factors to remove their function once it is no

166 enes in S. agalactiae 874391 that encode key virulence factors, including beta-h/c and HvgA, but not

167 are limited examples of direct regulation of virulence factors, PASTA kinases are critical for virule

168 substrates, including macrolide antibiotics, virulence factors, peptides and cell envelope precursors

169 ngle-chain toxins TcdA and TcdB are the main virulence factors.

170 on compared to strains lacking known E. coli virulence factors.

171 operate may represent a target for bacterial virulence factors.

172 on the expression and production of several virulence factors.

173 genes of foreign DNA elements and bacterial virulence factors.

174 addition, cell wall lipids are mycobacterial virulence factors.

175 ntibiotics and also to trigger production of virulence factors.

176 rectly regulates the two primary V. cholerae virulence factors.

177 accines to target the multitude of S. aureus virulence factors.

178 es four major proteases that are emerging as virulence factors: aureolysin (Aur), V8 protease (SspA),

179 ly consistent, HFMG isolates which differ in virulence for house finches-Virginia 1994 (VA1994), the

180 it nonetheless possessed several markers of virulence for mammals.

181 ticum (HFMG) spread rapidly and increased in virulence for the finch host in the eastern United State

182 ult from strains with mutations that enhance virulence gene expression but reduce subsequent transmis

183 is of its ability to both attract and induce virulence gene expression in EHEC, we propose that DHMA

184 2457T, including induced drug resistance and virulence gene expression.

185 ch wHTH proteins are important regulators of virulence gene transcription in many pathogens; they als

186 ies are possibly linked to pathogen-specific virulence genes and how they may influence pathology and

187 Multivariate analyses among H. pylori virulence genes and severity of hepatobiliary disease re

188 cement of the expression of CovRS-controlled virulence genes at the exponential growth phase; however

189 narrow host range, and potential transfer of virulence genes by generalized transduction.

190 ts had transcript levels of CovRS-controlled virulence genes comparable to those of a covS mutant but

191 rmosensing is critical for the expression of virulence genes in pathogenic bacteria that infect warm-

192 uencing, demonstrated that the EPEC and ETEC virulence genes of these hybrid isolates were differenti

193 We demonstrate that isolates lacking virulence genes promote beneficial plant growth, and tha

194 Virulence genes were consistently enriched in highly cod

195 ere further characterised for resistance and virulence genes, SCCmec and spa typing.

196 ule that activates the expression of several virulence genes.

197 ates of MYXV that fall in known or potential virulence genes.

198 vironmental cues activates the expression of virulence genes.

199 e last decade, chemical control of bacterial virulence has received considerable attention.

200 Investigations of parasite virulence have associated the expression of distinct var

201 Links between sugar metabolism and virulence have been demonstrated in GAS, where mutants i

202 us serotypes that coexist while differing in virulence.IMPORTANCE Most colds are caused by rhinovirus

203 tion in mammalian neuronal cells and reduced virulence in 2-day-old mice.

204 fitness is 0.41-0.78) and highly attenuated virulence in a Galleria mellonella infection model.

205 ion system 1 (T6SS-1), which is required for virulence in animals.

206 nd esterase activities and displayed reduced virulence in citrus.

207 In the current study, we assessed virulence in domestic poultry with two temporally distan

208 l sporulation, deoxynivalenol production and virulence in F. graminearum.

209 -attenuated CDV vaccines can retain residual virulence in highly susceptible species.

210 hogen Cochliobolus carbonum race 1, promotes virulence in maize through altering protein acetylation.

211 s into the parental virus conferred enhanced virulence in mice, although primary tropism for musculos

212 ct impact of the TBD on viral replication or virulence in mice.

213 vertebrate hosts and insect vectors, and for virulence in mice.

214 Thus, we evaluated inhibition of virulence in P. aeruginosa by a designed peptide (RpoN m

215 d norepinephrine, that are known to increase virulence in several pathogens, including enterohemorrha

216 ld on previous research highlighting induced virulence in Shigella flexneri strain 2457T following ex

217 The remaining two isolates exhibited low virulence in the pneumonia model but high virulence in t

218 ow virulence in the pneumonia model but high virulence in the subcutaneous infection model, suggestin

219 ty in ST3081 and may contribute to increased virulence in this clone.

220 ymbiont has previously enhanced Acanthamoeba virulence in vitro.

221 of alphaviruses were shown to contribute to virulence in vivo Nevertheless, a clear understanding of

222 Exg8 is largely dispensable for virulence in vivo, in contrast to Eng1.

223 tilocus sequence types with abnormally high 'virulence' in humans.

224 parasite induced host mortality, a proxy for virulence, in all B. bassiana lines.

225 isolates were differentially-expressed under virulence-inducing laboratory conditions, similar to ref

226 ht into the potential utility of non-biocide virulence inhibitors in treating skin infections.

227 azilian Peppertree) as a potential source of virulence inhibitors.

228 P. aeruginosa virulence is controlled partly by intercellular communic

229 Virulence is often under selection during host-parasite

230 onstruction accounts for the activity of 112 virulence-linked genes and virulence factor synthesis pa

231 Virulence-linked pathways in opportunistic pathogens are

232 omplex interrelationships between growth and virulence-linked pathways using a genome-scale metabolic

233 However, efficacy of virulence-linked targets may be affected by the contribu

234 Here the authors comparatively map virulence loci using the offspring from a P. yoelii YM a

235 uggest that H5N8 viruses can rapidly acquire virulence markers in mammalian hosts; thus, rapid spread

236 properties that can affect transmission and virulence may have contributed to the severity and scope

237 important insights regarding P. aeruginosa's virulence mechanisms.

