ライフサイエンスコーパス: staphylococcal

1 al survival and the long-term persistence of staphylococcal abscess communities.

2 rabbits, which reproduces the characteristic staphylococcal abscess.

3 The staphylococcal accessory regulator (sarA) plays an impor

4 The staphylococcal accessory regulator A locus (sarA) is a m

5 red important substances responsible by anti-staphylococcal activity in red propolis composition duri

6 us grown with HQNO and significantly reduced staphylococcal adhesion to fibronectin.

7 nding the role of homophilic interactions in staphylococcal adhesion, and for the design of new molec

8 e development of novel, urgently needed anti-staphylococcal agents.

9 ), and show that aggA and aggC contribute to staphylococcal agglutination with fibrin fibrils in huma

10 man keratinocytes from the lethal effects of staphylococcal alpha toxin through apolipoprotein L1-ind

11 man keratinocytes from cell death induced by staphylococcal alpha toxin.

12 The staphylococcal alpha-hemolysin is critical for the patho

13 We examined mutants of the staphylococcal alpha-hemolysin pore so severely truncate

14 on with Th1, Th2, Th17 and Th22 cytokines or staphylococcal alpha-toxin, respectively, at the mRNA an

15 Streptococcus pyogenes and protected against staphylococcal alpha-toxin-induced keratinocyte cell dea

16 were culture-positive, the most common being Staphylococcal and Streptococcal species.

17 Toxic shock syndrome (TSS) is caused by staphylococcal and streptococcal superantigens (SAgs) th

18 f antibiotic resistance genes for predicting staphylococcal antibacterial resistance need further dev

19 es ranging from 65.7 to 85.0% for predicting staphylococcal antibacterial resistance.

20 set for identifying pathogens and predicting staphylococcal antibacterial resistance.

21 tic resistance gene detection for predicting staphylococcal antibacterial susceptibility.

22 s ferric hydroxamate uptake D2 and conserved staphylococcal antigen 1A.

23 ly of structurally related proteins mediates staphylococcal attachment to host tissues, contributing

24 yphimurium bacteremia (n = 7) and those with Staphylococcal bacteremia (n = 7) with 100% correlation

25 tion strategy could help treat patients with Staphylococcal bacteremia without a need for novel antib

26 last resort treatment for streptococcal and staphylococcal bacteria including methicillin-resistant

27 ncated bacteriophage endolysin CHAPK and the staphylococcal bacteriocin lysostaphin have been co-admi

28 CRISPR-Cas9 system after infection with the staphylococcal bacteriophage varphi12.

29 However, it has yet to be determined if all staphylococcal bicomponent leukotoxin family members exh

30 The staphylococcal bicomponent pore-forming toxins Panton-Va

31 tanding the regulatory program that controls staphylococcal biofilm development, as well as the envir

32 ar biomass formation, biofilm formation, and staphylococcal biofilm in skin tissues.

33 tic intervention, we sought to identify anti-staphylococcal biofilm targets for the development of a

34 nt anti-biofilm activity against established staphylococcal biofilms and demonstrates the ability to

35 Staphylococcal biofilms are the most common cause of cen

36 en colonized with Staphylococcus aureus, and staphylococcal biofilms have been reported on adult AD s

37 electron microscopy verified the presence of staphylococcal biofilms on the skin of MPAACH children.

38 Staphylococcal biofilms sampled from MPAACH skin were vi

39 active and significantly reduced established staphylococcal biofilms.

40 enues for potential therapeutic targeting of staphylococcal biofilms.

41 clinical data supporting the elimination of staphylococcal breakpoints for other beta-lactam agents.

42 ated methicillin-resistant S. aureus (MRSA), staphylococcal BSI in cancer patients is associated with

43 otic therapy for MRSA-BSI; (4) management of staphylococcal BSIs in neonatal intensive care units; an

44 flanking conjugative transposon ICE6013, the staphylococcal cassette chromosome (SCC) and genomic isl

45 encoded by a conserved operon carried by the Staphylococcal Cassette Chromosome (SCCmec), an MGE that

46 ferent insertion of a genetic element in the staphylococcal cassette chromosome (SCCmec)-orfX junctio

47 ylococcus aureus (MRSA) with an unrecognized staphylococcal cassette chromosome mec (SCCmec) right-ex

48 Staphylococcal cassette chromosome mec (SCCmec) types II

49 MRSA isolates also underwent staphylococcal cassette chromosome mec (SCCmec) typing a

50 n a large (20 kb to > 60 kb) genomic island, staphylococcal cassette chromosome mec (SCCmec), that ex

51 resistant Staphylococcus aureus strains were staphylococcal cassette chromosome mec IV.

