ライフサイエンスコーパス: PVL

1 PVL and LukGH have potent cytolytic activity in vitro, a

2 PVL cells clustered into two states consistent with a di

3 PVL enhanced the virulence of a subset of MRSA strains i

4 PVL expression augmented the cytotoxicity of S. aureus o

5 PVL genes are consistently associated with skin and soft

6 PVL improved postprocedure (P<0.001) and was none (33.3%

7 PVL is capable of lysing human white blood cells, but at

8 PVL production ranged from 0.02 to 4.865 mug/ml and corr

9 PVL strains are strongly associated with skin and soft-t

10 PVL was significantly reduced in L-treated mice compared

11 PVL was the predominant factor determining late-stage bo

12 PVL-positive (PVL(+)) S. aureus was frequent in the lesi

13 PVL-positive S. aureus colonization is associated with a

14 PVL-positive skin and soft-tissue infections are more li

15 PVL-treated mice were subjected to splenic, renal, or pu

16 accine was associated with lower ATI week 16 PVL even after controlling for viral and host genetic fa

17 RSA isolates, we identified 30 spa types, 47 PVL-negative and 15 scn-negative isolates, and no ST398

18 sertion sites were also identified in all 52 PVL-harboring CC30 strains.

19 The ALPPS group received 90% PVL combined with parenchyma transection.

20 riventricular neural apoptosis resulted in a PVL-like phenotype that recapitulates the primary perive

21 We assigned isolates to a PVL R or H sequence type based on a polymorphism that re

22 ate odds of infection or colonisation with a PVL-positive strain with fixed-effects or random-effects

23 on for seemingly contradictory results about PVL's role in virulence.

24 PS-treated mice was injected into mice after PVL.

25 s with the gp120 outer domain, including all PVL signature and CD4 mimicry interactions, but not crit

26 all in 2009 but accounted for a third of all PVL-CSMRSA strains in 2010.

27 ttenuated forms of Hla (HlaH35L/H48L) alone, PVL components (LukS-PVT28F/K97A/S209A and LukF-PVK102A)

28 Activated HSC were detected in ALPPS, PVL+DMOG and DMOG, again not in PVL.

29 HSC activation were assessed in PVL, ALPPS, PVL+DMOG and DMOG alone.

30 white blood cells, but at sublytic amounts, PVL can activate protective host immunity in the absence

31 erall stent diameter difference was 2.6% and PVL was correctly identified with a post-processing algo

32 rginine catabolic mobile element (ACME), and PVL-carrying prophage, PhiSa2 or PhiSa2-like regions on

33 ALPPS and PVL+DMOG accelerated liver growth and HC proliferation i

34 ensity, which was also observed in ALPPS and PVL+DMOG.

35 Documenting the presence of arcA and PVL genes by PCR was an efficient and accurate means of

36 hat neutralized not only alpha-hemolysin and PVL, but also other related toxins, produced by USA300 a

37 as well as a combined occurrence of tst and PVL in 3 (8.8%) isolates.

38 and the presence of mecA, SCCmec types, and PVL genes were confirmed by PCR.

39 model that explains how influenza virus and PVL act together to cause necrotizing pneumonia: an infl

40 proved optimal for HEp3 tumors and another (PVL 2) for MDA-MB-435.

41 ted transient increases in anti-Hla and anti-PVL antibodies; however, subsequent infection risk was s

42 Treatment of mice with anti-PVL antibody also enhanced bacterial clearance.

43 ore likely to be treated surgically than are PVL-negative infections, and children with PVL-positive

44 Of these, 70 (18.1%) were identified as PVL-CSMRSA.

45 ingle putative virulence determinant such as PVL.

46 L-positive, methicillin-resistant S. aureus (PVL-MRSA) strains, although three novel spa types and a

47 methicillin-resistant Staphylococcus aureus (PVL-MRSA) in adult patients who were screened systematic

48 methicillin-sensitive Staphylococcus aureus (PVL-MSSA) clinical isolates.

