ライフサイエンスコーパス: EBV infection

1 umors and select NHL subtypes are related to EBV infection.

2 for robust and long-lasting immunity against EBV infection.

3 factors for the development of a symptomatic EBV infection.

4 endogenous iNKT antigen is expressed during EBV infection.

5 and 5-y-old EBV-naive children for in vitro EBV infection.

6 reat disorders associated with or induced by EBV infection.

7 Kissing was a significant risk for primary EBV infection.

8 sion of cyclin D1 is closely associated with EBV infection.

9 cells were comparable before and after acute EBV infection.

10 teins and thus had an abortive lytic form of EBV infection.

11 omas (NPCs) are commonly present with latent EBV infection.

12 constitution after preemptive R treatment of EBV infection.

13 have been postulated to predispose cells to EBV infection.

14 ymphomas that are frequently associated with EBV infection.

15 to the pathogenesis of acute and persistent EBV infection.

16 -cell and epithelial cell fusions as well as EBV infection.

17 mediates the switch between latent and lytic EBV infection.

18 es sharply in the same individuals following EBV infection.

19 AP deficiency causes lymphocytosis following EBV infection.

20 is effective and approved for use in primary EBV infection.

21 w much there is still to learn about primary EBV infection.

22 agent-based model and computer simulation of EBV infection.

23 sed independently or in the context of lytic EBV infection.

24 developed into a diagnostic tool for primary EBV infection.

25 may alter disease phenotypes associated with EBV infection.

26 tiviral response, involving IFNs, to chronic EBV infection.

27 ric renal transplant recipients with primary EBV infection.

28 he rhesus lymphocryptovirus animal model for EBV infection.

29 gulated on B cells when activated and during EBV infection.

30 enomes to further understand the genetics of EBV infection.

31 letion did not further aggravate symptoms of EBV infection.

32 tested in the most accurate animal model for EBV infection.

33 ss II and CD74 in B cells is repressed after EBV infection.

34 opathological diseases could be generated by EBV infection.

35 (+) T cell expansion in response to an acute EBV infection.

36 by overexpression or EGF treatment enhances EBV infection.

37 us challenge in the rhesus macaque model for EBV infection.

38 reatment of EBV with soluble NRP1 suppresses EBV infection.

39 owever, NRP2, the homologue of NRP1, impairs EBV infection.

40 or tyrosine kinase (RTK) signalling promotes EBV infection.

41 ily environment contribute to acquisition of EBV infection.

42 The NKG2C(hi) NK subset was not expanded by EBV infection.

43 quisitely susceptible to Epstein-Barr virus (EBV) infection.

44 Mg(2+) homeostasis after Epstein-Barr virus (EBV) infection.

45 and were associated with Epstein-Barr virus (EBV) infection.

46 s mainly associated with Epstein-Barr virus (EBV) infection.

47 re highly susceptible to Epstein-Barr virus (EBV) infection.

48 closely associated with Epstein-Barr virus (EBV) infection.

49 y associated with latent Epstein-Barr virus (EBV) infection.

50 ere were a total of 46 patients with primary EBV infection: 11 developed PTLD, 12 had symptomatic inf

51 To identify epigenetic events following EBV infection, a transient infection model was establish

52 ble differences in the course of the primary EBV infections across treatment groups.

53 tained from individuals experiencing primary EBV infection (acute infectious mononucleosis [AIM]) and

54 ric renal transplant recipients with primary EBV infection, adolescents are at significantly higher r

55 Primary Epstein-Barr virus (EBV) infection affects the host differently according to

56 is an effective strategy to control CMV and EBV infection after HSCT, conferring protection in 70%-9

57 A role for primary EBV infection after transplantation is supported by the

58 effective treatment for controlling CMV and EBV infections after HSCT; however, new practical method

59 Seropositivity for CMV or EBV infection alters B cell repertoires, regardless of t

60 ) NK cells are CMV specific and suggest that EBV infection alters the repertoire of NK cells in the b

61 ical and virologic manifestations of primary EBV infection among infants born to HIV-infected women,

62 2 years), and there was a trend toward early EBV infections among the case subjects.

