ライフサイエンスコーパス: EBV

1 EBV contacts show nearly 2-fold enrichment in host regio

2 EBV encodes 44 mature micro (mi)RNAs, mostly exhibiting

3 EBV establishes latent infection in B cells, which is th

4 EBV genomes are maintained by EBNA1, which tethers EBV e

5 EBV infection activates multiple cell signaling pathways

6 EBV infects more than 90% of the human population worldw

7 EBV is one of the most common viruses found in humans an

8 EBV nuclear antigens also repress CDKN2A to suppress sen

9 EBV nuclear proteins usurp normal transcriptional progra

10 EBV reactivation was associated with longer ICU stay (12

11 EBV's BZLF1 gene product, Zta, usually controls this rea

12 EBV-encoded proteins, along with noncoding RNAs and micr

13 EBV-negative Burkitt lymphoma cell lines infected with e

14 EBV/KSHV co-infection (OR = 5.71(1.58-7.12)), HIV positi

15 nic electron microscopy images of just 2,048 EBV virions obtained by chemical induction.

16 We have recently shown that the EBV type 2 (EBV-2) strain has the unique ability to infect mature T

17 ytic lymphohistiocytosis, and chronic active EBV disease.

18 -MHC-tetramer binding and reactivity against EBV-LMP2-expressing cell-lines.

19 re observed for nasopharyngeal carcinoma, an EBV-associated cancer, and CLL/SLL forms of non-Hodgkin

20 ld be targeted to enhance the efficacy of an EBV-specific vaccine or treat severe EBV infection and p

21 between groups following stimulation with an EBV-infected cell lysate.

22 oncogenic viruses such as SV40, JCV, BKV and EBV in patient-derived colorectal carcinoma (CRC) cells

23 s support the theory that persistent CMV and EBV shedding could contribute to the dynamics of the HIV

24 Subclinical CMV and EBV shedding could contribute to the dynamics of the HIV

25 er time were analyzed in relation to CMV and EBV shedding status.

26 Cytomegalovirus and EBV mismatch were avoided in 90% (9/10) and 100% (5/5) o

27 the required binding sites within EphA2 and EBV gH/gL that mediate the interaction of these two prot

28 synthetic peptides presenting the HCMV- and EBV-specific NEC hook sequences, we characterized the un

29 d to ubiquitination in both EBV-infected and EBV-negative cells.

30 lights complex interactions between KSHV and EBV, in addition to distinct genetic architectures resul

31 (EphA2) is a cellular receptor for KSHV and EBV.

32 n important entry receptor for both KSHV and EBV.

33 ocorticoid-induced TNF-receptor-related) and EBV-induced-3 (EBI3, an IL-35 subunit) in patients' Treg

34 as 'cargoes', and should inform future anti-EBV strategies.

35 In the absence of anti-EBV agents, however, therapeutic options for EBV-related

36 nhibitors that may be pursued for their anti-EBV and possibly even antiherpesviral potential, as this

37 ly only express the less immunogenic antigen EBV nuclear antigen-1 (EBNA-1), rendering them sensitive

38 h products, since no T cells recognizing any EBV-derived peptide in this common HLA allele have been

39 er prevalence of periodontal viruses such as EBV and CMV in CAD patients with periodontitis suggestin

40 Periodontal viruses such as EBV and CMV were significantly higher (62.5% and 75% res

41 ors or mediators in lymphoblasts may benefit EBV gene expression, suggesting a novel mechanism of tra

42 A significant association between EBV and CAL was revealed by multiple logistic regression

43 to identify genome-wide associations between EBV episomes and host chromosomes.

44 ntified 15,000 reproducible contacts between EBV episome(s) and the human genome.

45 , our analysis supports interactions between EBV episome(s) and active regions of the human genome in

46 tential interventional strategies that block EBV and KSHV infection of target epithelial cells.

47 of EBV-infected cells correlated with blood EBV loads.

48 Both EBV and malaria should, therefore, be considered as pote

49 t Zta is subjected to ubiquitination in both EBV-infected and EBV-negative cells.

50 y 2-fold enrichment in host regions bound by EBV nuclear antigen 2 (EBNA2) and EBNA3 transcription fa

51 ency I BL xenografts, decitabine followed by EBV-CTLs results in T-cell homing to tumors and inhibiti

52 t lymphoma (BL) sensitized cells to lysis by EBV-specific cytotoxic T cells (EBV-CTLs).

