ライフサイエンスコーパス: RSV infection

1 We enrolled previously healthy children with RSV infection.

2 rgeted at providing an effective therapy for RSV infection.

3 isease severity in infants hospitalized with RSV infection.

4 l efficacy in participants with experimental RSV infection.

5 ribe that high-fiber diet protects mice from RSV infection.

6 cterize the nasal microbiome of infants with RSV infection.

7 rity in both outpatients and inpatients with RSV infection.

8 ons significantly related to the severity of RSV infection.

9 receptor antagonist was administered during RSV infection.

10 ng the best available animal models to study RSV infection.

11 differentiation, stability, and function in RSV infection.

12 g lymph nodes in wild-type BALB/c mice after RSV infection.

13 group for severe pneumonia, independently of RSV infection.

14 LC3 responses in STAT1-deficient mice during RSV infection.

15 Treg cell phenotype and function to control RSV infection.

16 an was significantly downregulated following RSV infection.

17 products for the prevention and treatment of RSV infection.

18 There is no vaccine yet available to prevent RSV infection.

19 nalyze the permissiveness of CD4+ T cells to RSV infection.

20 rch tool for evaluating infants with primary RSV infection.

21 emental oxygen use among HCT recipients with RSV infection.

22 ctively, compared with wild-type mice during RSV infection.

23 essed in smaller airways in a mouse model of RSV infection.

24 of children who died with community-acquired RSV infection.

25 antibodies in serum from infants with acute RSV infection.

26 cies in both murine and cotton rat models of RSV infection.

27 ponses comparable to those generated by live RSV infection.

28 agent approved for use for the treatment of RSV infection.

29 y epithelial cells) to establish its role in RSV infection.

30 efficacious vaccine or therapy available for RSV infection.

31 therapeutic targeting of TSLP during severe RSV infection.

32 ot mount an IL-13-producing ILC2 response to RSV infection.

33 effective treatment or vaccine available for RSV infection.

34 treatment with recombinant cytokines before RSV infection.

35 e plays a fundamental role in the outcome of RSV infection.

36 study of the risk for hospitalization due to RSV infection.

37 re are no effective antiviral drugs to treat RSV infection.

38 f neutrophils to the immune response against RSV infection.

39 upregulated especially at the later stage of RSV infection.

40 at Sirt1 was upregulated in mouse lung after RSV infection.

41 ntiviral efficacy in the cotton rat model of RSV infection.

42 ependent co-correlates of protection against RSV infection.

43 itivity of BN for point-of-care detection of RSV infection.

44 ance the adaptive immune response with later RSV infection.

45 governing the pathogenic recall responses to RSV infection.

46 pment of AHR and airway inflammation, during RSV infection.

47 es exist of the incidence or epidemiology of RSV infection.

48 rophils did not change the viral load during RSV infection.

49 firming the role of autophagy in suppressing RSV infection.

50 ldren with a history of laboratory-confirmed RSV infection.

51 asopharyngeal samples of children with acute RSV infection.

52 32 in the inhaled RBV group had symptomatic RSV infection.

53 form the basis of new therapeutics to treat RSV infection.

54 but rather in its activation by a subsequent RSV infection.

55 l to understand the immune response to human RSV infection.

56 (17.7%) had no known risk factors for severe RSV infection.

57 in shaping the immune response early during RSV infection.

58 ome on the severity and clinical outcomes of RSV infection.

59 lightly inhibited in cells exhibiting robust RSV infection.

60 roles in protecting the host against IAV and RSV infections.

61 ldren annually require medical attention for RSV infections.

62 cine appeared safe, immunogenic, and reduced RSV infections.

63 ure was reduction in hospitalizations due to RSV infections.

64 nts treated with oral or aerosolized RBV for RSV infections.

65 f RSV-naive animals or after two consecutive RSV infections.

66 d to promote fast host recovery from IAV and RSV infections.

67 in response to respiratory syncytial virus (RSV) infection.