63 rast to reports in Hodgkin lymphoma in which EBV infection and A20 alteration are mutually exclusive,

64 NPC is characterized by clonal EBV infection and accounts for >78,000 annual cancer cas

65 ination approach against symptomatic primary EBV infection and against EBV-associated malignancies.

66 odies to EBV EAs are produced during primary EBV infection and are likely to be stimulated as a resul

67 d EBV-associated tumorigenesis, we monitored EBV infection and assessed tumor formation in humanized

68 The link between EBV infection and Burkitt lymphoma (BL) is strong, but t

69 PTLD is associated with EBV infection and can result in malignant B cell lymphom

70 oncentrations are also elevated during acute EBV infection and correlate with IL-18.

71 her had aplastic anemia in the course of his EBV infection and died from fulminant gram-positive bact

72 o contribution of the BHRF1 miRNA cluster to EBV infection and EBV-associated tumorigenesis, we monit

73 ns to facilitate the establishment of latent EBV infection and enhance viral replication.

74 suppressor, miR-34a, was strongly induced by EBV infection and expressed in many EBV and Kaposi's sar

75 model is a valid system for studying chronic EBV infection and for the preclinical development of the

76 ecapitulates features of symptomatic primary EBV infection and generates T cell-mediated immune contr

77 No association between EBV infection and HP infection or any clinicopathologica

78 egions of high malaria exposure have earlier EBV infection and increased EBV reactivation.

79 eversed transcriptional changes which follow EBV infection and it impaired the efficiency of EBV-indu

80 n p53 and LMP1 may play an important role in EBV infection and latency and its related cancers.IMPORT

81 ling the regulatory function of miR-BART6 in EBV infection and latency.

82 replication; however, parameters of chronic EBV infection and pathogenesis in the A-T population rem

83 The germinal-center (GC) model of EBV infection and persistence proposes that EBV gains ac

84 e EBV positive highlight the role of primary EBV infection and poor immune control of this virus.

85 Latent EBV infection and reactivation are associated with vario

86 The relationship between EBV infection and sensitivity to death receptor (DR)-ind

87 f SLE and suggest a mechanistic link between EBV infection and SLE.

88 transactivated upon IFN-alpha treatment and EBV infection and stimulates human Vbeta13+ T cells.

89 sion is repressed in GC cells independent of EBV infection and suggest that TET2 promotes type III EB

90 suggest that there is an association between EBV infection and the appearance of pathogenic Abs found

91 that drive cellular PARylation during latent EBV infection and the effects of PARylation on host gene

92 esponses can influence the nature of primary EBV infection and the level of viral persistence.

93 es fresh insight into the natural history of EBV infection and the pathogenesis of EBV-associated epi

94 9 years, we investigated the epidemiology of EBV infection and the relationship between EBV load, EBV

95 ogical functions of Necdin in the context of EBV infection and transformation.

96 dulate expression of COX-2 in the context of EBV infection and transformation.

97 that IL-18 is markedly elevated during acute EBV infections and EBV-associated diseases, while ferrit

98 (MSI), 73% of those with Epstein-Barr virus (EBV) infection and 11% of those that were not infected w

99 tive immune responses to Epstein-Barr virus (EBV) infection and are activated by human DCs to mount a

100 Latent Epstein-Barr virus (EBV) infection and cellular hypermethylation are hallmar

101 cancer characterized by Epstein-Barr virus (EBV) infection and dense lymphocyte infiltration.