49 A relationship between PVL production and clinical presentation or patient demo

50 In this model, both PVL and Hla seemed to be required for early lung involve

51 -resolution X-ray crystal structures of both PVL and alpha-toxin in their soluble, monomeric, and oli

52 We found that both PVL-positive CA-MRSA and isogenic Deltapvl strains attac

53 n immune cells in vitro against cytolysis by PVL and alpha-toxin and hence may serve as the basis for

54 recruited neutrophils are rapidly killed by PVL, resulting in uncontrolled release of neutrophil pro

55 One candidate (PVL 10) proved optimal for HEp3 tumors and another (PVL

56 model systems identified the same candidate (PVL 10) as the most active promoter of vasopermeation in

57 e were no VISA or VRSA isolates that carried PVL genes or ACME, and most strains (69.8%) were staphyl

58 l phage insertion sites in 52 S. aureus CC30 PVL-harboring isolates, collected from four continents o

59 d with community-onset-PVL-negative MRSA (CO-PVL-negative MRSA vs. all other MRSA), with adjusted odd

60 The association with CO-PVL-negative MRSA infection increased across quartiles o

61 -knockout mutant (Deltapvl) and complemented PVL-positive derivative, to evaluate the role of PVL in

62 genic Deltapvl strains and further confirmed PVL's capacity to activate proinflammatory responses fro

63 In contrast, PVL was associated with BT in all animals but did not af

64 Conversely, PVL lowered the levels of tumor necrosis factor alpha (T

65 The current PVL Academic Research Consortium provides recommendation

66 e of TDR mutations increased with decreasing PVL (rate ratio [RR], 0.91 per 1000 decrease in PVL; P =

67 -AIN2+ prevalence than those with detectable PVL (crude OR 0.84, 0.72-0.98; I(2) 0%, p=0.80) in 16 st

68 We determined PVL's toxicity on infected mouse and cultured human corn

69 es from inflammatory-CAFs and differentiated-PVL cells in independent TNBC patient cohorts revealed s

70 that, independent of its cytotoxic effects, PVL also plays an important and positive immunomodulator

71 Three hundred eight PVL closure procedures were attempted in 259 patients in

72 or design of immunogens capable of eliciting PVL antibodies is that VH1-2*02 germ-line BCR interactio

73 Here, we used an endemic PVL-positive SSTI-causing CA-MRSA strain from Taiwan, to

74 A 5-class grading scheme to evaluate PVL was developed in concordance with VARC recommendatio

75 in experimental cirrhosis with BT (excluding PVL).

76 c resection performing surgical exploration, PVL, and ISS results in a marked and rapid hypertrophy o

77 e-associated (HA) MRSA isolate, negative for PVL, that carried SCCmec type II.

78 has now become the first-line treatment for PVL.

79 IVa, CC121-MRSA-V/VT, CC152-MRSA-[V + fusC] (PVL+).

80 teracts this pathogen strategy by generating PVL-neutralizing antibodies and by neutralizing the rele

81 HIV PVL and HSV shedding were more important determinants of

82 d the association of ART, CD4+ count, or HIV PVL on histology-confirmed CIN2+ detection at follow-up.

83 ut ART users with sustained undetectable HIV PVL had 44% lower risk of anal cancer than those without

84 = .30).In 3 populations, ART users with HIV PVL <50 copies/ml were less likely to have CIN2+ detecti

85 0 copies/mL) was closely associated with HIV PVL (beta = 0.51 per log10 copies/ml increase, 95%CI:0.4

86 hat higher antibody levels against Hla, Hld, PVL, SEC-1, and PSM-alpha3 may protect against sepsis in

87 ariants of pandemic CC8-MRSA-[IVa + ACME I] (PVL+) USA300 were detected and majority of CC772 strains

88 vascular disease, diabetes, SCCmec type II, PVL negativity, and higher vancomycin MIC (all P values

89 PVL is an effective procedure that improves PVL severity and symptoms.

90 density and HSC activation were assessed in PVL, ALPPS, PVL+DMOG and DMOG alone.

