ライフサイエンスコーパス: RSV infection

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

2 f neutrophils to the immune response against RSV infection.

3 upregulated especially at the later stage of RSV infection.

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

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

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

7 ependent co-correlates of protection against RSV infection.

8 ance the adaptive immune response with later RSV infection.

9 governing the pathogenic recall responses to RSV infection.

10 emained fully pathogenic in a mouse model of RSV infection.

11 ndritic cells (pDCs), in the pathogenesis of RSV infection.

12 eased lung viral load and weight loss during RSV infection.

13 ed immune deficiency syndrome and persistent RSV infection.

14 izures and ataxia, have been associated with RSV infection.

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

16 class II and innate cytokine production upon RSV infection.

17 RSV, as has been shown in the mouse model of RSV infection.

18 ein-specific T cells and were protected from RSV infection.

19 possible involvement in SG activities during RSV infection.

20 mbda IFNs, especially IL-29, were induced by RSV infection.

21 regulatory T cells (Tregs) during A2-strain RSV infection.

22 or advanced glycation end products (RAGE) in RSV infection.

23 he role of TSLP signaling in the response to RSV infection.

24 and sRAGE in modulating the host response to RSV infection.

25 Treg cell phenotype and function to control RSV infection.

26 /-) mice were given doses of sRAGE following RSV infection.

27 omal lymphopoietin (TSLP) in the response to RSV infection.

28 products for the prevention and treatment of RSV infection.

29 lls was used to examine TSLP induction after RSV infection.

30 th atopic asthma than clinically significant RSV infection.

31 lowed a productive period on the dynamics of RSV infection.

32 us virus unless RAV is added during or after RSV infection.

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

34 s understood about their role in response to RSV infection.

35 atory genes by transcriptional elongation in RSV infection.

36 irate samples from severely ill infants with RSV infection.

37 ficant inhibition of mucus production during RSV infection.

38 differentiation, stability, and function in RSV infection.

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

40 rch tool for evaluating infants with primary RSV infection.

41 emental oxygen use among HCT recipients with RSV infection.

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

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

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

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

46 antibodies in serum from infants with acute RSV infection.

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

48 ponses comparable to those generated by live RSV infection.

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

50 group for severe pneumonia, independently of RSV infection.

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

52 efficacious vaccine or therapy available for RSV infection.

53 therapeutic targeting of TSLP during severe RSV infection.

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

55 effective treatment or vaccine available for RSV infection.

56 treatment with recombinant cytokines before RSV infection.

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

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

59 ure was reduction in hospitalizations due to RSV infections.

60 y of illness following primary and secondary RSV infections.

61 , and viral determinants for severe hMPV and RSV infections.

62 reased severity of infant rhinovirus but not RSV infections.

63 te that IL-17 plays a pathogenic role during RSV infections.

64 ldren annually require medical attention for RSV infections.

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

66 re disease from respiratory syncytial virus (RSV) infection.

67 sequent natural respiratory syncytial virus (RSV) infection.

68 xis in neonatal respiratory syncytial virus (RSV) infection.

69 nduced by acute respiratory syncytial virus (RSV) infection.

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

71 he treatment of 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 Respiratory syncytial virus (RSV) infection accounts for approximately 64 million cas

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 a were more likely to have rhinovirus versus RSV infection (adjusted odds ratio, 2.42; 95% CI, 1.19-4

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

78 Interestingly, IL-10R blockade during acute RSV infection altered CD4(+) T cell subset distribution,

79 ossible risk factors and severe outcomes for RSV infection among HIV-infected and uninfected children

80 limited data on respiratory syncytial virus (RSV) infection among children in settings with a high pr

81 Mice were protected against RSV infection and against RSV-induced airway mucin expre

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

83 of the ER stress response in the setting of RSV infection and identify the IRE1 stress pathway as a

84 ay was as sensitive as rtRT-PCR in detecting RSV infection and is a good adjunct assay for diagnostic

85 RSV infection and maturation of primary human DCs are re

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

87 ti-RSV CD8(+) T cells protected mice against RSV infection and pathogenesis, and waning protection co

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

89 not the only one, in which SH contributes to RSV infection and replication.

90 RSV infection and RSV hospitalization were positively as

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 ring from acute respiratory syncytial virus (RSV) infection and healthy infant controls.