52 rences also were seen between HAHO-MRSA (60% staphylococcal cassette chromosome mec type II [SCCmec I

53 s using pulsed-field gel electrophoresis and staphylococcal cassette chromosome mec, and Panton-Valen

54 oneal infection, the particulate form of the staphylococcal cell envelope (PCE) induced the productio

55 Here, using two different forms of the staphylococcal cell envelope of Staphylococcus aureus RN

56 However, the small size of staphylococcal cells has impaired analysis of changes in

57 -associated genetic lineage that carries the staphylococcal chromosomal cassette mec (SCCmec) type IV

58 from and inserts site-specifically into the staphylococcal chromosome.

59 Two screening methods to detect staphylococcal colonization in humans were compared.

60 underlying mechanisms suggest that the anti-staphylococcal compound facilitating P. aeruginosa domin

61 rocin-resistant derivative of the pGO1/pSK41 staphylococcal conjugative plasmid lineage, and pGO400::

62 ng lipoproteins, the TLR2 agonists, from the staphylococcal cytoplasmic membrane.

63 ed on DL1a, a synthetic peptide derived from staphylococcal delta-lysin.

64 essential role for autophagy in tolerance to Staphylococcal disease and highlight how a single virule

65 ades have witnessed an alarming expansion of staphylococcal disease caused by community-acquired meth

66 TIRAP and anti-LTA Ab deficiencies underlie staphylococcal disease in this patient.

67 In contrast, invasive staphylococcal disease is less commonly associated with

68 Life-threatening staphylococcal disease occurred during childhood in the

69 In a mouse model of systemic staphylococcal disease, a pstSCAB-overexpressing strain

70 few years to become the predominant cause of staphylococcal disease, but it also appears to have incr

71 infectious synergy, leading to disseminated staphylococcal disease.

72 abI inhibitors that will inspire future anti-staphylococcal drug development.

73 hways regulating retinal innate responses in staphylococcal endophthalmitis.

74 Labeled staphylococcal enterotoxin (SE) A, SED, and SEE were use

75 monstrate that bacterial isolates containing staphylococcal enterotoxin A (SEA) from the affected ski

76 ogress towards reference materials (RMs) for Staphylococcal enterotoxin A (SEA) in cheese.

77 Ovalbumin (OVA)-specific, staphylococcal enterotoxin A (SEA)-nonreactive naive CD4

78 on of three bacterial toxins: cholera toxin, staphylococcal enterotoxin A, and toxic shock syndrome t

79 -10 (Fo = 0.16% versus 0.007%; p = 0.04) and staphylococcal enterotoxin B (Fo = 0.49% versus 0.26%; p

80 Detection of staphylococcal enterotoxin B (SEB) as a bacterial toxin

81 ed quantitative detection in various food of staphylococcal enterotoxin B (SEB) as a model up to 6 pg

82 Staphylococcal enterotoxin B (SEB) causes food poisoning

83 s article, we present the x-ray structure of staphylococcal enterotoxin B (SEB) in complex with its r

84 Staphylococcal enterotoxin B (SEB) is a bacterial supera

85 Staphylococcal enterotoxin B (SEB) is a superantigen tha

86 Systemic exposure to staphylococcal enterotoxin B (SEB) rapidly and selective

87 Staphylococcal enterotoxin B (SEB), a potential biologic

88 develop an antibody (Ab) therapeutic against staphylococcal enterotoxin B (SEB), a potential incapaci

89 ufficient counterparts for responsiveness to staphylococcal enterotoxin B (SEB).

90 isms with particular emphasis on the role of staphylococcal enterotoxin B (SEB).

91 lls are hyperresponsive to SAgs, typified by staphylococcal enterotoxin B (SEB); ii) the human MAIT c

92 n of naive CD4(+) T lymphocytes with soluble staphylococcal enterotoxin B and anti-CD28.

