ライフサイエンスコーパス: CMV infection

1 l some of the direct and indirect effects of CMV infection.

2 ction, and during a persistent/latent murine CMV infection.

3 elta2(neg) gammadelta T cells in controlling CMV infection.

4 ated in relation to treatment outcome during CMV infection.

5 Of 101,111 infants, 328 (0.3%) had postnatal CMV infection.

6 te-onset sequelae in asymptomatic congenital CMV infection.

7 n response to both transfected DNA and mouse CMV infection.

8 ine IL-10 was defined during extended murine CMV infection.

9 east milk is the primary source of postnatal CMV infection.

10 associated with increased odds of congenital CMV infection.

11 y regulator of ISG expression during primary CMV infection.

12 recisely, being ultimately at lower risk for CMV infection.

13 es should allow efficient protection against CMV infection.

14 in patients with asymptomatic or symptomatic CMV infection.

15 h significantly increased odds of congenital CMV infection.

16 pM92 and pUL92 share a conserved function in CMV infection.

17 dding in vivo in the rhesus macaque model of CMV infection.

18 Patients underwent weekly surveillance for CMV infection.

19 d in a cohort of pregnant women with primary CMV infection.

20 e response of B lymphocytes to primary human CMV infection.

21 l-time PCR assay for diagnosis of congenital CMV infection.

22 developing symptomatic disease after primary CMV infection.

23 cells treated with gB-GNP gain resistance to CMV infection.

24 n of anti-CMV immunity or increased risk for CMV infection.

25 ctivating and inhibitory KIRs in immunity to CMV infection.

26 ess responses that are capable of inhibiting CMV infection.

27 of the plant, while not having any effect on CMV infection.

28 l infection or disease subsequent to primary CMV infection.

29 ug and received preemptive treatment against CMV infection.

30 C1C1(+) iDCs was maintained independently of CMV infection.

31 ated with premature rupture of membranes and CMV infection.

32 s the only small animal model for congenital CMV infection.

33 oint of this nested study was time to infant CMV infection.

34 e during immune maturation following primary CMV infection.

35 toxin as an effective compound that inhibits CMV infection.

36 of this immunoglobuline preparation against CMV infection.

37 ies using the guinea pig model of congenital CMV infection.

38 fe and promising approach against congenital CMV infection.

39 ment for ganciclovir-resistant or refractory CMV infection.

40 tem and may have a direct relevance to human CMV infection.

41 otential to suppress the indirect effects of CMV infection.

42 ation is at a particularly increased risk of CMV infection.

43 e critical during the early viremic phase of CMV infection.

44 AS-STING pathway in the initial detection of CMV infection.

45 women including 57 primary and 23 nonprimary CMV infections.

46 jority of birth defects caused by congenital CMV infections.

47 tive subjects developed asymptomatic primary CMV infections.

48 erapy in transplant patients with refractory CMV infections.

49 who receive prophylaxis for cytomegalovirus (CMV) infection.

50 the diagnosis of congenital cytomegalovirus (CMV) infection.

51 ) is associated with latent cytomegalovirus (CMV) infection.

52 .001) and had a higher 1-year probability of CMV infection (0.89 vs 0.69; P < .001).

53 We matched infants with postnatal CMV infection 1:1 to comparison infants using propensity

54 Postnatal CMV infection acquired by exposure to raw maternal milk

55 In preterm infants cytomegalovirus (CMV) infection acquired through maternal milk has been r

56 ciated with CMV infection occurred in 4, and CMV infection adversely affected patient survival (P = 0

57 e also demonstrate that long-term control of CMV infection after HSCT is primarily mediated through t

58 Limited clinical data exist regarding CMV infection after IIT/MVT.

59 In conclusion, CMV infection after LTx, rather than persistence of allo

60 lls was observed in patients who experienced CMV infection after LTx.

61 had a significantly lower incidence of late CMV infection after prophylactic therapy.

62 ategies are used to prevent cytomegalovirus (CMV) infections after solid organ transplant.