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

97 (2) saturation [O(2) sat] </= 87%) and fatal RSV infection, and characterized risk factors for life-t

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

99 the C3aR fail to develop AHR following acute RSV infection, and production of Th17 cytokines was sign

100 portance of mucosal immune responses against RSV infection, and the development of novel mucosal vacc

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

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

103 1 released by airway epithelial cells due to RSV infection appears to function as a paracrine factor

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

105 Life-threatening and fatal RSV infections are a heavy burden on infants in the deve

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

107 Severe respiratory syncytial virus (RSV) infections are characterized by airway epithelial c

108 These findings implicate RSV infection as an important mechanism of recurrent whe

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

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

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

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

113 p, we developed an ex vivo/in vitro model of RSV infection based on well-differentiated primary pedia

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

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

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

117 Given intranasally before RSV infection, BPZE1 markedly attenuated RSV, preventing

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

119 Cells preinfected with RAV interfere with RSV infection, but RSV does not produce infectious virus

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

121 Prevention of RSV infection by BPZE1 seems in part to be caused by ind

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

123 Suppressing RSV infection by RSV immunoprophylaxis might increase th

124 n of CD4(+) and CD8(+) cells during neonatal RSV infection caused a striking increase in anti-RSV ant

125 In mice, acute RSV infection causes airway hyperresponsiveness (AHR), i

126 his study, we use an in vitro model of human RSV infection comprised of human peripheral blood mononu

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

128 Although cases of RSV infection could be detected throughout the year, the

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

130 ble of producing IFN-alpha prior to neonatal RSV infection decreased Th2-biased immunopathogenesis du

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

132 L-SIGN on primary human DCs did not inhibit RSV infection, demonstrating that interactions between R

133 omal cells may be a frequent target of human RSV infection, develop structural and functional changes

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

135 ls in Hong Kong with virologically confirmed RSV infection during 2009-2011 (N = 607).

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

137 We find that RSV infection enhances the activated fraction of cyclin-

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

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

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

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

142 In response to respiratory syncytial virus (RSV) infection, expression of LLT1 was upregulated in th

143 from rural Kenya were closely monitored for RSV infection from birth through 3 consecutive RSV epide

144 We used the proportion of RSV infections from population-based surveillance with d

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

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

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

148 Adults with RSV infection identified in both outpatient and inpatien

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

150 ge, are independently associated with severe RSV infection in adults.

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

152 the current standard of care for preventing RSV infection in at-risk neonates.

153 efficacy for reducing pulmonary inflammation RSV infection in BALB/c mice.

154 RSV infection in both cultures was restricted to apical

155 y mucin production are two manifestations of RSV infection in children.

156 We investigated RSV infection in Chilean adults with CAP using direct vi

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

158 umab has shown efficacy in preventing severe RSV infection in high-risk infants.

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

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

161 ated remarkable similarities to hallmarks of RSV infection in infant lungs.

162 known about the relative cytopathogenesis of RSV infection in infant URT and LRT.

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

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

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

168 RSV infection in neonates induced limited type I IFN and

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

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

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

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

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

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

175 Upon RSV infection in vivo, lungs of Beclin-1(+/-) mice showe

176 epithelial cells are the primary targets of RSV infection in vivo, so the generation and exploitatio

177 ial cells (WD-PBECs), the primary targets of RSV infection in vivo.

178 13 expression, cytokines not produced during RSV infection in wild-type mice.

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 ted with severe respiratory syncytial virus (RSV) infection in adults have not been performed.

182 epidemiology of respiratory syncytial virus (RSV) infection in Africa is limited for crowded urban ar

183 h influenza and respiratory syncytial virus (RSV) infection in children in low- and middle-income cou

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

185 he incidence of respiratory syncytial virus (RSV) infection in low- or middle-income countries are av

186 ior to neonatal respiratory syncytial virus (RSV) infection in mice.