93 mulation by two fundamentally distinct SAgs, staphylococcal enterotoxin B and Mycoplasma arthritidis

94 PBMC were cultured for 7 d with staphylococcal enterotoxin B or IL-7 in the absence or p

95 Choric exposure to staphylococcal enterotoxin B precipitated a lupus-like i

96 versus unoriented constructs in an assay for staphylococcal enterotoxin B spiked into buffer showed t

97 hanced activation-induced proliferation (via staphylococcal enterotoxin B stimulation) but inhibited

98 cytokine production by cells in response to staphylococcal enterotoxin B stimulation.

99 with CpG and stimulation of the TCR with the staphylococcal enterotoxin B superantigen.

100 T, mmCT, or dmLT plus a polyclonal stimulus (staphylococcal enterotoxin B) or specific bacterial Ags,

101 This phenotype was reproduced with staphylococcal enterotoxin B, a heterologous SAg that al

102 of an additional T cell-activating stimulus, staphylococcal enterotoxin B, Abs to CTLA-4 and PD-1 rev

103 potential biological warfare agents, ricin, staphylococcal enterotoxin B, and epsilon toxin, in comp

104 In the absence of staphylococcal enterotoxin B, only the combination of Ab

105 vo with myelin oligodendrocyte glycoprotein, Staphylococcal enterotoxin B, or in vitro with anti-CD3

106 strated decreased pulmonary HIV-specific and staphylococcal enterotoxin B-reactive CD4(+) memory resp

107 and structure to the bacterial superantigen staphylococcal enterotoxin B.

108 induced by the atopic dermatitis-associated staphylococcal enterotoxin B.

109 g genes per isolate and a high prevalence of staphylococcal enterotoxin D and the enterotoxin gene cl

110 ion with a MRSA strain carrying the gene for staphylococcal enterotoxin P (sep).

111 cell transfer with the bacterial enterotoxin staphylococcal enterotoxin-B (SEB), which naturally link

112 ns produced by Staphylococcus aureus, called staphylococcal enterotoxins (abbreviated SEA to SEU).

113 a mouse model of asthma to determine whether staphylococcal enterotoxins promote TH2 differentiation

114 e association between asthma and exposure to staphylococcal enterotoxins.

115 he immunometabolic roles for a newly defined staphylococcal enzyme family.

116 tached peptidoglycan are the determinants of staphylococcal escape from adaptive immune responses.

117 emphasize the critical role of coagulase in staphylococcal escape from opsonophagocytic killing and

118 lococcus aureus (S. aureus) that produce the staphylococcal exotoxin alpha-toxin.

119 Staphylococcal food poisoning is caused by enterotoxins

120 vealed that MntABC critically contributes to staphylococcal growth when S. aureus is subjected to man

121 -sequestering protein calprotectin surrounds staphylococcal heart abscesses, calprotectin is not rele

122 The current model for staphylococcal hemoglobin-iron acquisition proposes that

123 The four-domain staphylococcal immunoglobulin binding (Sbi) protein inte

124 itro and increased survival significantly in staphylococcal-induced bacteremia compared to treatment

125 We confirmed the importance of EPHA2 for staphylococcal infection in an EPHA2-knock-out cell line

126 ribe here a novel, spontaneous model of oral staphylococcal infection in double knockout mice, defici

127 thicillin-resistant S. aureus, many cases of staphylococcal infection in the ICU are now classified a

128 minase activity and heightened resistance to Staphylococcal infection in TOC keratinocytes.

129 inhibition by S. aureus in vitro and promote staphylococcal infection in vivo.

130 Staphylococcal infection of bone marrow-derived osteocla

131 We focused specifically on staphylococcal infection of bone, one of the most common

132 lucidate the metabolic pathways required for staphylococcal infection within bone and demonstrate tha

133 El-K is commonly expressed in the setting of staphylococcal infection, in significant amounts.

134 Thus, using in vitro models of intracellular staphylococcal infection, we demonstrate that EsxA inter

135 bers of neutrophils, the key defense against staphylococcal infection.

136 and IL-22 protects against severe pulmonary staphylococcal infection.

137 ORAI1/2-deficient mice highly susceptible to staphylococcal infection.

138 andidiasis predisposes the host to secondary staphylococcal infection.

139 infection to reduce bacterial burden during staphylococcal infection.

140 e revealed a critical role for MntABC during staphylococcal infection.

141 t antimicrobial strategies, leading to fatal staphylococcal infection.

142 ing truncated AIPs as a means of attenuating staphylococcal infections in species beyond Staphylococc

143 Persistent staphylococcal infections often involve surface-associat

144 unities are often associated with persistent staphylococcal infections that place a tremendous burden

145 The worse outcome of staphylococcal infections with a higher vancomycin MIC c

146 evelop better strategies to tackle foodborne staphylococcal infections.