63 strategies can be adopted to treat resistant CMV infections, albeit no randomized clinical trials exi

64 However, whether CMV infection also affects memory T cell responses to in

65 CMV infection also was associated with reduced CD8(+) T

66 ntly the only tool for assessing the risk of CMV infection, although cellular immune responses driven

67 Of the 592 women with early primary CMV infection, amniocentesis for CMV DNA detection was p

68 m was to investigate the association between CMV infection and disease and severe HCV recurrence (com

69 Investigation of prevention of CMV infection and disease as a strategy to mitigate recu

70 outcomes in clinical trials, definitions of CMV infection and disease were developed and most recent

71 ive graft may offer an advantage in terms of CMV infection and disease.

72 To determine the contribution of pp65 to CMV infection and immunity, we generated a rhesus CMV la

73 of CMV; however, direct association between CMV infection and incidence of glioma is lacking.

74 ecipient-; D+R-) are at high-risk for active CMV infection and increased mortality, however the immun

75 nt(-); D(+)R(-)) are at high risk for active CMV infection and increased mortality; however, the immu

76 These findings suggest a link between CMV infection and inflammation that also may influence t

77 ng mRNA translation has a dramatic impact on CMV infection and proliferation.

78 s the only small animal model for congenital CMV infection and recapitulates disease symptoms (e.g.,

79 r saliva specimens for diagnosing congenital CMV infection and saliva specimens are easier to collect

80 lated to a functional contribution of KIR in CMV infection and should be investigated in hematopoieti

81 escribed the relationship between congenital CMV infection and SNHL in children.

82 At present, a vaccine is not available for CMV infection and the available antiviral drugs suffer f

83 CD8(+) T cell repertoires following neonatal CMV infection and thus have important implications for t

84 s to analyze risk factors for posttransplant CMV infection and to assess the efficacy and validity of

85 sults suggest new approaches both to curtail CMV infection and to purge the virus from organ transpla

86 l models of viral dynamics upon initial oral CMV infection and validated them using clinical shedding

87 t viremia, but significantly more late-onset CMV infections and side effects (leukopenia and neutrope

88 Unlike cytomegalovirus (CMV) infection and aging, human immunodeficiency virus (

89 ed for associations between cytomegalovirus (CMV) infection and clinical and pathological markers of

90 ell repertoire during human cytomegalovirus (CMV) infection and demonstrate that primary co-infection

91 Cytomegalovirus (CMV) infection and disease are important causes of morbi

92 in patients with concurrent cytomegalovirus (CMV) infection and inflammatory bowel disease (IBD).

93 The relationship between cytomegalovirus (CMV) infection and mortality among immunocompetent indiv

94 ociation between congenital cytomegalovirus (CMV) infection and sensorineural hearing loss (SNHL) was

95 ve hearing losses occur following congenital CMV infection, and CMV-infected infants should be evalua

96 T-cell immunity is critical for control of CMV infection, and correction of the immune deficiency i

97 ipient origin, can protect against recurrent CMV infections, and significantly influence the chimeris

98 The symptomatic manifestations of CMV infection are compounded by adverse indirect effects

99 n older humans and both aging and persistent CMV infection are independent factors in this process.

100 The current FDA-approved treatments for CMV infection are intended to be virus specific, yet the

101 f adverse outcome in asymptomatic congenital CMV infection are not known, and it is important that fu

102 As more CMV infections are identified, it is important to recogn

103 entified patients who were protected against CMV infection as long as they had no graft-versus-host d

104 However, CMV infection associated significantly with CVEs only in

105 Overall, CMV infection (asymptomatic CMV viral load >/= 400 CMV D

106 fants, the cumulative incidence of postnatal CMV infection at 12 weeks was 6.9% (95% CI, 4.2%-9.2%);

107 A total of 124 pregnant women with primary CMV infection at 5 to 26 weeks of gestation were randoml

108 The mAbs inhibit CMV infection at a post-attachment step by interacting w

109 Infants with symptomatic congenital CMV infection at birth are at significantly increased ri

110 antiviral strategy that specifically blocks CMV infection at multiple stages of virus life cycle, bu