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

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

189 RSV infection induced an RSV-specific human gamma interf

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

191 We found that RSV infection induces a non-canonical ER stress response

192 RSV infection induces ISG54, ISG56, and CIG5 gene expres

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

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

195 esigned to stratify allo-HCT recipients with RSV infection into groups according to their risk for pr

196 Therefore, we asked whether RSV infection involves DC-SIGN (CD209) or its isoform L-

197 ies have outlined that autophagy in DC after RSV infection is a crucial mechanism for driving innate

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

199 cted as neonates, TSLP expression induced by RSV infection is an important upstream event that contro

200 Vertical RSV infection is associated with dysregulation of crucia

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

202 RSV infection is frequent in Chilean adults with CAP.

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

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

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

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

207 servational studies cannot determine whether RSV infection is the cause of recurrent wheeze or the fi

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

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

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

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

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

213 Respiratory syncytial virus (RSV) infection is associated with serious lung disease i

214 Respiratory syncytial virus (RSV) infection is associated with subsequent recurrent w

215 spitalized with respiratory syncytial virus (RSV) infection is necessary.

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

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

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

219 RSV infection led to a significant reduction in TEER and

220 is clearly cytopathic, but other aspects of RSV infection may also contribute to cytopathology.

221 absence of epithelial immune mediators after RSV infection may contribute to explaining the inadequac

222 mation during a respiratory syncytial virus (RSV) infection, mice harboring significant autophagy def

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

224 vivo, so the generation and exploitation of RSV infection models based on morphologically and physio

225 nactivated RSV virus made disease, following RSV infection, more severe.

226 Despite the high morbidity rates of RSV infection, no highly effective treatment or vaccine

227 However, when coexpressed with NS2, as in RSV infection, NS1 could be detected in the mitochondria

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

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

230 EC model provides an authentic surrogate for RSV infection of airway epithelium in vivo.

231 RSV infection of BECs from subjects with asthma, compare

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

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

234 ticity of the RSV-WD-PAEC models relative to RSV infection of human airway epithelium in vivo, and fu

235 Furthermore, RSV infection of IL-10(-/-) mice resulted in more severe

236 RSV infection of IL-10-deficient mice resulted in more s

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

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

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

240 Together, these data indicate that RSV infection of the airway epithelium, via the action o

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

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

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

244 in response to respiratory syncytial virus (RSV) infection of dendritic cells (DC).

245 Respiratory syncytial virus (RSV) infection of most cultured cell lines causes cell-c

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

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

248 Here, we studied the effect of RSV infection on the airway epithelial barrier using mod

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

250 76 or placebo 12 hours after confirmation of RSV infection or 6 days after inoculation.

251 5 expression in nasal epithelia during acute RSV infection (OR, 3.8; 95% CI, 1.2-2.4; P < .001).

252 orders, corroborating the specific effect of RSV infection over the central nervous system.

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

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

255 Unlike A(RSV) infection, P(C+RSV) infection was found to be dynam

256 neonates with OX40L antibody during primary RSV infection prevented the subsequent enhancement of ai

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

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

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

260 Administration of anti-TSLP before neonatal RSV infection reduced the accumulation of lung DCs, decr

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

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

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

264 ent the exaggerated inflammatory response to RSV infection seen in children with bronchiolitis.

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

266 on for young infants and children at risk of RSV infection, since this population is naive to adenovi

267 ron (IFN-gamma) production by NK cells after RSV infection, suggesting that the protective effects ma

268 orm vital anti-inflammatory functions during RSV infection, suppressing pathogenic T cell responses a

269 vation-induced autophagy in combination with RSV infection synergistically enhanced DC cytokine expre

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

271 d significantly greater levels of TSLP after RSV infection than cells from healthy children.

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

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

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

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

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

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

278 In a mouse model of RSV infection, time-dependent increases in pulmonary IL-

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

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

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

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

283 tigate the role of the ER stress response in RSV infection using an in vitro A549 cell culture model.

284 27 signaling in respiratory syncytial virus (RSV) infection using IL-27Ralpha-deficient mice (IL-27rK

285 Compared to CD8(+) T cells responding to RSV infection, vaccine-elicited anti-RSV CD8(+) T cells

286 After RSV infections, viral levels were not significantly incr

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

288 Unlike A(RSV) infection, P(C+RSV) infection was found to be dynamin dependent and to

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

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

291 -10-producing cells in the lung during acute RSV infection were CD4(+) T cells.

292 RSV infections were identified by immunofluorescence tes

293 ta reveal a crucial sequence following acute RSV infection where initial C3a production causes tachyk

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

295 , and B cell memory, in striking contrast to RSV infection, which did not.

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

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

298 s in the lung were increased following acute RSV infection, with maximum production corresponding to

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