53 s was found to be the inhibition of TPPP1 by EBV-miRNA-BART12, which, in turn, inhibits the acetylati

54 to lysis by EBV-specific cytotoxic T cells (EBV-CTLs).

55 In interphase cells, EBV promoters drive the expression of latency genes, whi

56 patients had increased numbers of NK cells, EBV predominantly in NK cells, and immature NK cells in

57 imiting EBV DNAemia (SLD; n = 11) or chronic EBV DNAemia (CD; n = 19) at enrollment and 4-8 weeks lat

58 ng TCR clones to common viral epitopes (CMV, EBV, and influenza A) demonstrated that Ag specificity i

59 Whether persistent CMV/EBV replication could be targeted as a strategy to reduc

60 f the CD8(+) T cell response toward a common EBV determinant in HLA-B*07:02(+) individuals.

61 Comparing EBV types, viral genes displayed differential variation

62 uld enable monitoring of globally consistent EBVs at regional scales, by flexibly integrating differe

63 enrichment methods conclusively demonstrate EBV type 1 to be more prevalent in eBL patients than in

64 To evade immune detection, EBV switches between latent and lytic programs.

65 Eight patients developed EBV reactivation at a median of 96 days with no incidenc

66 nce-specific DNA-binding protein can disrupt EBV latency by driving the transcription of target genes

67 etylase (HDAC) inhibitor vorinostat disrupts EBV/HHV-8 latency, enhances chemotherapy-induced cell de

68 ires the concerted actions of nearly a dozen EBV proteins and numerous small non-protein-coding RNAs.

69 ce protein (EMP), namely LANA (KSHV), EBNA1 (EBV), and E2 (HPV).

70 ected B cells and is important for efficient EBV-induced transformation of B cells in vitro In this s

71 suggest that EBNA3A contributes to efficient EBV-induced lymphomagenesis in CBH mice.IMPORTANCE The E

72 ent protein BGLF2 activates p38 and enhances EBV reactivation.

73 CT (n = 33) or SOT (n = 13) with established EBV-PTLD, who had failed rituximab therapy, with third-p

74 Exploring EBV-mediated transcription regulatory networks is critic

75 CD8pos/DeltaTCR T cells modified to express EBV-LMP2-specific TCRs showed IFNgamma secretion and cyt

76 s available only for recombinantly expressed EBV proteins.

77 ytometry assay that detects cells expressing EBV-encoded small RNAs (EBERs), allowing rapid identific

78 we provide evidence that SM also facilitates EBV gene transcription.

79 gnificant increase in chronic GVHD following EBV reactivation (62.5% versus 8%; P = 0.01).

80 reased substantially and persisted following EBV reactivation and chronic GVHD, with a reciprocal dec

81 For EBV, associations are identified for VCA (rs71542439, p

82 Controlling for EBV type, we also performed a genome-wide association st

83 This lytic phase is also essential for EBV to cause infectious mononucleosis and cancers, inclu

84 , we demonstrated that CD21 is necessary for EBV entry into the Jurkat T-cell line.

85 EBV agents, however, therapeutic options for EBV-related diseases are limited.

86 k viral DNA concentrations, particularly for EBV and VZV.

87 coprotein and cellular receptor required for EBV-2 infection of T cells.

88 gether, our data point to a central role for EBV in mediating the tumour suppressive effects of MAOA

89 Multiplexed seroprofiles for EBV, malaria, and KSHV were generated for 266 eBL patien

90 use of antivirals as suppressive therapy for EBV lytic reactivation may aid efforts aimed at disease

91 provide evidence that peptides derived from EBV latent cycle proteins can impair the recognition of

92 On the other hand, EBV represents the first identified oncogenic virus, cap

93 Moreover, using HCMV::EBV hook domain swap constructs, computational predictio

94 Historically, EBV genes that contribute to virus replication have been

95 However, EBV reactivation was associated with a sustained alterat

96 However, EBV-specific antiviral agents are not yet available.

97 cell epitopes and peptides eluted from human EBV-transformed B cells.

98 ted invariant chain peptides (CLIP) in human EBV-positive and not EBV-negative B cell lines.

99 Decitabine treatment of latency I EBV+ Burkitt lymphoma (BL) sensitized cells to lysis by

100 programme, consisting of highly immunogenic EBV nuclear antigen (EBNA) and latent membrane proteins

101 ecitabine as a potent inducer of immunogenic EBV antigens, including LMP1, EBNA2, and EBNA3C.

