ライフサイエンスコーパス: rotavirus infection

1 al of B lymphocytes in PBMC of patients with rotavirus infection.

2 r in intracellular calcium regulation during rotavirus infection.

3 ion of intestinal lymphoid hyperplasia after rotavirus infection.

4 the normal pathogenic sequence of homologous rotavirus infection.

5 ting non-human primates against experimental rotavirus infection.

6 ing intestinal epithelial gene expression in rotavirus infection.

7 L-12 in the induction of immune responses to rotavirus infection.

8 initiate intestinal B-cell activation during rotavirus infection.

9 significantly associated with G. lamblia and rotavirus infection.

10 ques (Macaca mulatta) was observed following rotavirus infection.

11 , immunology, and clinical manifestations of rotavirus infection.

12 rotavirus in vivo, we used a mouse model of rotavirus infection.

13 of the human intestinal cell line Caco-2 to rotavirus infection.

14 ldren were similar to those of children with rotavirus infection.

15 in intestinal epithelial cells and restricts rotavirus infection.

16 tralizing antibody responses upon subsequent rotavirus infection.

17 an active component of the host response to rotavirus infection.

18 rred only with cells that are permissive for rotavirus infection.

19 ells were completely unable to clear chronic rotavirus infection.

20 mples to determine the prevalence of group C rotavirus infection.

21 ion and modulation of the immune response to rotavirus infection.

22 hat lactadherin protects against symptoms of rotavirus infection.

23 ntranasal routes in the adult mouse model of rotavirus infection.

24 ve delayed but complete clearance of primary rotavirus infection.

25 induced following homologous or heterologous rotavirus infection.

26 a 1- to 4-day delay in clearance of primary rotavirus infection.

27 in western New York have experienced group C rotavirus infection.

28 T cells from perforin +/+ mice in clearing a rotavirus infection.

29 the mechanism used by CD8+ T cells to clear rotavirus infection.

30 ice participate in the resolution of primary rotavirus infection.

31 atment led to a dose-dependent resistance to rotavirus infection.

32 e associated with partial protection against rotavirus infection.

33 tosis is a mechanism of host defense against rotavirus infection.

34 for IgA ASC responses in the intestine after rotavirus infection.

35 er T1D risk exhibit reduced activity against rotavirus infection.

36 re hyper-susceptible to initiation of murine rotavirus infection.

37 wing the development of laboratory-confirmed rotavirus infection.

38 tively associated with a risk of symptomatic rotavirus infection.

39 laboratory testing, diagnostic imaging, and rotavirus infection.

40 nd duration of diarrhea in male infants with rotavirus infection.

41 d B cell activation after in vivo intestinal rotavirus infection.

42 re not absolutely required in the setting of rotavirus infection.

43 han 5 years due to diarrhoea attributable to rotavirus infection.

44 riglycerides were significantly increased by rotavirus infection.

45 downregulation of lipid synthesis induced by rotavirus infection.

46 ets for antiviral development is limited for rotavirus infection.

47 transcription and IFN-beta secretion during rotavirus infection.

48 ge, 75% of children experienced a documented rotavirus infection.

49 ea, 131 (34%) were estimated to be caused by rotavirus infection.

50 ency to protect against murine norovirus and rotavirus infections.

51 ith concomitant HIV infection resolved acute rotavirus infections.

52 ally milder (diarrhea, vomiting, fever) than rotavirus infections.

53 derstanding of the host range restriction of rotavirus infections.

54 s potential as a new approach for control of rotavirus infections.

55 venting primary and resolving chronic murine rotavirus infections.

56 heir winter peaks, which have been linked to rotavirus infections.

57 teritis symptoms compared to that of natural rotavirus infections.

58 otects breastfed infants against symptomatic rotavirus infections.

59 and vaccine-reassortant strains in pediatric rotavirus infections.

60 tors are responsible for recovery from acute rotavirus infection?

61 31 infants developed rotavirus infection; 15 were symptomatic and 16 had no s

62 o observed more commonly among patients with rotavirus infection (54% vs. 9%; P = .033 for both).

63 s crucial for the immune response to enteric rotavirus infection, a proposed etiological agent for T1

64 variables were significantly associated with rotavirus infection after adjusting for seasonality and

65 CD8+ cells were highly efficient at clearing rotavirus infection, alpha4beta7- memory cells were inef

66 the early stages of autophagy are initiated, rotavirus infection also blocks autophagy maturation.

67 ea-related deaths previously associated with rotavirus infection among children 4-23 months old.