68 ng important in respiratory syncytial virus (RSV) infection.

69 llowing IAV and respiratory syncytial virus (RSV) infections.

70 he treatment of respiratory syncytial virus (RSV) infections.

71 3 (HPIV3), and respiratory syncytial virus (RSV) infections.

72 ) is approved to treat high-risk infants for RSV infection(7,8), but other treatments, as well as vac

73 of infants from respiratory syncytial virus (RSV) infection, a severe acute lower respiratory tract d

74 RSV infection activates BRD4 acetyltransferase activity

75 n histone H3 Lys (K) 122, demonstrating that RSV infection activates BRD4 in vivo These data validate

76 stration of the chemoattractant CXCL1 during RSV infection affected disease severity as measured by w

77 RSV infection after Cd pre-exposure also caused widespre

78 chment of epithelial cells than is seen with RSV infection alone.

79 As a potential response to this loss, RSV infection also significantly shortened nymphal stage

80 Inhibiting UA and IL-1beta during RSV infection ameliorates RSV immunopathology, reduces t

81 Infants with RSV infection and >=24 months of continuous enrollment w

82 sociated with respiratory sequelae following RSV infection and characterizing the viral load, RSV who

83 ion, transcriptome profiles of children with RSV infection and H. influenzae- and Streptococcus-domin

84 r matrix accumulation of HA occurs following RSV infection and may contribute to airway inflammation.

85 e target for preventative strategies against RSV infection and may inform the design of novel therape

86 months of life and identify risk factors for RSV infection and progression to severe disease.

87 rotein conformations, in vitro inhibition of RSV infection and propagation, and protective efficacy i

88 RSV infection and RSV hospitalization were positively as

89 that Cd burden by dietary intake potentiates RSV infection and severe disease with associated mitocho

90 association was observed between early life RSV infection and subsequent childhood recurrent wheeze,

91 demiological and immunological background to RSV infection and subsequently focus on the promising pi

92 be useful for the prevention or treatment of RSV infection and support the use of the pre-F protein a

93 airway inflammation and resistance following RSV infection and suppressed the level of MMP-12.

94 for children at risk for severe outcomes of RSV infection and thereby lower rates of hospitalization

95 However, both respiratory syncytial virus (RSV) infection and mutations in the receptor for advance

96 45) or evaluated as outpatients (n = 20) for RSV infection, and healthy noninfected age-matched contr

97 ed on APC after respiratory syncytial virus (RSV) infection, and its inhibition leads to exaggerated

98 During primary respiratory syncytial virus (RSV) infection, anti-Axl mAb treatment significantly inc

99 1 released by airway epithelial cells due to RSV infection appears to function as a paracrine factor

100 However, clinical data for fatal RSV infection are scarce.

101 antibody responses established after natural RSV infections are poorly protective against reinfection

102 at the site of respiratory syncytial virus (RSV) infection are sparse despite nearly five decades of

103 The lead peptide inhibits RSV infection as effectively as does a peptide correspon

104 ls play a critical role in clearing an acute RSV infection, as well as contributing to RSV-induced di

105 ess disease and pulmonary inflammation after RSV infection associated with reduced viral load.

106 Acute RSV infection associates with elevated IL-17 and accumul

107 f IFI44 or IFI44L was sufficient to restrict RSV infection at an early time postinfection.

108 ificantly reduced the following responses to RSV infection: augmenting of inflammatory cells, especia

109 oped a model of respiratory syncytial virus (RSV) infection based on well-differentiated pediatric pr

110 g index for respiratory syncytial virus (ISI-RSV) infection, based on a cohort of 237 allogeneic hema

111 han 5 years who died with community-acquired RSV infection between Jan 1, 1995, and Oct 31, 2015, thr

112 y showed a complete lack of efficacy against RSV infection but also induced severe lung disease enhan

113 findings, Myd88/Trif/Mavs(-/-) mice survived RSV infection but displayed higher viral load and weight