91 (rate ratio [RR], 0.91 per 1000 decrease in PVL; P = .033).

92 The acute administration of droxidopa in PVL and BDL rats caused a significant and maintained inc

93 -MSSA identical to those previously found in PVL-MRSA isolates highlights the role these strains may

94 he detection of PVL phages and haplotypes in PVL-MSSA identical to those previously found in PVL-MRSA

95 carrying M184V (RR, 1.50 per 100 increase in PVL; P < .001).

96 ative for L90M (RR, 0.75 per 100 increase in PVL; P = .022).

97 sent for K103N (RR, 1.00 per 100 increase in PVL; P = .99) and negative for L90M (RR, 0.75 per 100 in

98 on with oligodendrocyte and axonal injury in PVL.

99 nd subplate region is significantly lower in PVL cases compared to non-PVL controls.

100 ed in ALPPS, PVL+DMOG and DMOG, again not in PVL.

101 central white matter, and subplate region in PVL cases and controls.

102 ular foci, including the subplate region, in PVL, and may contribute to abnormal cortical formation a

103 However, by 2 hours after infection PVL-positive CA-MRSA more effectively disrupted endosome

104 train from Taiwan, together with an isogenic PVL-knockout mutant (Deltapvl) and complemented PVL-posi

105 on isolate characteristic was ST8/SCCmec IV, PVL+ MRSA (USA300) (53%).

106 ly sutured surgical valve paravalvular leak (PVL) closure.

107 f prosthetic mitral valve paravalvular leak (PVL) has emerged as an alternative to surgical treatment

108 Paravalvular leak (PVL) is a complication that occurs in 5-17% of patients

109 Paravalvular leak (PVL) is a frequent complication of transcatheter aortic

110 Paravalvular leak (PVL) occurs in 5% to 17% of patients following surgical

111 resents complications: paravalvular leakage (PVL) and onset of conduction abnormalities leading to pe

112 Significant prosthetic paravalvular leakage (PVL) could have serious clinical consequences and impair

113 SCCmec) typing, Panton-Valentine leucocidin (PVL) screening, and pulsed field gel electrophoresis (PF

114 associated with Panton-Valentine leucocidin (PVL) toxin.

115 tantly, using a Panton-Valentine leucocidin (PVL)-negative MRSA isolate from patient sputum, we show

116 t currently for Panton-Valentine leucocidin (PVL)-positive, methicillin-sensitive Staphylococcus aure

117 and HlgCB) and Panton-Valentine leukocidin (PVL or LukSF) were shown to assemble from soluble subuni

118 xins, including Panton-Valentine leukocidin (PVL) and alpha-hemolysin (Hla), although supporting evid

119 Panton-Valentine leukocidin (PVL) and alpha-toxin are exotoxins that create lytic por

120 nd detection of Panton-Valentine leukocidin (PVL) and scn genes.

121 ains expressing Panton-Valentine leukocidin (PVL) are associated with severe skin and soft tissue inf

122 The lukF/lukS Panton-Valentine leukocidin (PVL) genes did not directly correlate with the ISS, bein

123 n, detection of Panton-Valentine leukocidin (PVL) genes, arginine catabolic mobile element (ACME), an

124 assays for the Panton-Valentine leukocidin (PVL) genes, the protein A gene (spa), and arcA and opp3,

125 The Panton-Valentine leukocidin (PVL) is a cytotoxin expressed by many methicillin-resist

126 Panton-Valentine leukocidin (PVL) is common in African Staphylococcus aureus and can

127 S. aureus toxin Panton-Valentine leukocidin (PVL) is most likely causative for necrotizing diseases,

128 The impact of Panton-Valentine leukocidin (PVL) on the outcome in Staphylococcus aureus pneumonia i

129 Panton-Valentine leukocidin (PVL) production by methicillin-resistant Staphylococcus

130 re subjected to Panton-Valentine leukocidin (PVL) screening, and SCCmec, pulsed-field gel electrophor

131 Panton-Valentine leukocidin (PVL) was present in 21.9%, and vancomycin heteroresistan

132 Panton-Valentine leukocidin (PVL), a bacteriophage encoded toxin that has been epidem

133 d with those of Panton-Valentine leukocidin (PVL), a well-characterized S. aureus leukotoxin.