102 an genome in lymphoblastoid cells.IMPORTANCE EBV is associated with ~200,000 cancers each year.

103 d that this can occur in EBV-negative and in EBV-infected cells.

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

105 Stable knockdown of CLEC16A in EBV-positive Raji B cells resulted in an upregulation of

106 izing this multisubunit repressor complex in EBV-positive cells.

107 Similar TCRs were identified in EBV(RPP)-specific CD8(+) T cell repertoires across multi

108 itin modification and that this can occur in EBV-negative and in EBV-infected cells.

109 ut rather rewires intracellular signaling in EBV-infected B cells that optimizes cell survival and pr

110 and HIF-1alpha-stabilizing drugs can induce EBV reactivation.

111 Unexpectedly, DFO failed to induce EBV reactivation in cell lines that express mutant or no

112 synergized with DFO and MLN-4924 in inducing EBV reactivation.

113 used clinically for HIV prevention, inhibit EBV lytic DNA replication, with respective IC(50) values

114 ycle-associated proteins, which then inhibit EBV-associated tumor cell proliferation.

115 lead compounds or may be modified to inhibit EBV and potentially other herpesviruses, and (ii) be dev

116 ng latency for 24 h with TAF still inhibited EBV lytic DNA replication at 72 h after drug was removed

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

118 erapy) can also induce remissions if initial EBV-CTLs are ineffective.

119 Interestingly, EBV is also the first virus found to carry genes encodin

120 thus providing significant new insight into EBV biology and oncogenic potential.

121 Although KSHV-EBV dual infection does not increase eBL risk, EBV appea

122 ticipants with detectable CMV and high-level EBV DNA, while it significantly declined among participa

123 30 transplant recipients with self-limiting EBV DNAemia (SLD; n = 11) or chronic EBV DNAemia (CD; n

124 Lytic EBV transcription differs from cellular transcription in

125 FG-4592, induced accumulation of both lytic EBV proteins and phosphorylated p53 in cell lines that c

126 We adapted a 13-marker EBV antigen signature for NPC risk identified by proteom

127 [10/54]), Epstein-Barr virus (EBV) mismatch (EBV) (9.3% [5/54]), age/size mismatch (51.9% [28/54]), o

128 Most EBV-encoded miRNAs were found to be involved in the occu

129 e compare the phenotypes of an EBNA3A mutant EBV (Delta3A) and wild-type (WT) EBV in a cord blood-hum

130 ther wild-type or two different BHLF1 mutant EBVs were initially indistinguishable in supporting late

131 sly found that one EBV-encoded miRNA, namely EBV-miR-BART6-3p, acts as a tumor suppressor by inhibiti

132 ment methods and generated a total of 98 new EBV genomes from both eBL cases (n = 58) and healthy con

133 eptides (CLIP) in human EBV-positive and not EBV-negative B cell lines.

134 2, we compared the EphA2 binding activity of EBV gH/gL and the EBV gH/gL-N(69)L/S(71)V mutant.

135 BHLF1, indeed contributes to key aspects of EBV latency, including its ability to promote the contin

136 tive disorder; however, immune correlates of EBV DNAemia in the transplant setting are limited.

137 erize innate and T-cell immune correlates of EBV DNAemia.

138 to determine the incidence and correlates of EBV-positivity in a large sepsis cohort.

139 While the lytic cycle of EBV can be triggered by chemicals and immunologic ligand

140 n plays a central role in the development of EBV-driven cancers and may contribute to other EBV-assoc

141 le of EBV-miRNA-BART12 in the development of EBV-related tumors as well as the mechanism underlying t

142 nvolved in the occurrence and development of EBV-related tumors.

143 etely unilateral MFC following an episode of EBV positive mononucleosis that showed a dramatic respon

144 atency III critical for the establishment of EBV latency and lifelong persistence within its host, wh

145 ost defense that tip the balance in favor of EBV can have catastrophic effects.