68 consistent with the conclusion that natural rotavirus infection, an enteric pathogen, results in a s

69 irst examination was 3.0 mm in patients with rotavirus infection and 2.0 mm in control subjects (P =

70 The rapid declines in rotavirus infection and AGE in vaccinated and unvaccinat

71 ses were found to correlate with the risk of rotavirus infection and all P[8]/P[4] rotavirus infected

72 ation of a cause-effect relationship between rotavirus infection and biliary atresia in humans.

73 s, have also been shown to protect mice from rotavirus infection and clear chronic infection in SCID

74 Thirteen pairs of patients with rotavirus infection and control subjects were enrolled.

75 were evaluated in a gnotobiotic pig model of rotavirus infection and disease and were compared to pre

76 hese results suggest that protection against rotavirus infection and disease is primarily VP7/VP4 hom

77 Rotavirus infection and disease were common, but with si

78 months of age) without evidence of previous rotavirus infection and examined for rotavirus antigen.

79 Rotavirus infection and genotype were determined by anti

80 raintestinally in animals used as models for rotavirus infection and in children.

81 ound measurements, in infants with confirmed rotavirus infection and in healthy control subjects, of

82 lity of a causal association between natural rotavirus infection and intussusception.

83 n is required for viroplasm formation during rotavirus infection and is hyperphosphorylated into 32-

84 ssess STIM1 activation (puncta formation) by rotavirus infection and NSP4 expression.

85 s determined characteristics of asymptomatic rotavirus infection and potential risk factors for infec

86 antibody that is essential for clearance of rotavirus infection and protection from reinfection.

87 As with many other pathogens, rotavirus infection and replication leads to rearrangeme

88 Rotavirus infection and replication was assessed by enzy

89 he histological changes observed were due to rotavirus infection and replication.

90 a model that characterized susceptibility to rotavirus infection and RVGE among children, accounting

91 ified greater variation in susceptibility to rotavirus infection and RVGE in Vellore than in Mexico C

92 In both cohorts, susceptibility to rotavirus infection and RVGE were associated with male s

93 Mexico City belong to a high-risk group for rotavirus infection and RVGE, and demonstrate that unmea

94 timate naturally-acquired protection against rotavirus infection and RVGE, and to understand how diff

95 rstand naturally acquired protection against rotavirus infection and RVGE.

96 ich intestinal epithelial cells (IECs) sense rotavirus infection and signal IFN-beta production, and

97 mic IgA is not essential for protection from rotavirus infection and suggest that in the absence of I

98 Experience gained through studies of natural rotavirus infection and the clinical trials for the curr

99 to assess the disease burden associated with rotavirus infection and the distribution of rotavirus st

100 pathogens, we evaluated the OPN response to rotavirus infection and the extent of diarrhea manifeste

101 Our study supported the association between rotavirus infection and the host HBGA phenotypes, which

102 omposing the incidence rate into the rate of rotavirus infection and the risk of RVGE given infection

103 We used the neonatal mouse model of rotavirus infection and virus strains SA11-clone 4 (SA11

104 sized that the gut microbiota might modulate rotavirus infection and/or antibody response and thus po

105 There were 206 389 laboratory-confirmed rotavirus infections and 3 657 651 hospitalizations for

106 virus-unvaccinated children experienced 1418 rotavirus infections and 371 episodes of RVGE over 17,63

107 one rotavirus strain, 14 (30.4%) were mixed rotavirus infections and 4 (8.8%) was non-typeable.

108 erval [CI], .16-.32) in laboratory-confirmed rotavirus infections and a 26% decline (RR, 0.74; 95% CI

109 tained declines in both laboratory-confirmed rotavirus infections and AGE hospitalizations across all

110 ith large reductions in laboratory-confirmed rotavirus infections and hospitalizations due to acute g

111 estimated the impact on laboratory-confirmed rotavirus infections and hospitalizations for all-cause

112 ed to evaluate potential association between rotavirus infections and human HBGA phenotypes.

113 that antigenemia/viremia occurs routinely in rotavirus infections and imply that infectious rotavirus

114 iggering relationship between some wild-type rotavirus infections and T1D, but the potential effect o

115 ay have bearing on our full understanding of rotavirus infections and the effects of vaccination in d

116 ome activation upon mouse hepatitis virus or rotavirus infection, and in steady state stimulated by i

117 fferentially regulated >2-fold at 16 h after rotavirus infection, and only one gene was similarly reg

118 tric-scale organization of VPs formed during rotavirus infection, and quantitatively describe the str

119 emonstrated that viremia and extraintestinal rotavirus infection are common in acutely infected human