102 Symptomatic primary Epstein-Barr virus (EBV) infection and elevated humoral immune responses to

103 s highly associated with Epstein-Barr virus (EBV) infection and exhibits remarkable ethnic and geogra

104 The combination of Epstein-Barr virus (EBV) infection and high malaria exposure are risk factor

105 Epstein-Barr virus (EBV) infection and lytic replication are known to induce

106 The current model of Epstein-Barr virus (EBV) infection and persistence in vivo proposes that EBV

107 We compared primary Epstein-Barr virus (EBV) infection and suppression between Kenyan human immu

108 r acquisition of primary Epstein-Barr virus (EBV) infection and the virologic and immune correlates o

109 ', characterized by CD4 lymphopenia, chronic EBV infection, and EBV-related lymphoproliferative disor

110 IRF-5 was induced following EBV infection, and IRF-5 was expressed in B-cell lines w

111 nked immunodeficiency with magnesium defect, EBV infection, and neoplasia" (XMEN) disease characteriz

112 the XMRV LTR, suggesting that inflammation, EBV infection, and other conditions leading to NF-kappaB

113 haryngeal carcinoma (NPC) is associated with EBV infection, and the EBV-encoded LMP1 is believed to b

114 (+) T cells expand dramatically during acute EBV infection, and their persistence is important for li

115 activatability of CD4(+) T cells in primary EBV infection, and their role in B-cell differentiation,

116 s were predominantly associated with CMV and EBV infections, and T-cell receptor gammadelta(+) T cell

117 y with magnesium defect, Epstein-Barr virus (EBV) infection, and neoplasia' (XMEN) disease and its cl

118 s 68 (MHV68), a model of Epstein-Barr virus (EBV) infection, and then after latency was established,

119 Although the early events of EBV infection are poorly understood, increasing knowledg

120 Malaria and Epstein-Barr virus (EBV) infection are cofactors in the pathogenesis of ende

121 e-specific prevalence of Epstein-Barr virus (EBV) infection are relevant for determining when to admi

122 ytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections are a significant cause of morbidity and

123 responses to human diseases, such as HIV and EBV infections, as well as to assay new vaccine strategi

124 However, events regulating EBV infection at early stages of the disease and the rol

125 y, was downregulated in primary B cells post-EBV infection at the transcriptional and translational l

126 During acute EBV infection, both preexisting CMV- and Flu-specific me

127 cant EBNA-1-specific CD8+ T-cell response to EBV infection, but the immune response to this tumor ant

128 The probability of EBV infection by 1 year of age was .78 (95% CI, .67-.88)

129 However, despite documentation of EBV infection by expression of EBNA2 and LMP1, B-CLL cel

130 tious mononucleosis (AIM) and chronic active EBV infection (CAEBV) that were also compared with a pub

131 light upon the potential mechanisms by which EBV infection can lead to cellular transformation.

132 However, EBV infection can result in various, and often fatal, cl

133 However, EBV infection caused a decrease in the absolute number o

134 Infrequently, EBV infection causes infectious mononucleosis (IM) or Bu

135 ons in some aging humans, but whether CMV or EBV infection contributes to alterations in the B cell r

136 rtoires, regardless of the individual's age: EBV infection correlates with the presence of persistent

137 oproliferative disease [PTLD] or symptomatic EBV infection, defined as flu-like symptoms or infectiou

138 Subclinical CMV infection and subclinical EBV infection each associated with approximately fourfol

139 ped primary asymptomatic Epstein-Barr virus (EBV) infection, followed by EBV+ B-cell lymphoma and hep

140 ytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections following allogeneic hematopoietic stem

141 EBV infection gives rise to B cell lines that readily pr

142 ontinuous antigen presence due to persistent EBV infection, half of the proliferating EBNA1-specific

143 BRLF1(R) gene products, but its role during EBV infection has not been well defined.

144 Epstein-Barr virus (EBV) infection has been linked to systemic lupus erythem

145 nical syndrome that can arise during primary EBV infection, has allowed the evolution of the response

146 carcinoma cells containing the lytic form of EBV infection have enhanced expression of a gene (DHRS9)

147 , X-linked lymphoproliferative disease; (ii) EBV infection in a range of new, genetically defined, pr

148 of information on prevalence and sequelae of EBV infection in adult renal transplantation beyond the

149 significantly younger age at time of primary EBV infection in children from Kisumu compared with chil

150 evaluated the prevalence of HP, HP CagA+ and EBV infection in gastric cancer (GC) samples from adults

151 e the lymphocytosis that occurs during acute EBV infection in humans, but it is unclear whether bysta

152 a longitudinal prospective study of primary EBV infection in humans.

