ライフサイエンスコーパス: EBV infection

1 enomes to further understand the genetics of EBV infection.

2 letion did not further aggravate symptoms of EBV infection.

3 rm of non-Hodgkin's lymphoma associated with EBV infection.

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

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

6 opathological diseases could be generated by EBV infection.

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

8 by overexpression or EGF treatment enhances EBV infection.

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

10 reatment of EBV with soluble NRP1 suppresses EBV infection.

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

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

13 ily environment contribute to acquisition of EBV infection.

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

15 ell line confirmed that CD21 is required for EBV infection.

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

17 factors for the development of a symptomatic EBV infection.

18 endogenous iNKT antigen is expressed during EBV infection.

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

20 Kissing was a significant risk for primary EBV infection.

21 by EBNA-antisense transcription during lytic EBV infection.

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

23 cells were comparable before and after acute EBV infection.

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

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

26 constitution after preemptive R treatment of EBV infection.

27 have been postulated to predispose cells to EBV infection.

28 ymphomas that are frequently associated with EBV infection.

29 to the pathogenesis of acute and persistent EBV infection.

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

31 mediates the switch between latent and lytic EBV infection.

32 es sharply in the same individuals following EBV infection.

33 AP deficiency causes lymphocytosis following EBV infection.

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

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

36 ormal EBV life cycle reminiscent of a latent EBV infection.

37 As (lncRNAs) differentially expressed during EBV infection.

38 m latency to the lytic replication stages of EBV infection.

39 4-1BB costimulation in host immunity against EBV infection.

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

41 reat disorders associated with or induced by EBV infection.

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

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

44 undant requirements for host defense against EBV infection.

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

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

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

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

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

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

51 NPC), a cancer caused by Epstein-Barr virus (EBV) infection.

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

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

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

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

56 EBV infection activates multiple cell signaling pathways

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

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

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

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

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

62 hose who acquire primary Epstein-Barr virus (EBV) infection after solid organ transplantation.

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

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

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

66 2 years), and there was a trend toward early EBV infections among the case subjects.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 y of an EBV-specific vaccine or treat severe EBV infection and pathological consequences in immunodef

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

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

89 Latent EBV infection and reactivation are associated with vario

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

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

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

93 9 years, we investigated the epidemiology of EBV infection and the relationship between EBV load, EBV

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

95 the production of type I IFN which inhibits EBV infection and virus-induced B-cell transformation.

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

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

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

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

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

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

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

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

104 agnesium deficiency with Epstein-Barr virus (EBV) infection and neoplasia (XMEN), a disease that has

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

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

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

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

109 osis, a symptomatic manifestation of primary EBV infection, and in long-term healthy carriers of EBV.

110 to infectious mononucleosis, chronic active EBV infection, and lymphoid and epithelial cancers.

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

112 nked immunodeficiency with magnesium defect, EBV infection, and neoplasia) is a complex primary immun

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

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 s has been hindered by latency-a hallmark of EBV infection-and atomic structures are thus available o

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

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

122 at more than 11,000 genes are regulated upon EBV infection as naive B cells exit quiescence to enter

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

124 d explain why their children acquire primary EBV infection at an earlier age than white children.

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

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

127 y immunodeficiency, characterized by chronic EBV infections attributed to a Mg(2+) homeostasis defect

128 PAL1), EBV cell entry (ITGB6), modulation of EBV infection (BCL2L12, NEDD4L), telomere biology (CLPTM

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

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

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

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

133 stein-Barr virus (EBV) causes chronic active EBV infection (CAEBV) characterized by T cell lymphoprol

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

135 In addition, we found that EBV infection can down-regulate MAOA expression in both

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

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

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

139 EBV-associated cancers harbor a latent EBV infection characterized by a lack of viral replicati

140 cell transcriptional changes in response to EBV infection classified tumors into two molecular subty

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

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

143 No vaccine against EBV infection currently exists, but such vaccines are in

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

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

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

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

148 ential source of primary Epstein-Barr virus (EBV) infection for young children is parental oral secre

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

150 whether HPV-positive cells support a latent EBV infection has not been demonstrated.

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

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

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

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

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

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

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

158 Using a model examining the establishment of EBV infection in HPV-immortalized tissues, we showed an

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

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

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

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

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

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

165 hanisms, effects that might be attributed to EBV infection in NPE cells.

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

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

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

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

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

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

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

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

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

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

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

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

178 The pathogenesis of Epstein-Barr virus (EBV) infection, including development of lymphomas and c

179 EBV infection increased RPL4 expression and redistribute

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

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

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

183 EBV infection induced redistribution between B cell subs

184 Using a model of direct EBV infection into HPV16-immortalized tonsillar cells gr

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

186 EBV infection is associated with development of the auto

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

188 EBV infection is linked to the development of approximat

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

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

191 EBV infection is rapidly followed by activation and incr

192 EBV infection is typically benign and is well controlled

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

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

195 isk factors, among which Epstein-Barr virus (EBV) infection is a strong suspect.

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

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

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

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

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

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

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

203 Epstein-Barr virus (EBV) infection is ubiquitous worldwide and is associated

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

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

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

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

208 The mechanisms by which chronic EBV infection leads to subsequent disease remain incompl

209 Epstein-Barr virus (EBV) infection leads to cancers with an epithelial origi

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

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

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

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

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

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

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

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

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

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

220 EBV infection of B cells triggers activation of several

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

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

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

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

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

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

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

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

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

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

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

232 Although EBV infection of preneoplastic epithelial cells is not i

233 EBV infection of primary B lymphocytes resulted in globa

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

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

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

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

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

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

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

241 Epstein-Barr virus (EBV) infection of human primary resting B lymphocytes (R

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 butes new insights into the understanding of EBV infection-related carcinogenesis.

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

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

259 n memory B cells, the reservoir for lifelong EBV infection, remains incompletely understood.

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

261 EBV infection resulted into a pronounced immunologic ske

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

263 malignancies as well as symptomatic primary EBV infection should be further explored for clinical de

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

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

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

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

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

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

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

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

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

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

274 During EBV infection, type III EBV latency genes were expressed

275 EBV infection upregulated APC-related markers on B cells

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

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

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

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

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

281 Time of EBV infection was determined by measuring antibody titer

282 Primary EBV infection was not associated with gastroschisis, but

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

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

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

286 To further understand the role of BGLF2 in EBV infection, we used mass spectrometry to identify cel

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

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 ry that is manipulated by LMP1 during latent EBV infections, which can affect oncogenesis.

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

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

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.