147 nly 1 initiated CAS; 67% (8/12) of these had staphylococcal infections.

148 a rise in enterococci and coagulase-negative staphylococcal infections.

149 gnificant clinical implications for relapsed staphylococcal infections.

150 nd develop therapeutic approaches to control staphylococcal infections.

151 for attenuating current multidrug resistant staphylococcal infections.

152 that improve our understanding of persistent staphylococcal infections.

153 potential treatment for multidrug-resistant staphylococcal infections.

154 he development of novel targets for treating staphylococcal infections.

155 ctams with approved clinical indications for staphylococcal infections.

156 ng into question the role of Agr in invasive staphylococcal infections.

157 hway holds potential for managing persistent staphylococcal infections.

158 activation and the protection of hosts from staphylococcal infections.

159 Finally, the effects of staphylococcal invasion on the integrity of different ce

160 a, providing broad-spectrum efficacy against staphylococcal invasive disease.

161 model involving Duts in the transfer of the staphylococcal islands (SaPIs) has been suggested, quest

162 Sixty-two percent of staphylococcal isolates (sampled from 400 subjects) form

163 Staphylococcal isolates from elderly patients were more

164 Methicillin resistance was prevalent among staphylococcal isolates from ocular infections, with man

165 We found that strain-level variation in staphylococcal isolates governs the interactions between

166 The biofilm propensity of staphylococcal isolates was assessed by crystal violet a

167 All staphylococcal isolates were susceptible to vancomycin.

168 ith resistance trends reported for nonocular staphylococcal isolates.

169 e important insight into the pathogenesis of staphylococcal joint infection and the mechanisms underl

170 and chemokinesis were markedly impaired, but staphylococcal killing was normal, and neutrophil oxidat

171 r antagonist anakinra to whole blood reduced staphylococcal killing, supporting a functional signific

172 r antagonist anakinra to whole blood reduced staphylococcal killing, supporting an IL-1beta functiona

173 Patients suffer from cold staphylococcal lesions and mucocutaneous candidiasis, se

174 identifies HlgAB and HlgCB as major secreted staphylococcal leukocidins.

175 activation and reveals an unexpected role of staphylococcal lipoproteins in EV biogenesis.

176 e whole-blood response to the TLR2/6 agonist staphylococcal lipoteichoic acid (LTA) was abolished onl

177 ti-LTA Abs rescue TLR2-dependent immunity to staphylococcal LTA in individuals with inherited TIRAP d

178 activity of Podoviridae, a unique family of staphylococcal lytic phages with short, non-contractile

179 Here, we investigate the staphylococcal malate-quinone and l-lactate-quinone oxid

180 ary epithelial cells and in a mouse model of staphylococcal mastitis.

181 etter understand the roles that BSH plays in staphylococcal metabolism, we constructed and examined s

182 We recently described Tudor-staphylococcal/micrococcal-like nuclease (TSN)-mediated

183 pic analyses demonstrate that CP outcompetes staphylococcal MntC and streptococcal PsaA for Mn(II).

184 VH3 idiotype Ig; however, the mechanisms for staphylococcal modification of immune responses are not

185 f the biofilm repress the production of anti-staphylococcal molecules.

186 A mediates the specific replicon assembly of staphylococcal multiresistant plasmids.

187 This process is essential for staphylococcal nasal colonization and resistance to the

188 (CPHMD(MSlambdaD)) framework to a series of staphylococcal nuclease (SNase) mutants with buried ioni

189 ic volumetric properties of various forms of staphylococcal nuclease (SNase), including three variant

190 Tudor Staphylococcal Nuclease (TSN or Tudor-SN; also known as

191 ivated point mutants of two target proteins (staphylococcal nuclease and ribose binding protein).

192 Staphylococcal nuclease and tudor domain containing 1 (S

193 nditions by interacting with and stabilizing Staphylococcal nuclease domain-containing 1 (SND1).

194 ormed a 1.1-mus MD simulation of crystalline staphylococcal nuclease, providing 100-fold more samplin

195 ogen prevalence, in particular a more common staphylococcal origin, have affected outcomes, which hav

196 We conclude that Nfu is necessary for staphylococcal pathogenesis and establish Fe-S cluster m

197 amily of peptides with multiple functions in staphylococcal pathogenesis.