153 pported by histologic evidence, suggest that EBV infection in IM tonsils involves extrafollicular B c

154 pe III) of viral latency; however, long-term EBV infection in immunocompetent hosts is limited to B c

155 higher rate of EBV expansion during primary EBV infection in infants and during subsequent episodes

156 RTK signalling, which subsequently promotes EBV infection in nasopharyngeal epithelial cells.

157 rguing against a defective control of latent EBV infection in RA.

158 results point to an important role for lytic EBV infection in the development of B cell lymphomas in

159 T-cell and natural killer cell responses to EBV infection in these patients.

160 -specific antibodies capable of neutralizing EBV infection in vitro The majority of gp350-directed va

161 that lead to switching from latent to lytic EBV infection in vivo are still elusive.

162 major clinically relevant features of human EBV infection in vivo, opening the way to new therapeuti

163 Epstein-Barr virus (EBV) infection in humans is a major trigger of malignant

164 Diseases resulting from Epstein-Barr virus (EBV) infection in humans range from the fairly benign di

165 cytomegalovirus (CMV) or Epstein-Barr virus (EBV) infection in immunocompromised patients can be trea

166 miology and morbidity of Epstein-Barr virus (EBV) infection in pediatric renal transplant recipients

167 que opportunity to track Epstein-Barr virus (EBV) infection in the context of the reconstituting B-ce

168 sing different stages of Epstein-Barr virus (EBV) infections in clinical serum samples.

169 EBV infection increased RPL4 expression and redistribute

170 ysis suggested that both subclinical CMV and EBV infection independently associate with significant d

171 improved NK cell-mediated immune control of EBV infection, indicating that mixed hematopoietic cell

172 unstable as carcinoma cells, indicating that EBV infection induced an epigenetic mutator phenotype.

173 EBV infection induced redistribution between B cell subs

174 To assess whether EBV infection is a characteristic feature of multiple sc

175 EBV infection is associated with development of the auto

176 d CD8(+) lymphocytosis associated with acute EBV infection is composed largely of EBV-specific T cell

177 EBV infection is controlled initially by the innate immu

178 EBV infection is linked to the development of approximat

179 The switch between latent and lytic EBV infection is mediated by the two viral immediate-ear

180 nctionality and phenotype are ablated, i.e., EBV infection is not consistent with GC function.

181 Our data show that the regulation of EBV infection is perturbed in RA and suggest that increa

182 EBV infection is rapidly followed by activation and incr

183 EBV infection is typically benign and is well controlled

184 falciparum exposure affects the dynamics of EBV infection is unclear.

185 e in multiple sclerosis brain indicates that EBV infection is unlikely to contribute directly to mult

186 Epstein-Barr virus (EBV) infection is associated with a broad spectrum of di

187 Epstein-Barr virus (EBV) infection is associated with B cell lymphomas in hu

188 Epstein-Barr virus (EBV) infection is associated with many human malignancie

189 Latent Epstein-Barr virus (EBV) infection is associated with several lymphoprolifer

190 Epstein-Barr virus (EBV) infection is associated with the development of man

191 Diagnosis of Epstein-Barr virus (EBV) infection is based on clinical symptoms and serolog

192 Latent Epstein-Barr virus (EBV) infection is causally linked to several human cance

193 Primary Epstein-Barr virus (EBV) infection is characterized by the presence of IgM a

194 Primary Epstein-Barr virus (EBV) infection is the most common cause of infectious mo

195 Primary Epstein-Barr virus (EBV) infection is the most important risk factor for dev

196 ss-associated DNA damage, which results from EBV infection, is detected by DDR.

197 nuation of DDR, discovered in the context of EBV infection, is of broad interest as the biology of ce

198 We have used a modeling approach to study EBV infection kinetics in a longitudinal cohort of child

199 circulating B cells in patients with primary EBV infection, leading us to investigate whether STAT3 c

200 Epstein-Barr virus (EBV) infection leads to lifelong viral persistence throu

201 Production of RA during the lytic form of EBV infection may enhance viral replication by promoting

202 nfectious mononucleosis occurs after primary EBV infection may include age, dose of virus received, a

203 e distinctive responses with the progress of EBV infection might facilitate the management of EBV-med

204 mphocryptovirus-infected rhesus macaques, an EBV infection model.