114 ected BMDCs exacerbate a live challenge with RSV infection but was inhibited when BMDCs were treated

115 ble to influenza (seasonal and pandemic) and RSV infection by applying Poisson regression models to m

116 ur results provide a strategy for inhibiting RSV infection by mucosal and endotracheal delivery of do

117 Suppressing RSV infection by RSV immunoprophylaxis might increase th

118 The combined results show that RSV infection can quite effectively prime animals for th

119 Respiratory syncytial virus (RSV) infection causes significant morbidity in hematopoi

120 Among 201 episodes of RSV infection, children with higher viral load had signi

121 s higher in samples collected at the time of RSV infection compared with samples collected one month

122 Murine models of RSV infection confirmed that LPS exposure, Tlr4 genotype

123 s in the lungs of juvenile mice during acute RSV infection could potentiate extracellular matrix remo

124 ion of UA or IL-1beta during neonatal murine RSV infection decreased mucus production, reduced cellul

125 able of inducing IFN-alpha prior to neonatal RSV infection decreased Th2-biased immunopathogenesis du

126 ease in vivo, in a murine model of pulmonary RSV infection, demonstrating maximal efficacy when appli

127 s elicited by Ad5.RSV-F and those seen after RSV infection; differences in antibody profiles were als

128 ed as any day while alive after diagnosis of RSV infection during which </=2 L of supplemental oxygen

129 data from hospitalized adults with confirmed RSV infections during 2 North American RSV seasons.

130 to spread, the high frequency of symptomless RSV infection episodes highlights a potentially importan

131 Tests on 16,928 samples yielded 205 RSV infection episodes in 179 individuals (37.1%) from 4

132 iated with an increased risk of asymptomatic RSV infection episodes were higher age, shorter duration

133 Upon RSV infection, EX-527-treated DCs, Sirt1 small interferi

134 versican promotes airway inflammation during RSV infection further demonstrating that versican's role

135 econd decline >=5% and >=10% at 90 days post-RSV infection had a higher 1-year mortality (P = 0.004 a

136 HCT recipients with RSV infections had similar outcomes when treated with ae

137 Healthcare-associated RSV infections (HAIs) accounted for 29 deaths (36.7%), w

138 Infant RSV infection has a significant long-term healthcare-res

139 sease following respiratory syncytial virus (RSV) infection has been linked to enhanced proinflammato

140 Early life respiratory syncytial virus (RSV) infection has been linked to the onset of asthma.

141 ific T cells mediate disease following acute RSV infection have been hampered by the lack of defined

142 Although risk factors for RSV infection have been identified, the role of microbia

143 nts after acute respiratory syncytial virus (RSV) infection have been obtained from animal experiment

144 omatic cases of respiratory syncytial virus (RSV) infection have not been well described.

145 uction of versican was not altered following RSV infection; however, BEC production of versican was s

146 ciated with the inflammatory response during RSV infection (i.e., CCL-2, CCL-3, CCL-5, IL-6) as well

147 During RSV infection, IL-33 is elevated and promotes immune cel

148 These studies showed that after RSV infection, immunization with a single dose of VLPs c

149 st but not by a post-F VLP boost or a second RSV infection.IMPORTANCE Humans may experience repeated

150 function for IFI44 and IFI44L in controlling RSV infection.IMPORTANCE RSV infects all children under

151 s, like IAV and respiratory syncytial virus (RSV) infections, impose great challenges to public healt

152 shown to induce pulmonary eosinophilia upon RSV infection in a mouse model.

153 age worldwide; therefore, the prevention of RSV infection in all infants represents a significant un

154 tected against severe lung injury induced by RSV infection in an experimental mouse model and in pedi

155 ines, and encourage more specific studies on RSV infection in BPD patients, including vaccine develop

156 with deaths among children hospitalized with RSV infection in Canadian pediatric centers.