111 n group) revealed prevalent cytomegalovirus (CMV) infection at diagnosis in childhood ALL, demonstrat

112 studies of such a vaccine against congenital CMV infection based on a virus with a targeted deletion

113 in the present study no difference in murine CMV infection between Ncr1(gfp/pfp) and wild-type (WT) m

114 We correlated CMV infection, biopsy-proven graft rejection, and graft

115 -three newborns with congenital asymptomatic CMV infection born to women with primary CMV infection d

116 novel cell-targeting antiviral that inhibits CMV infection by decreasing the synthesis of viral prote

117 ich are important for effectively inhibiting CMV infection by targeting the expression of immediate-e

118 e estimated the likelihood of transient oral CMV infections by comparing their observed frequency to

119 how adaptive NK cells arising in response to CMV infection can escape MDSC-mediated suppression, and

120 on of ganR- and ganciclovir-sensitive (ganS) CMV infection can risk factors and outcomes attributable

121 Postnatal cytomegalovirus (CMV) infection can cause serious morbidity and mortality

122 Congenital CMV infection (cCMV) is the most common congenital infec

123 er it poses an increased risk for congenital CMV infection (cCMV).

124 vertant T cells in the context of persistent CMV infection, combined with lack of regulatory T cells,

125 CMV infection conferred a vulnerability of C2C2(+) iDCs

126 persistent clonal B cell expansions, whereas CMV infection correlates with the proportion of highly m

127 an IgG-seropositive allograft do not develop CMV infection despite not receiving prophylaxis.

128 Cumulative incidence of postnatal CMV infection, detected by serum or urine NAT.

129 .2%); 5 of 29 infants (17.2%) with postnatal CMV infection developed symptomatic disease or died.

130 Cytomegalovirus (CMV) infection directly targets vascular endothelium and

131 ere independently associated with late-onset CMV infection/disease (hazard ratio, 4.04 [95% confidenc

132 irus (CMV) infection/disease (i.e., incident CMV infection/disease after cessation of prophylactic an

133 Cumulative incidence estimates for CMV infection/disease after prophylaxis cessation in D+/

134 on may be at an increased risk of late-onset CMV infection/disease and should be considered for more

135 other potential risk factors for late-onset CMV infection/disease in kidney transplant recipients.

136 The cumulative incidence of late-onset CMV infection/disease was assessed using the Kaplan-Meie

137 Potential risk factors for late-onset CMV infection/disease were examined using Cox proportion

138 ts who completed treatment for an episode of CMV infection/disease were included.

139 risk factor for late-onset cytomegalovirus (CMV) infection/disease (i.e., incident CMV infection/dis

140 tic CMV infection born to women with primary CMV infection during pregnancy were enrolled.

141 ay be available to prevent or treat maternal CMV infection during pregnancy, especially for women wit

142 t significantly modify the course of primary CMV infection during pregnancy.

143 o pregnant women who have acquired a primary CMV infection during pregnancy.

144 Cytomegalovirus (CMV) infection during fetal life causes severe symptoms

145 l-to-fetal rates of primary cytomegalovirus (CMV) infection during pregnancy have been between 30% an

146 Primary cytomegalovirus (CMV) infection during pregnancy is the leading infectiou

147 Primary cytomegalovirus (CMV) infection during the first half of pregnancy is res

148 revention, diagnosis and treatment of active CMV infection enhance transplant outcomes, and are the f

149 duced-intensity HSCT and collated details on CMV infection episodes and T-cell chimerism.