238 nsistent with the rare occurrence of loss-of-virulence mutations, we show that prfA and hly are under

239 ggregation, which may lead to characteristic virulence not present in the monoinfection.

240 The moderate virulence observed in mammalian models and the capacity

241 Mechanistically, the attenuated virulence of 10-del ZIKV may be due to decreased viral R

242 we hypothesized that the relative degree of virulence of a chlamydial population dictates the microR

243 sses in holobiont physiology, instead of the virulence of any single etiological agent, environmental

244 genetic studies demonstrating the attenuated virulence of bacterial strains in which modified carbohy

245 e of glioma cancer stem cells (GCSCs) in the virulence of gliomas.

246 ignalling modules that are essential for the virulence of human pathogenic fungi.

247 ld help define strategies for mitigating the virulence of important human pathogens, such as Streptoc

248 pathotyping model) to predict the potential virulence of isolates of H. parasuis based on a subset o

249 could provide important clues regarding the virulence of P. aeruginosa in albumin-depleted versus al

250 for varying survivability, pathogenicity and virulence of pathogen strains, and varying abilities of

251 results suggest that SsCP1 is important for virulence of S. sclerotiorum and that it can be recogniz

252 culum size, immune status of the infant, and virulence of the causative agent influence the clinical

253 ossible that disease severity depends on the virulence of the chlamydial inoculum.

254 lity by the infecting phage and the level of virulence of the E. coli strain.

255 essential process for the proliferation and virulence of this parasite.

256 role of this chaperone in the physiology and virulence of Yersinia enterocolitica serotype O:3.

257 is, resistance to host defense peptides, and virulence of Yersinia, we constructed DeltarfaH mutants

258 on-withholding strategies to reduce pathogen virulence or to locally increase iron levels to activate

259 e host environment and implement appropriate virulence pathways.

260 o the index isolate, notably demonstrating a virulence phenotype in chickens inversely related to tha

261 ts of a carcinogenic host environment on the virulence phenotype of H. pylori to understand how only

262 everal effector mutants displaying different virulence phenotypes using genetic complementation studi

263 proteins resulted in host-specific or broad virulence phenotypes.

264 plant growth, and that the acquisition of a virulence plasmid is sufficient to transition beneficial

265 Similar virulence plasmids have been acquired by other B. cereus

266 nthrax pathogenesis are located on two large virulence plasmids.

267 effectors that contribute to L. pneumophila virulence positively or negatively and has demonstrated

268 the disease and is capable of elevating the virulence potential of the periodontal microbial communi

269 ic resistance modulate bacterial fitness and virulence potential, thus influencing the ability of pat

270 typic properties of P. gingivalis related to virulence potential.

271 s suggest that low NF-kappaB activation is a virulence property of pneumococci and that the appropria

272 S. aureus toxins and virulence proteases often circulate in host blood vessel

273 vided here indicates that CT694/CTL0063 is a virulence protein involved in chlamydial invasion.

274 ts by delivering transferred DNA (T-DNA) and virulence proteins into host plant cells.

275 hes, intracellular pathogens secrete various virulence proteins, called effectors, to manipulate host

276 The role of the S. agalactiae global virulence regulator, CovR, in UTI pathogenesis is unknow

277 hanisms involved in a previously undescribed virulence regulatory pathway of an important human patho

278 rgets may be affected by the contribution of virulence-related genes to metabolism.

279 anisms that modulate the expression of their virulence repertoire in response to signals from the mic

280 tions by strains of a CC22 background, these virulence-specific factors had little influence on morta

281 cavity, demonstrating that PlrS coordinates virulence specifically in the LRT.

282 oteins, including many involved in bacterial virulence such as toxins, adhesins, flagella, and pili,

283 bolic potential of genes involved in stress, virulence, sulfur cycle, metal resistance, degradation o

284 ation, indicating that VPS52 is an important virulence target.

285 hitherto unknown features of attenuation of virulence that could be used as markers of product quali

286 s potentially may qualify as targets of anti-virulence therapy and that ajoene could be a lead struct

287 e fungal metabolism plays a critical role in virulence though specific nutrient sources utilized by h

288 ted by Bacillus anthracis to promote disease virulence through disruption of host signaling pathways.

289 formation, exopolysaccharide production and virulence to crustacean hosts.

290 ange can play a role in the emergence of new virulence traits in Pgt.

291 We discuss the Liberibacter virulence traits, including secretion systems, putative

292 luate candidate drugs that inhibit bacterial virulence traits.

293 make slight but significant contributions to virulence underscores the incremental contributions to f

294 Bacterial pathogens coordinate virulence using two-component regulatory systems (TCS).

295 There is evidence suggesting virulence vary with mating types in fungi, including the

296 C12-HSL), that promote biofilm formation and virulence via interbacterial communication.

297 ghtly more pronounced decreases were seen in virulence via intrahemcoel injection assays (G. mellonel

298 ectin-3 and protease expression on S. aureus virulence was studied in a murine skin infection model.

299 t when CotE is absent, both colonization and virulence were markedly reduced.

300 ated by the multifaceted nature of bacterial virulence, which has so far prevented a robust mapping b