134 element (ACME), Panton-Valentine leukocidin (PVL), and other toxins that may contribute to disease se

135 strains produce Panton-Valentine leukocidin (PVL), but its contribution to CA-MRSA pathogenesis is po

136 Panton-Valentine leukocidin (PVL), encoded by the lukSF-PV genes, is a putative virul

137 actors, such as Panton-Valentine leukocidin (PVL), have been proposed to drive this epidemic.

138 xins, including Panton-Valentine leukocidin (PVL), leukotoxin GH (LukGH; also known as LukAB), leukot

139 characteristics Panton-Valentine leukocidin (PVL), SCCmec IVa, the arginine catabolic mobile element

140 emolysin (Hld), Panton Valentine leukocidin (PVL), staphylococcal enterotoxin C-1 (SEC-1), and phenol

141 A and those for Panton-Valentine leukocidin (PVL), USA300, and USA400.

142 ing part of the Panton-Valentine leukocidin (PVL), was observed in the codY mutant.

143 lysin (Hla) and Panton-Valentine leukocidin (PVL), we evaluated whether active immunization with atte

144 USA300 and its Panton-Valentine leukocidin (PVL)- and alpha-hemolysin (Hla)-negative isogenic deriva

145 CCmec type, and Panton-Valentine leukocidin (PVL)-producing genes on an S. aureus genome.

146 proteases, and Panton-Valentine leukocidin (PVL).

147 lysin (Hla) and Panton-Valentine leukocidin (PVL; LukF-PV/LukS-PV subunits), both premier targets of

148 Periventricular leukomalacia (PVL) is a structural loss of white matter pathways that

149 m infants with periventricular leukomalacia (PVL) is uncertain.

150 disease (HD), periventricular leukomalacia (PVL), and kidney dysfunction; Fer-1 inhibited lipid pero

151 ogies, notably periventricular leukomalacia (PVL), which is distinguished by bilateral necrosis of ne

152 ria for proliferative verrucous leukoplakia (PVL).

153 tic cirrhosis and 2-day portal vein-ligated (PVL) animals.

154 Sham, portal vein-ligated (PVL), and 4-week biliary duct-ligated (BDL) rats receive

155 ng liver partition and portal vein ligation (PVL plus transection=ALPPS) or the addition of the proly

156 Portal vein ligation (PVL) induces liver growth prior to resection.

157 ALPPS combines portal vein ligation (PVL) with liver transection (step I), followed by resect

158 y (PH), intraoperative portal vein ligation (PVL), and associated liver partition and portal vein lig

159 cal exploration, right portal vein ligation (PVL), and in situ splitting (ISS) of the liver parenchym

160 fibroblast (CAF) and two perivascular-like (PVL) subpopulations.

161 of signature features for potent VRC01-like (PVL) antibodies, and verify the importance of these feat

162 Potent VRC01-like (PVL) HIV-1 antibodies derived from the VH1-2*02 germ-lin

163 drawn for HTLV-1 serology and proviral load (PVL).

164 of TDR mutations and population viral load (PVL) among treated patients during 1997-2011 was estimat

165 unodeficiency virus (HIV) plasma viral load (PVL) on high-grade cervical intraepithelial neoplasia (C

166 tal HIV shedding with HIV plasma viral load (PVL), herpetic lesions, HSV shedding and other factors w

167 tive ART [HAART], HIV-RNA plasma viral load [PVL], and nadir or current CD4 cell count) with outcomes

168 h no vision loss (NVL), partial vision loss (PVL), and severe vision loss (SVL) were matched 1:1:1 ba

169 receptor 5a, the cellular target of the lukS PVL subunit.