146 unambiguous diagnoses of different forms of EBV-driven LPD and represents a powerful tool to study t

147 tometry was used to measure the frequency of EBV-specific T-cell responses between groups following s

148 the mutations located in the large groove of EBV gH/gL (R(152)A and G(49)C) also have decreased bindi

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

150 As (EBERs), allowing rapid identification of EBV-infected cells among PBMCs.

151 There was no impact of EBV reactivation on acute graft-versus-host disease (GVH

152 In order to better understand the impact of EBV variation in eBL tumorigenesis, we improved viral DN

153 We prospectively evaluated the incidence of EBV reactivation and its impact on transplantation outco

154 ation was associated with a low incidence of EBV reactivation without EBV-lymphoproliferative disorde

155 We observed a 37% incidence of EBV-positivity.

156 nt cycles consisted of 3 weekly infusions of EBV-CTLs and 3 weeks of observation.RESULTSEBV-CTLs did

157 reby promoting the invasion and migration of EBV-related cancers, such as nasopharyngeal cancer and g

158 ) is retained among an unknown percentage of EBV isolates.

159 ase (CAL) is associated with the presence of EBV in coronary artery plaque samples in the current stu

160 reviously underrepresented the prevalence of EBV type 2.

161 s supporting the latency I or III program of EBV protein expression and is more complex than original

162 Proportions of EBV-infected cells correlated with blood EBV loads.

163 ptides derived from seven latent proteins of EBV in the interaction of NKG2A and its ligand HLA-E.

164 The close proximity of EBV episomes and the super enhancers that are enriched f

165 similar distributions in genomic regions of EBV-positive cells and is associated with oncogenic supe

166 his is the first study to reveal the role of EBV-miRNA-BART12 in the development of EBV-related tumor

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

168 underlying defective immune surveillance of EBV, patients with high-grade disease may have a recurre

169 In contrast to those of EBV and HCMV, the KSHV lytic cycle occurs while the APC/

170 ial therapeutic targets for the treatment of EBV-associated cancers.

171 targets and strategies for the treatment of EBV-related tumors.

172 The tropism of EBV for B cells and epithelial cell infection has been w

173 a indicate that the binding site of EphA2 on EBV gH/gL is at least in part proximal to the EBV gL gly

174 However, we have previously found that one EBV-encoded miRNA, namely EBV-miR-BART6-3p, acts as a tu

175 ZEBRA then transcriptionally activates other EBV genes and, together with some of those gene products

176 transcription but not transcription of other EBV genes or cellular genes.

177 V-driven cancers and may contribute to other EBV-associated diseases.

178 herapeutics licensed the bank of third-party EBV-CTLs from Memorial Sloan Kettering Cancer Center in

179 d failed rituximab therapy, with third-party EBV-CTLs.

180 t, frequencies of interferon-gamma-producing EBV-specific CD4 T cells were significantly lower in the

181 ers, we need a way to efficiently reactivate EBV into lytic replication.

182 ts with POD after a first cycle who received EBV-CTLs from a different donor achieved CR or durable P

183 erapy for patients with rituximab-refractory EBV-associated lymphoma after transplantation.TRIAL REGI

184 the first functional HLA-A*01:01-restricted EBV-LMP2-specific T-cell populations and TCRs, which can

185 cells transduced with HLA-A*01:01-restricted EBV-LMP2-specific TCRs was optimized by knocking out the

186 V dual infection does not increase eBL risk, EBV appears to suppress reactivation of KSHV while malar

187 nning residues 379-387 of EBNA-3 (RPPIFIRRL [EBV(RPP)]).

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

189 In this study, EBV-infected cell lines derived from gastric cancers and

190 In summary, EBV BGLF2 interacts with Tyk2, inhibiting Tyk2, STAT1, a

191 teracts the ability of IFN-alpha to suppress EBV reactivation.IMPORTANCE Type I interferons are impor

192 nomes are maintained by EBNA1, which tethers EBV episomes to the host chromosomes during mitosis.

193 is important for higher KSHV fusion and that EBV gH/gL does not utilize a similar motif for fusion ac

194 Our findings 1) demonstrate that EBV dovetails its escape strategy to a key cellular dang

195 These results demonstrate that EBV latent antigens can function as master regulators of

196 Functional analysis demonstrated that EBV peptides can bind to HLA-E and block inhibition of N

197 We found that EBV gH/gL-N(69)L/S(71)V had higher binding affinity for

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

199 with EBV latent antigens, and we found that EBV latent antigens cooperatively facilitate KLF14 expre

200 Using our unbiased methods, we found that EBV type 1 was significantly more prevalent in eBL patie

201 We reported previously that EBV tegument protein BGLF2 activates p38 and enhances EB

202 Indeed, our experiments reveal that EBV exploits several inflammasome sensors to actually ac

203 findings of the current study revealed that EBV-miR-BART12 binds to the 3'UTR region of Tubulin Poly

204 nalysis of population structure reveals that EBV type 2 exists as two genomic subgroups and was more

205 We showed that EBV-infected T cells had an effector memory activated ph

206 EphA2 binding activity of EBV gH/gL and the EBV gH/gL-N(69)L/S(71)V mutant.

207 molecular link between B-cell state and the EBV latency programme.