157 antibodies play a role in protection against RSV infection in early life, but data regarding the conc

158 The pathological features induced by RSV infection in HIS mice included peribronchiolar infla

159 Diagnosis of RSV infection in hospitalized adults is often delayed, w

160 RSV infection in hospitalized older adults often manifes

161 and airway resistance, two manifestations of RSV infection in humans, in mice.

162 fusion inhibitor with the potential to treat RSV infection in infants and adults is reported.

163 ghlight the dominance of type-2 responses to RSV infection in infants and suggest an important role o

164 ithelium that reproduce several hallmarks of RSV infection in infants, indicating that they represent

165 that they represent authentic surrogates of RSV infection in infants.

166 n clinical development for the prevention of RSV infection in infants.

167 olar macrophages (rAMs) to susceptibility to RSV infection in mice that recovered from allergic airwa

168 been shown to confer robust immunity against RSV infection in mice, cotton rats, and nonhuman primate

169 RSV infection in neonates induced limited type I IFN and

170 Here we show that RSV infection in neonates induced limited type I interfe

171 expression of NbP3IP conferred resistance to RSV infection in Nicotiana benthamiana.

172 ts caused by Spn and NTHi, with a concurrent RSV infection in sOP children.

173 Studies examining RSV infection in susceptible BALB/c mice indicate that b

174 by wt G, but not by wt F, completely blocked RSV infection in the absence of added complement.

175 Infants with RSV infection in the first year of life (n = 38 473) wer

176 Confirmation of RSV infection in the lower respiratory tract provides pr

177 They also protected against RSV infection in the mouse lung.

178 provided nearly complete protection against RSV infection in the upper and lower respiratory tract a

179 Natural RSV infection in young children does not elicit long-las

180 es polygyrus on respiratory syncytial virus (RSV) infection in a mouse model.

181 ciation between respiratory syncytial virus (RSV) infection in early life and subsequent respiratory

182 Respiratory syncytial virus (RSV) infection in infants has recognizable clinical sign

183 Respiratory syncytial virus (RSV) infection in lung transplant recipients (LTRs) caus

184 Respiratory syncytial virus (RSV) infection in mouse and human lung is associated wit

185 spitalized with respiratory syncytial virus (RSV) infection in the United States.

186 s have examined respiratory syncytial virus (RSV) infections in adults.

187 Per 1000 children, the average annual RSV infection incidence rates among children aged <3, 3-

188 development for respiratory syncytial virus (RSV) infection, including small molecules that target vi

189 RSV infection induced an RSV-specific human gamma interf

190 We discovered that RSV infection induces a complex of bromodomain containin

191 Respiratory syncytial virus (RSV) infection induces asthma exacerbations, which leads

192 in response to respiratory syncytial virus (RSV) infection induces bacterial biofilm formation throu

193 We suggest that protection from RSV infection is a function of a complex interplay betwe

194 Vertical RSV infection is associated with dysregulation of crucia

195 RSV infection is associated with neutrophil influx into

196 bronchiolitis revealed that the severity of RSV infection is determined by the TLR4 genotype of the

197 Our study suggests that RSV infection is frequent in Laos and commonly associate

198 ested, estimating the under-ascertainment of RSV infection is imperative.

199 We postulate that the severity of RSV infection is influenced by modulation of the host im

200 nses that play a role in the pathogenesis of RSV infection is needed for therapeutic development.

201 Because RSV infection is restricted to the respiratory tract, an

202 RSV infection is typically associated with secondary bac

203 Whether T cells are permissive to RSV infection is unknown.

204 wever, the role of mast cells in response to RSV infection is unknown.