205 promoters triggering the prelatent phase of EBV infection, noncoding EBV-encoded RNA transcripts ind

206 Subclinical CMV and EBV infection occurred in 22 and 36%, respectively.

207 These findings imply that EBV infection occurring in mesenchymal, endothelial, and

208 ed PTLD is more frequently seen when primary EBV infection occurs after transplant, a common scenario

209 EBV infection occurs early in infants born to HIV-infect

210 e show that exosomes released during primary EBV infection of B cells harbored LMP1, and similar leve

211 EBV infection of B cells in vitro induces the release of

212 In this report, we show that EBV infection of B cells leads to the downregulation of

213 EBV infection of B cells triggers activation of several

214 that antibodies to gp350/220, which inhibit EBV infection of B cells, enhance infection of epithelia

215 ) envelope glycoprotein 350, 72A1, inhibited EBV infection of B lymphocytes in vitro.

216 tained at 6 months postdiagnosis neutralized EBV infection of cultured and primary target cells.

217 We show that EBV infection of GC B cells is followed by upregulation

218 hat genes differentially expressed following EBV infection of GC B cells were significantly enriched

219 the pattern of expression observed following EBV infection of GC B cells.

220 phosphatase receptor kappa (PTPRK), followed EBV infection of HL cells and was also more frequently o

221 aques accurately models acute and persistent EBV infection of humans.

222 Overall, these observations suggested that EBV infection of keratinocytes leaves a lasting epigenet

223 monocytes into the epithelium and inhibited EBV infection of keratinocytes.

224 Furthermore, EBV infection of lymphoma cells in HIV-positive individu

225 We have modeled acute EBV infection of naive and GC B cells in mice through ti

226 The mechanisms of cell-free EBV infection of nasopharyngeal epithelial cells remain

227 However, EBV infection of normal oral epithelial cells is confine

228 However, the mechanisms of EBV infection of oral epithelium are poorly understood.

229 Here, we show that EBV infection of oral keratinocytes led to CpG island hy

230 Although EBV infection of preneoplastic epithelial cells is not i

231 EBV infection of primary B lymphocytes resulted in globa

232 Furthermore, EBV infection of primary blood B cells led to downregula

233 IMP1alpha expression is down-regulated after EBV infection of primary germinal center B cells and tha

234 s detected in all three latencies and during EBV infection of primary human B cells.

235 We show here that EBV infection of primary human B lymphocytes leads to th

236 We investigated EBV infection of resting B lymphocytes, which leads to c

237 ranscriptional changes induced during latent EBV infection of these same cells, where the BARTs are e

238 Epstein-Barr virus (EBV) infection of B cells leads to the sequential activa

239 Epstein-Barr virus (EBV) infection of primary B cells causes B-cell activati

240 Epstein-Barr virus (EBV) infection of primary human B cells drives their ind

241 Epstein-Barr virus (EBV) infection of resting B lymphocytes results in their

242 ytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections of humans.

243 memory B cells but are highly susceptible to EBV infection, often developing fatal symptoms resemblin

244 d NKG2D, receptors implicated in controlling EBV infection, on memory CD8(+) T cells from CD70-defici

245 ange of cellular immune responses induced by EBV infection, on viral strategies to evade those respon

246 e considered in patients with severe primary EBV infection or EBV-associated cancer, especially in th

247 t been investigated in the context of either EBV infection or IRF7 responses.