208 us to precisely map the contacts between the EBV episome(s) and the human host genome.

209 on of dATP into a primed DNA template by the EBV DNA polymerase in vitro.

210 ed, and disruption of this loop disables the EBV lytic cascade.

211 d lymphomagenesis in CBH mice.IMPORTANCE The EBV protein EBNA3A is expressed in latently infected B c

212 (or to allow at maximum 10% of change in the EBV predicted from progeny data).

213 These results offer insights into the EBV capsid assembly and a mechanism for recruiting cell-

214 ned near-atomic-resolution structures of the EBV capsid with an asymmetrically attached DNA-transloca

215 ade is activated only when expression of the EBV latent-to-lytic switch protein ZEBRA is turned on.

216 r findings highlight the complexities of the EBV population structure and provide new insight into vi

217 utant tumors expressed similar levels of the EBV protein EBNA2 and cellular protein p16, but in some

218 infectivity is particularly dependent on the EBV SM protein, a nuclear protein expressed early during

219 ession from an intact BHLF1 ORF required the EBV posttranscriptional regulator protein SM, whose expr

220 lows a subpopulation of cells to support the EBV lytic cycle.IMPORTANCE Transition from latency to th

221 ding affinity for EphA2, indicating that the EBV gL N-glycosylation site might be responsible for inh

222 We have recently shown that the EBV type 2 (EBV-2) strain has the unique ability to infe

223 These results indicate that the EBV-miR-BART6-3p/LOC553103/STMN1 axis regulates the expr

224 BV gH/gL is at least in part proximal to the EBV gL glycosylation site, which in part accounts for di

225 re followed by sequencing (4C-seq) using the EBV origin of plasmid replication (oriP) as a "bait" in

226 of target genes and by interacting with the EBV lytic origin of replication.

227 Therefore, EBV BGLF2 might protect virus-infected cells from the ty

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

229 Methods of augmenting the immune response to EBV in low-grade LYG include treatment with interferon-a

230 of EBNA3A in T cell and NK cell responses to EBV-infected tumors.

231 protein, LMP1, which alters NK responses to EBV.

232 igen-1 (EBNA-1), rendering them sensitive to EBV-specific cells.

233 complex that binds to TATT motifs unique to EBV late lytic promoters.

234 emonstrate that SM binds and recruits XPB to EBV promoters during lytic replication.

235 IFNgamma secretion and cytotoxicity towards EBV-LMP2-expressing malignant cell-lines.

236 be used in future TCR gene-therapy to treat EBV-associated latency type II/III malignancies.

237 f new therapeutic interventions for treating EBV-associated lymphomas.IMPORTANCE Epstein-Barr virus (

238 pomorph mutant virus (Delta3A) and wild-type EBV.

239 ins from Burkitt's lymphoma cells undergoing EBV replication, followed by tandem mass tag (TMT) mass

240 has not only revealed mechanisms underlying EBV-induced disease in these primary immunodeficiencies

241 e human gammaherpesvirus Epstein-Barr virus (EBV) (human herpesvirus 4 [HHV4]) infects most adults an

242 s other viruses, such as Epstein-Barr virus (EBV) and cytomegalovirus (CMV), were detected at compara

243 nk between B cell-tropic Epstein-Barr virus (EBV) and disease onset.

244 biological carcinogens, Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV)

245 Both Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV)

246 n upregulate immunogenic Epstein-Barr virus (EBV) antigens on Burkitt lymphoma (BL) that normally onl

247 56 angstrom structure of Epstein-Barr virus (EBV) BFRF1-BFLF2, as well as an increased resolution 1.4

248 We have found that the Epstein-Barr virus (EBV) BGLF2 tegument protein binds to a protein in the ty

249 The Epstein-Barr virus (EBV) BHLF1 gene encodes an abundant linear and several c

250 tomegalovirus (HCMV) and Epstein-Barr virus (EBV) both impair the activity of APC/C during their lyti

251 ered human cancer virus, Epstein-Barr virus (EBV) causes Burkitt's lymphoma and nasopharyngeal carcin

252 Epstein-Barr virus (EBV) DNAemia is a major risk factor for posttransplant l

253 tomegalovirus (HCMV) and Epstein-Barr virus (EBV) entry glycoproteins have defined the interaction si

