ライフサイエンスコーパス: rotavirus infection

1 in intestinal epithelial cells and restricts rotavirus infection.

2 the normal pathogenic sequence of homologous rotavirus infection.

3 ting non-human primates against experimental rotavirus infection.

4 ing intestinal epithelial gene expression in rotavirus infection.

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

6 initiate intestinal B-cell activation during rotavirus infection.

7 significantly associated with G. lamblia and rotavirus infection.

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

9 , immunology, and clinical manifestations of rotavirus infection.

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

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

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

13 tralizing antibody responses upon subsequent rotavirus infection.

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

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

16 ells were completely unable to clear chronic rotavirus infection.

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

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

19 hat lactadherin protects against symptoms of rotavirus infection.

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

21 ve delayed but complete clearance of primary rotavirus infection.

22 induced following homologous or heterologous rotavirus infection.

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

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

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

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

27 ice participate in the resolution of primary rotavirus infection.

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

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

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

31 tively associated with a risk of symptomatic rotavirus infection.

32 laboratory testing, diagnostic imaging, and rotavirus infection.

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

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

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

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

37 riglycerides were significantly increased by rotavirus infection.

38 downregulation of lipid synthesis induced by rotavirus infection.

39 ets for antiviral development is limited for rotavirus infection.

40 transcription and IFN-beta secretion during rotavirus infection.

41 e associated with partial protection against rotavirus infection.

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

43 er T1D risk exhibit reduced activity against rotavirus infection.

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

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

46 r in intracellular calcium regulation during rotavirus infection.

47 ion of intestinal lymphoid hyperplasia after rotavirus infection.

48 ith concomitant HIV infection resolved acute rotavirus infections.

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

50 derstanding of the host range restriction of rotavirus infections.

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

52 venting primary and resolving chronic murine rotavirus infections.

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

54 otects breastfed infants against symptomatic rotavirus infections.

55 and vaccine-reassortant strains in pediatric rotavirus infections.

56 tors are responsible for recovery from acute rotavirus infection?

57 31 infants developed rotavirus infection; 15 were symptomatic and 16 had no s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Rotavirus infection and disease were common, but with si

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

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

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

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

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

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

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

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

81 Rotavirus infection and replication was assessed by enzy

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

83 rstand naturally acquired protection against rotavirus infection and RVGE.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Correlates of protection from rotavirus infection are controversial.

101 Although rotavirus infections are generally considered to be conf

102 Human group C rotavirus infections are routinely diagnosed by electron

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

104 3 serum samples from children with confirmed rotavirus infection but in none of 35 samples from contr

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

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

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

108 -1991) due to diarrhea and weekly reports of rotavirus infection by 74 laboratories were reviewed to

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

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

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

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

113 Rotavirus infection decreased TER before the appearance

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

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

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

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

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

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

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

121 Although rotavirus infection has generally been felt to be restri

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

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

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

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

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

127 Rotavirus infection in adults is poorly understood and f

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

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

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

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

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

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

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

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

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

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

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

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

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

141 Although rotavirus infections in adults are relatively uncommon,

142 Chronic rotavirus infections in immunocompromised children may r

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

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

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

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

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

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

149 Finally, rotavirus infection induced the activation and expressio

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

151 Rotavirus infection induces the expression of a subset o

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

153 /41, astrovirus, nonpolio enteroviruses, and rotavirus) infections, interference among Sabin vaccine

154 Rotavirus infection is a leading cause of morbidity and

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

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

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

158 Rotavirus infection is one of the most common causes of

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

160 Rotavirus infection is systemic, with an acute active vi

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

162 Rotavirus infection is the foremost cause of severe gast

163 Rotavirus infection is the leading cause of severe diarr

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

165 Rotavirus infection is the most common cause of severe d

166 Rotavirus infection is the most common cause of severe d

167 Rotavirus infection is thought to be confined to the int

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 Rotavirus infection of intestinal epithelial cells and m

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

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

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

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

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

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

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

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

193 Rotavirus infection produces a serious health burden in

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

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

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

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

198 Rotavirus infection results in overexpression of interfe

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

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

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

202 We show that rotavirus infection significantly enhanced serum tumor n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

220 We studied whether rotavirus infection was associated with antigenemia duri

221 Rotavirus infection was associated with increased distal

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

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

224 Rotavirus infection was identified using reverse-transcr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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