205 BACKGROUND Respiratory syncytial virus (RSV) infection is a cause of substantial morbidity and m

206 Respiratory syncytial virus (RSV) infection is a leading cause of severe acute lower

207 Severe respiratory syncytial virus (RSV) infection is a major cause of morbidity and mortali

208 Respiratory syncytial virus (RSV) infection is a major cause of severe lower respirat

209 Respiratory syncytial virus (RSV) infection is an important cause of pneumonia mortal

210 Respiratory syncytial virus (RSV) infection is epidemiologically linked to asthma.

211 Respiratory syncytial virus (RSV) infection is the leading cause of hospitalization a

212 Respiratory syncytial virus (RSV) infection is the major cause of bronchiolitis in yo

213 Respiratory syncytial virus (RSV) infection is the number one cause of bronchiolitis

214 virin (RBV) for respiratory syncytial virus (RSV) infections is not well studied.

215 at produces intracellular H2S, we found that RSV infection led to a reduced ability to generate and m

216 Inhibition of either UA or IL-1beta during RSV infection led to chronic reductions in pulmonary imm

217 ice [SPC-Cre(+) Vcan(-/-)] demonstrated that RSV infection led to increased HA accumulation compared

218 Therefore, in this model of RSV infection, lung neutrophils do not offer obvious ben

219 RSV infection may result in greater morbidity and mortal

220 Previous RSV infection may, however, impact responses to an RSV v

221 After RSV infection, mice pre-exposed to Cd had elevated lung

222 ted with protection in a healthy human adult RSV infection model.

223 nge the current paradigm that acquisition of RSV infection occurs only after birth and shift attentio

224 key roles in regulating inflammation during RSV infection of adult mice, we studied the role of thes

225 RSV infection of BEC/HLF cocultures led to decreased hya

226 RSV infection of BECs from subjects with asthma, compare

227 Despite their abundance in the lungs during RSV infection of both mice and man, the role of neutroph

228 We aimed to determine whether ex vivo RSV infection of bronchial epithelial cells (BECs) from

229 RSV infection of human airway epithelial cell, human lun

230 opy and Western blotting results showed that RSV infection of human airway epithelial cells induced a

231 ation and the peak severity of disease after RSV infection of mice.

232 ur findings suggest that (antibody-enhanced) RSV infection of NK cells induces a proinflammatory rath

233 RSV infection of OVA-sensitized/challenged BALB/c mice r

234 Finally, RSV infection of Sirt1(f/f)-CD11c-Cre(+) mice resulted i

235 d Th17 differentiation, we hypothesized that RSV infection of STAT4-/- mice would result in enhanced

236 ast, type I IFNs were not detected following RSV infection of WD-PBECs.

237 culating CD4+ and CD8+ T cells during severe RSV infection of young children.

238 Respiratory syncytial virus (RSV) infection of children previously immunized with a n

239 Respiratory syncytial virus (RSV) infection of seronegative children previously immun

240 dren with acute respiratory syncytial virus (RSV) infection often develop sequelae of persistent airw

241 tudies was to explore the effect of previous RSV infection on murine antibody responses to RSV F and

242 there are scarce data on the full impact of RSV infection on outpatient children.

243 tion with post-F-containing VLPs or a second RSV infection only weakly stimulated NA, even though tot

244 At the time of a positive test for RSV infection or 5 days after inoculation, whichever occ

245 76 or placebo 12 hours after confirmation of RSV infection or 6 days after inoculation.

246 , from either 12 hours after confirmation of RSV infection or 6 days after virus inoculation.

247 previously infected with RSV, while a second RSV infection or a postfusion F-containing VLP cannot.

248 ide epidemiology and public health burden of RSV infection over time.

249 ccinees (26/244) showed evidence of a recent RSV infection (P = .04).

250 Clinical diagnoses given to children with RSV infection presenting to ED or hospitalized were iden

251 At least one third of children with RSV infection presenting to ED were diagnosed as other i

252 To test the hypothesis that RSV infection promotes inflammation via altered HA and v

253 host iron-binding protein transferrin during RSV infection promotes P. aeruginosa biofilm development

254 evaluated over 180 days; immunogenicity and RSV infection rates were evaluated over 112 days.