198 PSMs have multiple functions in staphylococcal pathogenesis; for example, they lyse red

199 Staphylococcal pathogenicity islands (SaPIs) are the pro

200 ling molecules that induce the cycle of some Staphylococcal pathogenicity islands (SaPIs) by binding

201 s), the gene-transfer agents (GTAs), and the staphylococcal pathogenicity islands (SaPIs), the primar

202 bited by the highly mobile phage satellites, staphylococcal pathogenicity islands (SaPIs), which carr

203 Here we report that the staphylococcal pathogenicity islands have a dual role in

204 Staphylococcal peptidoglycan is characterized by pentagl

205 to S. aureus infection, and adjuvancy with a staphylococcal peptidoglycan O-acetyltransferase mutant

206 nts to rifampin are needed for management of staphylococcal periprosthetic joint infection.

207 es to rifampin in the clinical management of staphylococcal periprosthetic joint infections.

208 We have named this protein "staphylococcal peroxidase inhibitor" (SPIN).

209 cteristic extra motif VI, present in all the staphylococcal phage coded trimeric Duts, as well as the

210 We have recently proposed that the trimeric staphylococcal phage encoded dUTPases (Duts) are signali

211 Staphylococcal phage S83 was spray-dried with lactose an

212 For the AFM-IR measurements, spray-dried Staphylococcal phage Sa83 powder was embedded in resin,

213 The trimeric staphylococcal phage-encoded dUTPases (Duts) are signall

214 Since lytic staphylococcal phages are considered as anti-S. aureus a

215 Unlike most staphylococcal phages, Podoviridae require a precise wal

216 re essential for the life cycle of temperate staphylococcal phages.

217 ylation can prevent the infection by certain staphylococcal phages.

218 We identified the staphylococcal phenol-soluble modulin (PSM) peptides as

219 deletion of the nfu gene negatively impacts staphylococcal physiology and pathogenicity.

220 , the collective role of the CidR regulon in staphylococcal physiology is not clearly understood.

221 target antibiotic resistance genes destroys staphylococcal plasmids that harbor antibiotic resistanc

222 the host can be protected against secondary staphylococcal pneumonia after sub-lethal influenza infe

223 dly reduces susceptibility to post-influenza staphylococcal pneumonia and that this may represent a n

224 In as much as staphylococcal pneumonia is a disease driven in large pa

225 quiring sfb influences the susceptibility to staphylococcal pneumonia via induction of type 17 immuni

226 tate-dependent potentiation of cell death in staphylococcal populations.

227 Here we report the structures of a staphylococcal pore-forming cytotoxin, leukocidin GH (Lu

228 The staphylococcal pore-forming cytotoxins hijack important

229 er, our findings support a two-step model of staphylococcal prosthetic joint infection: As we previou

230 lso demonstrates a novel role for a secreted staphylococcal protease as a requirement for the develop

231 In conclusion, the staphylococcal protease SspB inactivates galectin-3, abr

232 Whether and which staphylococcal proteases account for Aap processing is y

233 The staphylococcal protein A (spa) gene was sequenced for al

234 eraction with virulence factor of S. aureus, staphylococcal protein A (SpA) in the presence of electr

235 Staphylococcal protein A (SpA) is an important virulence

236 Staphylococcal protein A (SpA) is anchored to the cell w

237 ntibiotic susceptibility, biofilm formation, Staphylococcal protein A (spa) typing, SCCmec typing, an

238 Staphylococcal protein A (SPA) was used to modify the si

239 d antigen presentation to CD4(+) T cells and staphylococcal protein A (SpA), a cell wall-anchored sur

240 and neutralizes the abundant surface-exposed Staphylococcal protein A (SpA).

241 cluded multilocus sequence typing (MLST) and staphylococcal protein A gene (spa) typing results as we

242 ted-residue force field, for the B domain of staphylococcal protein A, we are able to (i) provide the

243 of the common model protein, the B domain of staphylococcal protein A.

244 lved in AD augment the toxicity of the lytic staphylococcal protein alpha toxin.

245 However, few staphylococcal proteins that mediate intracellular survi

246 d TSST-1 can provide broad neutralization of staphylococcal SAgs.