120 Correlates of protection from rotavirus infection are controversial.

121 Although rotavirus infections are generally considered to be conf

122 Human group C rotavirus infections are routinely diagnosed by electron

123 Globally, rotavirus infections are the most common cause of diarrh

124 ells were rarely detectable in children with rotavirus infection at both acute and convalescent stage

125 to limited diagnosis of acute human group C rotavirus infections because no routine test is availabl

126 3 serum samples from children with confirmed rotavirus infection but in none of 35 samples from contr

127 CD8 cells helped resolve rotavirus infection but were less important in protectio

128 pithelial cells are the principal targets of rotavirus infection, but the response of enterocytes to

129 immune response induced in the intestine by rotavirus infection, but vaccination with virus-like par

130 -1991) due to diarrhea and weekly reports of rotavirus infection by 74 laboratories were reviewed to

131 od of a 12-month increment, and detection of rotavirus infection by enzyme immunoassay in at least 10

132 lls lining the gastrointestinal tract combat rotavirus infection by two key antiviral compounds known

133 Annually in Kenya, rotavirus infection causes 19% of hospitalizations and 1

134 d a delay of 1 to 2 days in the clearance of rotavirus infection compared to the clearance time for u

135 anges suggest a plausible mechanism by which rotavirus infection could cause intussusception.

136 Rotavirus infection decreased TER before the appearance

137 more than half of all deaths attributable to rotavirus infection: Democratic Republic of the Congo, E

138 Microbiota ablation resulted in reduced rotavirus infection/diarrhea and a more durable rotaviru

139 Individuals with laboratory-confirmed rotavirus infections during 2000-2018 and all-cause hosp

140 have been observed for laboratory-confirmed rotavirus infections during the 2014-2015 season.

141 In a mouse model of rotavirus infection, effects of oral administration of C

142 IFNs could efficiently protect cells against rotavirus infection, endogenous type III IFNs were found

143 pe for preventing the severe consequences of rotavirus infection, especially in resource-limited sett

144 pitalizations, and 20 to 40 deaths caused by rotavirus infections every year in the United States.

145 ected neighboring cells and the clearance of rotavirus infection from the epithelium.

146 apable of unambiguously discriminating mixed rotavirus infections from nonspecific cross-reactivity;

147 hildren presenting with laboratory-confirmed rotavirus infection had higher proportions of effector a

148 result from altered intestinal motility, but rotavirus infection had no effect on gastrointestinal tr

149 T cell-mediated immune protection following rotavirus infection has been observed in animal models,

150 Furthermore, rotavirus infection has been shown to modify T1D risk in

151 Although rotavirus infection has generally been felt to be restri

152 ics and patterns of cytokine responses after rotavirus infection has important implications for induc

153 ntroduced, the number of laboratory-detected rotavirus infections has been consistently lower than du

154 s vaccine would prevent 70% of deaths due to rotavirus infection if administered without age restrict

155 Following primary rotavirus infection, IgA knockout mice cleared virus as

156 ly assess the role of IgA in protection from rotavirus infection, IgA knockout mice, which are devoid

157 man milk was associated with delayed time to rotavirus infection, implying protective properties of a

158 f Th1-associated protective immunity against rotavirus infection in adult mice.

159 Rotavirus infection in adults is poorly understood and f

160 findings highlight the significant burden of rotavirus infection in Africa, and underscore the need f

161 New knowledge on rotavirus infection in children and well established mou

162 day care was a risk factor for asymptomatic rotavirus infection in children under age 5 years; livin

163 Although the VLA-2 integrin promotes rotavirus infection in CHO cells, it is clear that the V

164 han IgG were responsible for protection from rotavirus infection in IgA knockout mice, mice were depl

165 The early response to a homologous rotavirus infection in mice includes a T-cell-independen

166 er's patch B cell activation associated with rotavirus infection in mice requires dendritic cells, we

167 Rotavirus infection in mice was used to define host or v

168 shown that CD8+ T cells mediate clearance of rotavirus infection in mice.

169 ed CD8+ T cells mediate clearance of primary rotavirus infection in mice: JHD knockout (JHD -/-) (B-c

170 ole in mitigating clinical disease following rotavirus infection in neonatal swine and that the prote

171 ns identified during nosocomial outbreaks of rotavirus infection in New Delhi and Bangalore, India, m

172 Rotavirus infection in rats was evaluated by (i) clinica

173 multicountry birth cohort study, we describe rotavirus infection in the first 2 years of life in site

174 explained 5.9% to 6.2% of the variability in rotavirus infection in the pooled data and their predict

175 lobule membrane glycoprotein, inhibits human rotavirus infection in vitro, whereas bovine lactadherin

176 Although rotavirus infections in adults are relatively uncommon,

177 Reductions of 69-83% in laboratory-confirmed rotavirus infections in all age groups and 77-88% in inf

178 ral agents and could be used to help control rotavirus infections in children.