248 bstantial, but vaccines that prevent primary EBV infections or treat EBV-associated diseases are not

249 EBV+ PTLD can arise after primary EBV infection, or because of reactivation of a prior inf

250 e its role in modulating immune responses to EBV infection, our results suggest that the dUTPase coul

251 maternal antibodies was a major predictor of EBV infection outcome, because decay predicted time to E

252 Type I EBV infection, particularly type I BL, stimulates strong

253 Our results indicate that EBV infection persists, with virus readily detectable in

254 munosuppressed transplant recipients, handle EBV infections poorly, and many are at increased risk of

255 gA antibodies in 15 individuals with primary EBV infection reacted with 15%-55.6% of HH514-16 Burkitt

256 ytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections remain a major cause of morbidity and mo

257 The effect of persistent EBV infection remained significant even after adjustment

258 ablishment of persistent Epstein-Barr virus (EBV) infection requires transition from a program of ful

259 Acute Epstein-Barr virus (EBV) infection results in an unusually robust CD8(+) T c

260 Moreover, ethnicity, tumor location and EBV infection status might be potential key factors infl

261 A (miRNA) 200 (miR200) family members on the EBV infection status of cells.

262 e patients to development of IM upon primary EBV infection, suggesting that genetic variation in T ce

263 In conclusion, EBV infection switches MOG processing in B cells from de

264 ermethylation as an epigenetic scar of prior EBV infection that was retained after loss of the virus.

265 the immune response to acute and persistent EBV infection, their role in immune control of EBV repli

266 facilitate the development of acute systemic EBV infection, they do not enhance the overall oncogenic

267 regulated and downregulated miRNAs following EBV infection This occurs together with changes at histo

268 y is characterized by high susceptibility to EBV infection, though the underlying pathological mechan

269 s, most immune-competent individuals control EBV infection throughout their lives.

270 and players involved in the contribution of EBV infection to the aggressiveness of NPC are discussed

271 Epstein-Barr virus (EBV) infection transforms B cells in vitro and is associ

272 EBV infection upregulated APC-related markers on B cells

273 nchymal B cell aggregates, were examined for EBV infection using multiple methodologies including in

274 e signal transduction pathways during latent EBV infection via its C-terminal activating region 1 (CT

275 At 2 years, probability of EBV infection was .96 (95% CI, .89-.99) in HIV-infected

276 rclonal comparisons showed that each form of EBV infection was associated with a specific degree of p

277 Primary EBV infection was associated with cough, fever, otitis m

278 ining of EBV(+) and EBV(-) DLBCL, suggesting EBV infection was associated with reduced EphA4 expressi

279 Primary EBV infection was categorized as PTLD, symptomatic infec

280 Time of EBV infection was determined by measuring antibody titer

281 Primary EBV infection was not associated with gastroschisis, but

282 Our finding that CNS EBV infection was rare in multiple sclerosis brain indic

283 Although the rate of EBV infection was similar between groups, infants receiv

284 vel splice variant, V12, that was induced by EBV infection, was constitutively nuclear, and acted as

285 As somatic reversion correlated with EBV infection, we propose that the virus exerts a select

286 residence in Kisumu and younger age at first EBV infection were significant predictors for having a h

287 Risk factors for type 1 EBV infection were similar to those for EBV overall.

288 CMV and EBV infections were associated with significant expansio

289 due in part to these cells dying from lytic EBV infection when they differentiate and express wild-t

290 cells displaying either classical latency I EBV infection (where EBNA1 is the only EBV antigen expre

291 e significant risk factors for a symptomatic EBV infection, whereas there is no close association bet

292 RNA downregulates the IL-1 receptor 1 during EBV infection, which consequently alters the responsiven

293 y relevant BHRF1-2 miRNA interactions during EBV infection, which is an important step in understandi

294 e an association between subclinical CMV and EBV infections, which occur despite standard antiviral p

295 may interact with latent Epstein-Barr virus (EBV) infection, which in turn may predispose to the deve

296 remarkably high level of persistently lytic EBV infection with HeLa cervical cells that permit only

297 influence of the host cell on the outcome of EBV infection with regard to genome expression, amplific

298 ve implications for the close association of EBV infection with undifferentiated NPC.

299 was insufficient to prevent chronic CMV and EBV infections with a possible contribution of impaired

300 evidence has associated Epstein-Barr virus (EBV) infection with disease development.