170 mL), and 77 (72%) were viremic with a median PVL of 5450 copies/mL (interquartile range, 169-1 997 96

171 hundred sixty-two patients (70%) had </=mild PVL after the procedure.

172 Mitral PVL was associated with higher MACE (hazard ratio [HR],

173 e patients who underwent percutaneous mitral PVL closure at Mayo Clinic, Rochester, MN, between Janua

174 t of patients undergoing percutaneous mitral PVL closure, successful percutaneous reduction of the PV

175 f 231 patients underwent percutaneous mitral PVL repair at a mean age of 67+/-12 years.

176 ificantly lower in PVL cases compared to non-PVL controls.

177 Hla, but not PVL, significantly impacted severe sepsis-related mortal

178 0, 2.5 +/- 2.0, and 2.3 +/- 2.1 for the NVL, PVL, and SVL groups, respectively (P < 0.0001).

179 (n = 198), and 56.0% (n = 195) for the NVL, PVL, and SVL groups, respectively (P = 0.0005).

180 heat-killed organisms and in the absence of PVL and alpha-toxin.

181 fferent mammalian species, where activity of PVL is found to be restricted to fewer species than that

182 hitherto unrecognized low-level carriage of PVL-CSMRSA among patients being admitted to hospitals in

183 so describe the molecular characteristics of PVL-MRSA and antibiotic resistance phenotypes.

184 Characterization of PVL-MSSA isolates by multilocus sequence typing (MLST) a

185 Percutaneous closure of PVL is an effective procedure that improves PVL severity

186 linical evidence for percutaneous closure of PVL, including large national registries from Ireland, S

187 nsiderations for the percutaneous closure of PVL, such as access site and device selection.

188 l the frequency and clinical consequences of PVL closure.

189 Furthermore, the detection of PVL phages and haplotypes in PVL-MSSA identical to those

190 We determined here the distribution of PVL phages, PVL gene sequences, and chromosomal phage in

191 h the pvl gene variation and distribution of PVL-encoding phages are poorly understood.

192 ains sheds further light on the evolution of PVL-positive CA-MRSA.

193 The expression of PVL but not LukAB resulted in more-severe pulmonary infe

194 The genotypes of PVL(+) S. aureus in returnees were reported to be endemi

195 Inactivation of PVL in USA300 strains caused reduced pathology and bacte

196 um skin infection model, where low levels of PVL augmented innate immune resistance to infection.

197 Seven different lineages of PVL-CSMRSA were identified.

198 imaging in the assessment and management of PVL, including echocardiographic imaging and adjunctive

199 /or thick, may be the first manifestation of PVL.

200 es, but the precise pathogenic mechanisms of PVL and a possible contribution of influenza virus remai

201 rtant insights into the microepidemiology of PVL-harboring CC30 strains, while the discovery of PhiSa

202 n and each infection relative to the odds of PVL-positive skin and soft-tissue infection.

203 utant was not explained by overexpression of PVL.

204 The presence of PVL in S. aureus in travelers was associated with compli

205 Here we report the prevalence of PVL among a representative sample of 1,055 S. aureus inf

206 riginal research reporting the prevalence of PVL genes among Staphylococcus aureus pneumonia, bactera

207 l counts, suppressed bacterial production of PVL and Hla, and reduced production of the neutrophil-ch

208 In contrast, the colonization rate of PVL-CSMRSA increased over time, rising from 0.075% in 20

209 man corneal epithelial cells and the role of PVL and antibody to PVL in pathogenesis of murine kerati

210 We investigate the role of PVL in disease, colonisation, and clinical outcome.

211 sed studies are needed to define the role of PVL in mild, moderate, and severe disease and to inform

212 positive derivative, to evaluate the role of PVL in the pathogenesis of CA-MRSA in the RHEK-1 human k

213 es the temporal and spatial specificities of PVL and indicate that damage to VEGF-dependent, immature

214 Finally, we show that the toxicity of PVL, but not of HlgCB, is neutralized by various C5aR1 a

215 definitions to be used in clinical trials of PVL closure devices.