179 Chronic rotavirus infections in immunocompromised children may r

180 UT2 secretor status and laboratory-confirmed rotavirus infections in US children.

181 Taken together, our findings show that rotavirus infection, in the context of a normal immune r

182 Histopathological changes due to rotavirus infection included acute inflammation of the p

183 that the proportion of hospitalizations for rotavirus infection increased with income.

184 omach, bone, or lung were all susceptible to rotavirus infection, indicating a wider host tissue rang

185 t molecular basis for understanding neonatal rotavirus infections, indicating that glycan modificatio

186 Finally, rotavirus infection induced the activation and expressio

187 levels in acute-phase PBMC, we conclude that rotavirus infection induces robust proinflammatory and a

188 Rotavirus infection induces the expression of a subset o

189 pecific CD8 T cells in multiple organs after rotavirus infection initiated via the intranasal, oral,

190 We previously demonstrated that rotavirus infection initiates cellular autophagy and tha

191 /41, astrovirus, nonpolio enteroviruses, and rotavirus) infections, interference among Sabin vaccine

192 Rotavirus infection is a leading cause of morbidity and

193 Rotavirus infection is a potential trigger for autoimmun

194 Acute gastroenteritis caused by rotavirus infection is an important cause of morbidity a

195 Rotavirus infection is inhibited by bacteria, and we det

196 nfection, but the response of enterocytes to rotavirus infection is largely unknown.

197 Recent studies have confirmed that rotavirus infection is not confined only to the gut but

198 Rotavirus infection is one of the most common causes of

199 and MDA-5 and that IFN-beta secretion during rotavirus infection is regulated by PKR.

200 Rotavirus infection is significantly enhanced in prefold

201 Rotavirus infection is systemic, with an acute active vi

202 ation of both the rabbit and mouse models of rotavirus infection is that human rotavirus (HRV) strain

203 Rotavirus infection is the foremost cause of severe gast

204 Rotavirus infection is the leading cause of severe diarr

205 The target cell of rotavirus infection is the mature enterocyte of the smal

206 Rotavirus infection is the most common cause of severe d

207 Rotavirus infection is the most common cause of severe d

208 Rotavirus infection is thought to be confined to the int

209 The results suggest that asymptomatic rotavirus infection is transmitted through the same rout

210 We extracted data on laboratory-confirmed rotavirus infections (July 2000 through June 2015) and a

211 In developing countries, rotavirus infections lead to more than 200,000 deaths in

212 inflammatory protein-1beta expression during rotavirus infection localized to the intestinal epitheli

213 revented injury of the duct epithelium after rotavirus infection, maintained continuity of duct lumen

214 host genetic susceptibility to norovirus and rotavirus infection may be strain specific.

215 As childhood nutrition improves worldwide, rotavirus infection may remain a public health challenge

216 ell culture), we hypothesized that such dual-rotavirus infections might play a role in the pathogenes

217 egression analysis showed that resistance to rotavirus infection most closely correlated with higher

218 s, G1P[8] strains constitute the majority of rotavirus infections most years, but occasionally other

219 We find that MDA5 activity limits rotavirus infection not only through the induction of an

220 The peak incidence of rotavirus infection occurred from January through May, a

221 Rotavirus infection of 5-day-old but not > or =21-day-ol

222 ses to specific rotavirus proteins following rotavirus infection of adult mice.

223 Rotavirus infection of HT-29 cells induced mRNA for seve

224 We determined that rotavirus infection of HT-29 intestinal epithelial cells

225 ecurrence of bile duct obstruction following rotavirus infection of IFN-gamma-deficient mice.

226 Rotavirus infection of intestinal epithelial cells and m

227 The outcome of rotavirus infection of intestinal epithelial cells is mo

228 In this study, we used an in vivo model of rotavirus infection of mouse gallbladder with UK x RRV r

229 We found that rotavirus infection of neonatal mice has a unique tropis

230 o better understand mechanisms of persistent rotavirus infections of cultured cells, we established i

231 re selected during maintenance of persistent rotavirus infections of MA104 cells and suggest that mut

232 viruses and cells coevolve during persistent rotavirus infections of MA104 cells.

233 avirus vaccine trial with protection against rotavirus infection or disease was investigated.