255 Infants at high risk for severe RSV infection receive monthly injections of a prophylact

256 ment with the KDM6 inhibitor, GSK J4, during RSV infection reduced inflammatory DC in the lungs along

257 Respiratory syncytial virus (RSV) infections remain a major cause of respiratory dise

258 health problem, respiratory syncytial virus (RSV) infections remain without specific therapy.

259 ors contribute to airway inflammation during RSV infection remains unknown.

260 ously healthy infants <10 months of age with RSV infections representing the spectrum of disease seve

261 N-lambda airway secretion; (b) subjects with RSV infection showed the highest IFN-lambda airway level

262 tential to serve as a robust animal model of RSV infection, since human RSV does not fully replicate

263 ulmonary inflammation following both IAV and RSV infections, suggesting that macrophage PPAR-gamma is

264 dren with acute respiratory syncytial virus (RSV) infection, symptomatic non-RSV respiratory virus in

265 ic site O are more efficacious at preventing RSV infection than antibodies specific for antigenic sit

266 ote an altered Th2 immune response following RSV infection that leads to more severe immunopathology.

267 developed a severity score for infants with RSV infection that should be useful as an end point for

268 piratory disease (ERD) subsequent to natural RSV infection that was observed in clinical trials of fo

269 e are known clinical risk factors for severe RSV infection, the majority of those hospitalized are pr

270 For children who are at risk for severe RSV infections, the American Academy of Pediatrics recom

271 ted with autophagy-mediated processes during RSV infection, thereby directing efficient antiviral imm

272 way inflammation and airway resistance after RSV infection through mediating MMP-12 production via PA

273 d individuals remain susceptible to repeated RSV infections throughout life.

274 bjective was to develop an in vitro model of RSV infection to evaluate interindividual variation in r

275 review the use of a neonatal mouse model of RSV infection to mimic severe infection in human infants

276 We sought to determine the capacity of RSV infection to stimulate group 2 innate lymphoid cells

277 delivery, further preventing progression of RSV infection to the lung.

278 bution of adult respiratory syncytial virus (RSV) infections to the use of advanced healthcare resour

279 iewed the records of 124 HCT recipients with RSV infections treated with oral or aerosolized RBV from

280 including ILC2s and ST2(+) myeloid cells, in RSV infection-triggered pathophysiology.

281 g, and/or central cyanosis]) were tested for RSV infections using real-time reverse transcriptase-pol

282 nifestations of respiratory syncytial virus (RSV) infection vary widely from mild, self-limiting illn

283 The effect of acetate on RSV infection was abolished in Gpr43(-)(/)(-) mice.

284 In adjusted analyses, RSV infection was associated with greater odds of length

285 Epithelial damage in response to RSV infection was associated with neutrophil activation

286 RSV infection was confirmed by RT-qPCR with any positive

287 n use by day 28 after the first diagnosis of RSV infection was lowest in patients presenting with URT

288 Using an Ifitm1(-/-) mouse, we show that RSV infection was more severe, thereby extending the ran

289 codes to capture deaths where a diagnosis of RSV infection was present.

290 RSV infection was promoted in ATG5- or ATG7-silenced pla

291 erimental human respiratory syncytial virus (RSV) infection, we investigate systemic and local virus-

292 hybrid model of respiratory syncytial virus (RSV) infection, we previously demonstrated that the CD8(

293 The potential roles of NbP3IP in RSV infection were examined.

294 f enrollment, from infants hospitalized with RSV infection were quantified.Measurements and Main Resu

295 history and records of laboratory-confirmed RSV infections were obtained by linking the mortality da

296 ompared to non-adjvuanted G vaccine and live RSV infection, which correlated strongly with both neutr

297 of innate immunity may affect recovery from RSV infection will help guide the development of safe an

298 stigated the mechanism of action of HMGB1 in RSV infection with the aim of identifying new inflammato

299 Eight of 9 patients who cleared the RSV infection within 2 weeks mounted a >/=4-fold NAb res

300 lower peak viral load, absence of concurrent RSV infections within the household, infection by RSV gr