216 e positively associated with community-onset-PVL-negative MRSA (CO-PVL-negative MRSA vs. all other MR

217 Rabbits vaccinated with Hla toxoid alone or PVL components alone were only partially protected again

218 iver was compared to patients after ALPPS or PVL.

219 LukGH or PVL caused skin inflammation in rabbits and a monkey, bu

220 Controls underwent either transection or PVL alone.

221 strains, while USA400 strains overproducing PVL caused increased bacterial burdens.

222 isogenic DeltaPVL, or strains overproducing PVL.

223 lyvalerolactone-poly(ethylene glycol) (PAMAM-PVL-PEG).

224 While the hydrophobic PAMAM-PVL core can encapsulate hydrophobic drugs, the hydrophi

225 ist on the impact of successful percutaneous PVL closure on midterm outcomes.

226 rom mitral valve replacement to percutaneous PVL repair was 1.25 (0.31-7.25) years.

227 and Ireland centers undertaking percutaneous PVL closure submitted data to the UK PVL Registry.

228 temporally spaced at 24 h and 96 h after PH, PVL, and ALPPS.

229 ermined here the distribution of PVL phages, PVL gene sequences, and chromosomal phage insertion site

230 1 was Panton-Valentine leukocidin positive (PVL(+)).

231 he CC8/Panton-Valentine leukocidin-positive (PVL(+)) group of S. aureus clone USA300: 34 of these str

232 PVL-positive (PVL(+)) S. aureus was frequent in the lesional and nasal

233 toxins Panton-Valentine leukocidin LukSF-PV (PVL) and gamma-hemolysin CB (HlgCB) target human phagocy

234 ity of methods for assessing and quantifying PVL, and lack of consistency in the timing of such asses

235 Residual PVL is associated with 1-year mortality.

236 residual PVL, patients with </=mild residual PVL had lower rates of repeat surgical interventions (6%

237 Compared with those who had >mild residual PVL, patients with </=mild residual PVL had lower rates

238 7% in patients with higher grade of residual PVL (P=0.002).

239 Moderate to severe residual PVL was associated with all-cause mortality (hazard rati

240 LST) clonal complex associated with specific PVL phage types.

241 ntify the origin of a sudden increase of ST8 PVL-positive isolates in Geneva during 2013.

242 e thinning with inferior VF defects, suggest PVL.

243 rgeons score 7+/-4%) with severe symptomatic PVL in mitral (81%) or aortic (19%) position underwent t

244 alence, progression, and impact of post-TAVR PVL and to help direct future efforts regarding the asse

245 ffect of antibody treatment, it appears that PVL plays an inconsistent role in pathogenesis and immun

246 ns with their receptors, we demonstrate that PVL and HlgCB differentially interact with human C5aR1 a

247 ms of disease we identified no evidence that PVL affects outcome.

248 These findings indicate that PVL is an important virulence factor that enables CA-MRS

249 Our results indicate that PVL phages with icosahedral heads, including Phi108PVL a

250 Recent reports indicating that PVL may be correlated with increased late mortality have

251 We show that PVL and HlgCB feature distinct activity toward neutrophi

252 low doses induced apoptosis, suggesting that PVL also has the capacity to regulate inflammation.

253 oversial, with clinical data suggesting that PVL-producing strains may cause less severe disease in h

254 This finding challenges the view that PVL mainly causes invasive disease with poor prognosis.

255 The PVL Academic Research Consortium met to review evidence

256 sular polysaccharide gene cap5E Although the PVL-encoding phage varphiSa2USA was introduced into the

257 resence of SCCmec type IV, the ACME, and the PVL toxin gene and matched the t008 or t121 molecular sp

258 ons did not differ significantly between the PVL cases and controls.