234 fected PKR(-/-) MEFs, indicating that during rotavirus infection, PKR functions at a stage between IF

235 Rotavirus infection produces a serious health burden in

236 rted by studies demonstrating that wild-type rotavirus infection protects against subsequent rotaviru

237 ses following either natural or experimental rotavirus infection provide protection against subsequen

238 Current in vitro models of rotavirus infection rely primarily on the use of animal

239 Worldwide in 2008, diarrhoea attributable to rotavirus infection resulted in 453,000 deaths (95% CI 4

240 Rotavirus infection results in overexpression of interfe

241 vere rotavirus gastroenteritis for the first rotavirus infection season after vaccination.

242 rstood, but in analogy to Gardia lamblia and rotavirus infections, secondary lactose maldigestion (LM

243 Together, these data suggest that rotavirus infection sensitized mice to the inflammatory

244 We show that rotavirus infection significantly enhanced serum tumor n

245 a suite of hydrometeorological variables and rotavirus infection status ascertained through community

246 For this analysis of multisite cohort data, rotavirus infection status was ascertained through commu

247 ession recapitulated this rare resistance to rotavirus infection, suggesting a previously unrecognize

248 ted 5-fold by VP8* and were not activated by rotavirus infection, suggesting the differential regulat

249 Antibodies that neutralize rotavirus infection target outer coat proteins VP4 and V

250 We found that boys had a greatest risk of rotavirus infection than girls.

251 he clinical presentation and pathogenesis of rotavirus infection, the associated global disease burde

252 For the past 2 decades, rotavirus infection, the most common cause of severe dia

253 osal pDCs critically influence the course of rotavirus infection through rotavirus recognition and su

254 We used the neonatal mouse model of rotavirus infection to study extraintestinal spread foll

255 o age-related, antibody-independent risk for rotavirus infections to cause RVGE.

256 In infants with only rotavirus infection, total cumulative stool output was 3

257 A was induced in balb/cAnNCrl mice by rhesus rotavirus infection; uninfected mice were used as contro

258 ccine with use of data on health outcomes of rotavirus infection, vaccine effectiveness, and immuniza

259 eptibility to SA-dependent or SA-independent rotavirus infection varied depending on the cell line te

260 une responses to homologous and heterologous rotavirus infection vary both quantitatively and qualita

261 The age-adjusted prevalence of asymptomatic rotavirus infection was 11%; prevalence was highest in c

262 The maximum lymph node size in patients with rotavirus infection was 11.6 mm at the first examination

263 s, the percentage reduction in deaths due to rotavirus infection was 53%, 66%, and 69%, respectively.

264 en immediately before an infant's episode of rotavirus infection was assayed for lactadherin, butyrop

265 Prior rotavirus infection was associated with a 50% lower haza

266 We studied whether rotavirus infection was associated with antigenemia duri

267 Rotavirus infection was associated with increased distal

268 The number of events attributable to rotavirus infection was estimated by multiplying age-str

269 he degree of protection conferred by natural rotavirus infection was estimated through analyses of da

270 Rotavirus infection was identified using reverse-transcr

271 y cultured intestinal epithelial cells after rotavirus infection was investigated.

272 The neonatal rat model of rotavirus infection was used to determine the kinetics o

273 To identify correlates of resistance to rotavirus infection, we analyzed levels of serum immunog

274 To understand the role of cytokines during rotavirus infection, we assessed the kinetics of tumor n

275 ular mechanisms involved in the events after rotavirus infection, we identified host cellular genes w

276 es of hospitalization specifically coded for rotavirus infection were 14, 4, and 6 cases per 10,000 p

277 Human in vitro and murine in vivo models of rotavirus infection were used to delineate the role of p

278 Rotavirus infections were initially identified as possib

279 infection provided complete protection from rotavirus infection when rabbits were challenged orally

280 e syncytia with cells that are permissive to rotavirus infection whereas nonpermissive cells are refr

281 e importance of type III IFNs in controlling rotavirus infection, which could be exploited as antivir

282 ving childhood vaccines for pneumococcal and rotavirus infections while greatly expanding coverage of

283 s in our understanding of the mouse model of rotavirus infection will enhance the understanding of hu

284 the biology, immunology, and pathogenesis of rotavirus infection will help to explain the strengths a

285 Viremia was detected following rotavirus infection with RRV and HAL1166.

286 -/-) mice and lpr (fas-deficient) mice clear rotavirus infection with the same kinetics as control mi

287 n anti-IFN-gamma monoclonal antibody cleared rotavirus infection with the same kinetics as those for

288 pare exposures reported by participants with rotavirus infection with those of participants who teste

289 Repeated associations of rotavirus infections with a wide range of nongastroenter

290 However, research into associations of rotavirus infections with T1D development in humans have

291 indicate a balanced Th1/Th2 response during rotavirus infection, with higher cytokine levels early a