254 The Epstein-Barr virus (EBV) episome is known to interact with the three-dimensi

255 Epstein-Barr virus (EBV) genomes persist in latently infected cells as extra

256 ication cycle.IMPORTANCE Epstein-Barr virus (EBV) has significant oncogenic potential that is linked

257 The Epstein-Barr virus (EBV) immediate early transactivator Zta plays a key role

258 otype of the herpesvirus Epstein-Barr virus (EBV) indicate that upon exposure to lytic triggers, cert

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

260 Epstein-Barr virus (EBV) infects human B cells and reprograms them to allow

261 Epstein-Barr virus (EBV) is a human herpesvirus that can cause lymphomas, ep

262 Epstein-Barr virus (EBV) is a ubiquitous human gamma-herpesvirus that establ

263 Zta function.IMPORTANCE Epstein-Barr virus (EBV) is a ubiquitous human pathogen and associated with

264 Epstein-Barr virus (EBV) is an enigma; on one hand, it infects and persists

265 Epstein-Barr virus (EBV) is associated with a number of T-cell diseases, inc

266 Epstein-Barr virus (EBV) is associated with epithelial and lymphoid malignan

267 tical transplantation on Epstein-Barr virus (EBV) is largely unknown.

268 Epstein-Barr virus (EBV) is one of nine human herpesviruses that persist lat

269 ismatch (18.5% [10/54]), Epstein-Barr virus (EBV) mismatch (EBV) (9.3% [5/54]), age/size mismatch (51

270 nths following confirmed Epstein-Barr virus (EBV) positive mononucleosis.

271 Epstein-Barr virus (EBV) preferentially infects epithelial cells and B lymph

272 lifelong infection, the Epstein-Barr virus (EBV) switches between four viral genome latency and lyti

273 Epstein-Barr virus (EBV) was discovered as the first human tumor virus more

274 we investigated whether Epstein-Barr virus (EBV), an oncoherpesvirus, exploits inflammasomes to acti

275 ted lymphomas.IMPORTANCE Epstein-Barr virus (EBV), as the first human tumor virus, infects more than

276 sociated viruses such as Epstein-Barr virus (EBV), hepatitis B virus (HBV) and human papilloma virus

277 More than 70% of Epstein-Barr virus (EBV)-negative Hodgkin lymphoma (HL) cases display inacti

278 tissue infiltration with Epstein-Barr virus (EBV)-positive lymphocytes.

279 rane protein 1 (LMP1) of Epstein-Barr virus (EBV).

280 s latently infected with Epstein-Barr virus (EBV).

281 and Human herpesvirus 4 (Epstein-Barr virus [EBV]) were more prevalent in children with caries.

282 ytomegalovirus [CMV] and Epstein-Barr virus [EBV]).

283 hepatitis C virus [HCV], Epstein-Barr virus [EBV], and cytomegalovirus [CMV]) have limited breadth an

284 In vitro, EBV can transform primary human B lymphocytes into immor

285 However, little is known about where EBV episomes are located in interphase cells.

286 effector memory activated phenotype, whereas EBV-infected B cells expressed plasma cell differentiati

287 In this study, we determined which EBV-positive cell lines are reactivated by classes of HI

288 While EBV SM has been thought to act posttranscriptionally, we

289 induction therapy for treating patients with EBV-associated cancers, we need a way to efficiently rea

290 induction therapy for treating patients with EBV-positive malignancies that contain wild-type p53.

291 Ngamma and cytotoxicity when stimulated with EBV-LMP2-expressing cell-lines.

292 mediate monocytes following stimulation with EBV peptides has high sensitivity for the detection of o

293 les of the E2F-Rb-HDAC complex together with EBV latent antigens, and we found that EBV latent antige

294 Secondary treatment with EBV-CTLs restricted by a different HLA allele (switch th

295 a low incidence of EBV reactivation without EBV-lymphoproliferative disorder.

296 as at rates similar to their induction by WT EBV but with delayed onset.

297 compared to the onset of those caused by WT EBV, although the tumors occurred at a similar rate.

298 The WT EBV and EBNA3A mutant tumors expressed similar levels of

299 involving multiple cellular genes in the WT EBV- versus Delta3A-infected tumors and increased expres

300 NA3A mutant EBV (Delta3A) and wild-type (WT) EBV in a cord blood-humanized (CBH) mouse model.