150 Cytomegalovirus (CMV) infection following allogeneic bone marrow transpla

151 me-linked immunospot (ELISPOT) assay and for CMV infection from the period before transplantation to

152 SOT) recipients who control cytomegalovirus (CMV) infection from those who progress to CMV-disease (C

153 lantation, in which the beneficial impact of CMV infection has been reported on the graft-versus-leuk

154 Chronic cytomegalovirus (CMV) infection has been associated with immunosenescence

155 The vast majority of infants with congenital CMV infection have no clinical findings at birth (asympt

156 Cytomegalovirus(CMV) infections have a significant effect on morbidity a

157 We show that both aging and CMV infection impact independently on the gammadelta T c

158 of CMV disease and treatment outcomes during CMV infection in 291 solid organ transplant recipients r

159 r increased attention to screening of active CMV infection in advanced HIV patients in developing cou

160 significantly higher prevalence of in utero CMV infection in ALL cases (n = 268) than healthy contro

161 dies reported low CD4(+) T-cell responses to CMV infection in early life, contrasting with large resp

162 hymocyte globulin may be important to reduce CMV infection in high-risk serostatus group (D+/R-).

163 The efficiency of primary CMV infection in humans following oral exposure, however

164 gs that recapitulate key features of primary CMV infection in humans.

165 These observations indicate that oral CMV infection in infants typically begins with a single

166 CMV infection in kidney transplant recipients (KTRs) has

167 sible impact of viremia and risk factors for CMV infection in pediatric LT recipients managed with ga

168 , was effective in reducing the incidence of CMV infection in recipients of allogeneic hematopoietic-

169 Postnatal acquisition of primary CMV infection in rhesus macaques results in prolonged vi

170 logic features of naturally acquired primary CMV infection in rhesus macaques.

171 who had suffered posttransplant symptomatic CMV infection in the cross-sectional study.

172 omatic or asymptomatic disease after primary CMV infection in the immunocompetent host.

173 These findings suggest that active CMV infection in the setting of treated HIV may represen

174 The primary sources of postnatal CMV infection in this population are breast milk and blo

175 the potential clinical impact of congenital CMV infections in high-seroprevalence settings.

176 s (CMV) load is central to the management of CMV infections in immunocompromised patients, but quanti

177 We explored the role of cytomegalovirus (CMV) infection in CD8 lymphocytosis and inflammation in

178 erge rapidly during primary cytomegalovirus (CMV) infection in humans, they exhibit a state of prolon

179 rphisms on the incidence of cytomegalovirus (CMV) infection in solid-organ transplant recipients.

180 Cytomegalovirus (CMV) infection in solid-organ transplantation is associa

181 al (Staphylococcus aureus) and viral (murine CMV) infection in vivo.

182 aid to clinical features of cytomegalovirus (CMV) infections in individuals without human immunodefic

183 V shedding events, which we termed transient CMV infections, in a prospective birth cohort of 30 high

184 ns was linked to transfusion, resulting in a CMV infection incidence of 0.0% (95% CI, 0.0%-0.3%) per

185 respiratory status associated with postnatal CMV infection included a new requirement for vasopressor

186 Cytomegalovirus (CMV) infection increases the risk of complications after

187 cell functions in vivo, in a system of mouse CMV infection, indicated that licensing did not play a m

188 In utero CMV infection induced oligoclonal expansions of fetal CD

189 Cytomegalovirus (CMV) infection involves interaction between endothelial

190 Congenital CMV infection is a leading cause of mental retardation a

191 s the first study to suggest that congenital CMV infection is a risk factor for childhood ALL and is

192 CMV infection is a significant cause of morbidity and mo

193 a better understanding of how natural human CMV infection is acquired.

194 Primary CMV infection is associated with a high maternal-to-chil

195 These results suggest that CMV infection is associated with an increased risk of AD

196 We conclude that CMV infection is associated with asthma and may contribu

197 CMV infection is associated with higher CD8 T-cell count

198 The latent phase of CMV infection is characterized by intermittent episodes

199 Thus, although the incidence of CMV infection is high during infancy, our data provide a

200 Sustained control of CMV infection is largely accounted for by cellular immun

201 its multiple immunoregulatory effects during CMV infection is not clear.

202 These data imply that CMV infection is not directly responsible for the declin

203 cell hyporesponsive phenotype during murine CMV infection is tissue specific and not cell intrinsic.