247 alian New Zealand Cooperative on Outcomes in Staphylococcal Sepsis cohort for 1153 children with SAB

248 We identified staphylococcal serine protease-like proteins (Spls) as d

249 Here we identify Stk2, a staphylococcal serine/threonine kinase that provides eff

250 primary response gene 88 (MyD88) deficiency, staphylococcal skin and soft tissue infections are a lea

251 ntly of bone marrow-derived monocytes during staphylococcal skin infection leading to transiently inc

252 tients with AD may enhance susceptibility to staphylococcal skin infection.

253 ML-mediated inflammation in a mouse model of staphylococcal skin infection.

254 ; anti-interleukin (IL)-6 autoantibodies and staphylococcal skin infection; and anti-IL-17A, anti-IL-

255 cal antimicrobial agent for the treatment of staphylococcal skin infections.

256 of ebselen was evaluated in a mouse model of staphylococcal skin infections.

257 Here, we identify SosA as the staphylococcal SOS-induced cell division inhibitor.

258 , as well as representative enterococcal and staphylococcal species (including MRSA and VISA).

259 Non-Staphylococcus aureus staphylococcal species (non-SASS) are important pathogen

260 Transcriptomic mapping of different staphylococcal species confirmed that 3'UTRs were also v

261 ng bacteria, closely related less pathogenic staphylococcal species do not possess this importer.

262 t percent of subjects co-colonized with both staphylococcal species exhibited strains that formed coo

263 n be used to provide rapid identification of staphylococcal species in blood culture bottles to help

264 ylococcus agnetis are two coagulase-variable staphylococcal species that can be isolated from bovine

265 dis isolates was compared with that of other staphylococcal species.

266 faecalis isolates and other enterococcal and staphylococcal species.

267 binding specific positions on stem I and the Staphylococcal-specific stem Sa.

268 Staphylococcal SplB protease belongs to the chymotrypsin

269 We reveal that staphylococcal sRNA RsaD is overexpressed >20-fold in a

270 Glycopeptides reduce the risk of resistant staphylococcal SSIs and enterococcal SSIs, but increase

271 glycopeptides reduced the risk of resistant staphylococcal SSIs by 48% (relative risk, 0.52; 95% con

272 superficial and deep chest SSIs, susceptible staphylococcal SSIs, and respiratory tract infections.

273 hodology, and taking advantage of a singular staphylococcal strain that lacks the whole TCS machinery

274 Vn-binding activity was expressed by staphylococcal strains grown under iron starvation condi

275 infections are often associated with mutant staphylococcal strains that have decreased susceptibilit

276 t other clinically relevant enterococcal and staphylococcal strains.

277 se to 100% protection against four different staphylococcal strains.

278 pression levels of these enzymes vary across Staphylococcal strains.

279 thology elicited by acute challenge with the staphylococcal superantigen enterotoxin B were comparabl

280 The staphylococcal superantigen SEE induced the production o

281 Here we show Staphylococcal Superantigen-Like protein 11 (SSL11) from

282 us aureus secretes a potent TLR2 antagonist, staphylococcal superantigen-like protein 3 (SSL3), which

283 Staphylococcal superantigens cause toxic shock syndrome,

284 ding an array of virulence factors including staphylococcal superantigens, proteases, and leukotoxins

285 matory patterns, including IgE antibodies to staphylococcal superantigens; several studies using biol

286 vaccines and antibody therapeutics targeting staphylococcal surface molecules have thus far failed to

287 tionship between mechanics and adhesion in a staphylococcal surface protein, which may represent a ge

288 am infections by directing fibrinogen to the staphylococcal surface, generating a protective fibrin s

289 The mechanisms underlying T7SS-mediated staphylococcal survival during infection nevertheless re

290 te in particular is absolutely essential for staphylococcal survival in bone, despite the presence of

291 dings can help inform future developments in staphylococcal vaccine development and studies into the

292 nt vaccine failures and the design of future staphylococcal vaccines.

293 The role of alpha-toxin in pediatric staphylococcal-viral coinfection is unclear.

294 Production of Hla and restoration of staphylococcal virulence can be achieved in the psm muta

295 0-fold reduction in USA300 expression of the staphylococcal virulence regulator agr but had little ef

296 The Esx proteins are required for staphylococcal virulence, but their functions during inf

297 loss of any one transporter did not decrease staphylococcal virulence.

298 f the LacI family of metabolic regulators to staphylococcal virulence.

299 ular basis for the crucial role of MntABC in staphylococcal virulence.

300 Atl has also been identified previously as a staphylococcal vitronectin (Vn)-binding protein.