259 for the prophage insertion that harbored the PVL genes.

260 egions was 54 to 80% lower (p</=0.01) in the PVL cases (n=15) compared to controls adjusted for age a

261 By 6 hours after infection, the PVL-positive strain caused significantly more caspase-de

262 nce of the arcA gene and the presence of the PVL genes (area under the curve, 0.980; 95% confidence i

263 re, successful percutaneous reduction of the PVL to mild or less was associated with significant midt

264 imilar expression pattern to the PH than the PVL at the early phase of the regeneration.

265 ion M184V was positively associated with the PVL of nonresponding patients carrying M184V (RR, 1.50 p

266 Antibodies to PVL or control sera were topically applied to infected c

267 al cells and the role of PVL and antibody to PVL in pathogenesis of murine keratitis.

268 opical treatment with polyclonal antibody to PVL yielded significant reductions in corneal pathology

269 The open transapical approach to PVL closure in high-risk patients has a high procedural

270 growth and HC proliferation in comparison to PVL.

271 ature periventricular vessels contributes to PVL development.

272 se inhibitor dimethyloxalylglycine (DMOG) to PVL both accelerate growth via stabilization of HIF-alph

273 emnant liver after ALPPS doubled relative to PVL, whereas mice with transection alone disclosed minim

274 s of infection because mice are resistant to PVL and HlgCB.

275 in this study showed a genetic similarity to PVL-positive, methicillin-resistant S. aureus (PVL-MRSA)

276 ates (385/1,998, or 19.3%) were subjected to PVL testing.

277 cC, vanA, Panton-Valentine Leukocidin toxin (PVL), and toxic shock syndrome toxin-1 (tst) genes.

278 pacity and quality of life after transapical PVL closure.

279 d midterm clinical efficacy of transcatheter PVL closure using an open transapical approach.

280 ecutive patients who underwent transcatheter PVL closure in our center were prospectively enrolled.

281 ortic (19%) position underwent transcatheter PVL closure.

282 taneous PVL closure submitted data to the UK PVL Registry.

283 We hypothesized that a key to understanding PVL's action on host cells and, possibly, outcomes from

284 People living with HIV with undetectable PVL had lower HSIL-AIN2+ prevalence than those with dete

285 We found that, unlike PVL, LukGH did not prime human neutrophils for increased

286 clude routine detection of genes for USA300, PVL, or mupA, all of which were either of low frequency

287 majority of CC772 strains were CC772-MRSA-V (PVL+), "Bengal- Bay Clone".

288 However the reduction of in vivo PVL did not reach the statistical significance in V- tre

289 the CA-MRSA infection isolates, 8 (67%) were PVL(+).

290 cA-positive MRSA isolates, five (14.7%) were PVL-positive, seventeen (50%) were tst-positive, ten (29

291 Whether PVL is pathogenic or an epidemiological marker is unclea

292 The signature features explain why PVL antibodies derive from a single germ-line human V(H)

293 om nontemperate climates are associated with PVL(+) S. aureus and promote the emergence and spread of

294 e PVL-negative infections, and children with PVL-positive musculoskeletal disease might have increase

295 Circulating factors in combination with PVL seem to mediate enhanced liver regeneration, associa

296 gans or ALPPS-plasma injection combined with PVL induced liver hypertrophy similar to ALPPS.

297 ratios (aOR)(95% CI) among participants with PVL >= 1000 per 10 5 PBL were 7.08 (2.67, 18.74; p<0.001

298 d odds ratios (ORs) to compare patients with PVL-positive colonisation and each infection relative to

299 Upon superinfection with PVL-expressing S. aureus, the recruited neutrophils are

300 95% CI, 0.37-0.90; P = 0.01), and those with PVL had 44% decreased odds (OR, 0.56; CI, 0.36-0.87; P =