204 The immunology of human CMV infections is reflected in the murine CMV (MCMV) mod

205 Congenital cytomegalovirus (CMV) infection is a leading cause of hearing loss and ne

206 Cytomegalovirus (CMV) infection is a leading cause of illness and death i

207 Congenital cytomegalovirus (CMV) infection is a leading cause of mental retardation

208 Cytomegalovirus (CMV) infection is a significant complication in hematopo

209 Cytomegalovirus (CMV) infection is an ongoing clinical problem in solid-o

210 Cytomegalovirus (CMV) infection is associated with adverse outcomes in hu

211 Human cytomegalovirus (CMV) infection is associated with inferior survival in r

212 ral-resistant or refractory cytomegalovirus (CMV) infection is challenging, and salvage therapies, fo

213 The immune response to cytomegalovirus (CMV) infection is highly complex, including humoral, cel

214 Cytomegalovirus (CMV) infection is one of the most common persistent vira

215 Cytomegalovirus (CMV) infection is responsible for substantial morbidity

216 Congenital cytomegalovirus (CMV) infection is the major infectious cause of birth de

217 Cytomegalovirus (CMV) infection is the most prevalent infectious complica

218 memory inflation, as seen for example after CMV infection, is the maintenance of expanded, functiona

219 hus, although most people eventually acquire CMV infection, it usually requires numerous exposures.

220 ute to the control of early cytomegalovirus (CMV) infection, leading to a multiphasic type I interfer

221 Cytomegalovirus (CMV) infection leads to the development of adaptive and

222 This prompted us to investigate whether CMV infection limits immunologic space at sites where im

223 CMV infection may contribute to risk for morbid outcomes

224 n immunocompromised individuals, and chronic CMV infection may exacerbate a myriad of inflammatory co

225 ls in solid organ transplant recipients with CMV infection may reflect vascular inflammation and is a

226 Congenital and early infant CMV infections may have important consequences for child

227 svirus infections including cytomegalovirus (CMV) infection may be particularly important for telomer

228 Primary CMV infection mobilizes a large pool of memory B cells t

229 pically confirmed ganR-CMV (n = 37) and ganS-CMV infection (n = 109), matched by donor/recipient CMV

230 Cytomegalovirus (CMV) infection negatively influences both short- and lon

231 espite the defect in maturation, upon murine CMV infection, NK cells from NKp46-Cre-Gata3(fl/fl) mice

232 Mortality associated with CMV infection occurred in 4, and CMV infection adversely

233 Approximately one third of CMV infections occurred during the peripartum period, wi

234 Cytomegalovirus (CMV) infection occurs frequently in young children, who,

235 ium was optimized to improve its utility for CMV infection of maize.

236 altered neurodevelopment that follows murine CMV infection of the developing brain and that a subset

237 of neural progenitor cells or in vivo murine CMV infection of the mouse brain.

238 The impact of CMV infection on survival and cancer incidence was asses

239 g evidence of the effect of cytomegalovirus (CMV) infection on survival and the risk of cancer after

240 IE1 is expressed earlier than IE2 after CMV infection or MIE gene transfection.

241 ite antiviral treatment; (iv) CMV disease or CMV infection or risk factors, such as CMV-IgG-negative

242 ase, and patients with ganciclovir-resistant CMV infection or who are intolerant to antiviral therapy

243 e mainstay of treatment for cytomegalovirus (CMV) infection or CMV disease.

244 nting, renal dysfunction, diabetes mellitus, CMV infection, or malignancy was detected.

245 Rejection was significantly associated with CMV infection (P = 0.01, odds ratio = 2.61).

246 te rejection (P = 0.02) and cytomegalovirus (CMV) infection (P = 0.03) than controls.

247 cell subsets in response to cytomegalovirus (CMV) infection, paralleling antigen-specific T cell diff

248 sent pretransplant in patients who developed CMV infection posttransplant.

249 opositive SOT patients at risk of developing CMV infection posttransplant.

250 lin (>10 mg/kg) were associated with a lower CMV infection rate on univariate analysis.

251 However, congenital CMV infection remains a leading cause of SNHL in childre

252 Cytomegalovirus (CMV) infection remains a major complication after kidney

253 CMV infection represents a major complication in hematop

254 recipients of kidney transplants may predict CMV infection resolution and antiviral drug resistance.

255 T cell kinetics in peripheral blood predict CMV infection resolution and emergence of a mutant strai

256 These results suggest that CMV infection restrains CD8(+) T cell alloresponses afte

257 or treatment of mice with poly(I:C) or mouse CMV infection resulted in increased Ly49A expression and

258 Whether postnatal CMV infection results in long-term pulmonary sequelae in

259 mune globulin to pregnant women with primary CMV infection significantly reduced the rate of intraute

260 Cytomegalovirus (CMV) infection sometimes causes large expansions of CMV-

261 ide a major defense against cytomegalovirus (CMV) infection through the interaction of their surface

262 These findings thus associate CMV infection to a STAT3-dependent modulatory role in gl

263 vely studied 27 D(+)R(-) LTRs during primary CMV infection to determine whether acute CD4(+) T cell p

264 ectively studied 23 D+R- LTRs during primary CMV infection to determine whether acute CD8(+) T cell p

265 , we used the rhesus macaque animal model of CMV infection to investigate the in vivo function of the

266 ) pretransplant predicted the development of CMV infection under the immunosuppressive regime after t

267 Risk factors for CMV infection using multivariable analysis were D+R- ser

268 Greater knowledge of why CMV infection usually fails may provide insight into how

269 Time to the incidence of CMV infection (viremia and/or tissue invasive disease) a

270 CMV infection was assessed in 138 breastfed and 134 form

271 Primary CMV infection was associated with a sustained expansion

272 Postnatal CMV infection was associated with an increased risk for

273 In VLBW infants, postnatal CMV infection was associated with increased risk for BPD

274 Postnatal CMV infection was defined as a diagnosis of CMV or detec

275 The CMV infection was detected in 48 patients (49%) in the f

276 Congenital CMV infection was detected in 9 of 79 (11.4%; 95% confid

277 CMV infection was detected in juvenile and adult monkeys

278 CMV infection was monitored by polymerase chain reaction

279 CMV infection was observed in 34 of 210 (16%) with a med

280 both symptomatic and asymptomatic congenital CMV infection was performed.

281 Although CMV infection was self-limiting after syngeneic BMT, in

282 The CMV infection was significantly more frequent among adul

283 The only identified risk factor for CMV infection was the donor/recipient serostatus (odds r

284 57.5% (n = 310) of the infants; none of the CMV infections was linked to transfusion, resulting in a

285 rhesus macaques as a model of primary human CMV infection, we examined the virologic and immunologic

286 To describe features of postnatal CMV infection, we extracted clinical and laboratory data

287 fetal CD8(+) and CD4(+) T-cell responses to CMV infection were compared to those of adults with prim

288 ocompetent patients with primary symptomatic CMV infection were genotyped for KIR and their HLA ligan

289 olid-organ transplant recipients at risk for CMV infection were included, among whom 373 (44%) receiv

290 eropositive patients at intermediate risk of CMV infection were investigated, according to current al

291 issue invasive disease) and risk factors for CMV infection were investigated.

292 can American race, acute graft rejection and CMV infection were significantly associated with the dev

293 The odds of developing late-onset CMV infections were higher for the prophylactic compared

294 e T-cell counts, known to be associated with CMV infection, were measured before transplantation and

295 Of note, CMV infection, which is directly associated with the act

296 mmature LC (iLC) are remarkably resistant to CMV infection, while mature LC (mLC) are more permissive

297 in predicting which children with congenital CMV infection will develop hearing loss and, among those

298 An effective vaccine against human CMV infection will need to target genes that are essenti

299 RTANCE Nucleolar biology is important during CMV infection with the nucleolar protein, with nucleolin

300 Developing a vaccine to prevent CMV infection would be extremely valuable but would be f