ライフサイエンスコーパス: EBV

1 EBV and HHV6 reactivations were predictors for the occur

2 EBV expresses viral oncogenes that promote cell growth a

3 EBV infection upregulated APC-related markers on B cells

4 EBV is a common gammaherpes virus with tropism for B lym

5 EBV latency types are defined by DNA methylation pattern

6 EBV latent membrane protein 1 (LMP1) is required for the

7 EBV shedding rate and quantity decreased less dramatical

8 EBV treatment in hyperinflated patients with heterogeneo

9 EBV tropism is dictated by gp42 levels in the virion, as

10 EBV+ PTLD can arise after primary EBV infection, or beca

11 EBV-transformed lymphoblastoid B cell lines (LCLs) deriv

12 ovirus (hazard ratio [HR], 0.995; P = .022), EBV (HR, 0.994; P = .029), and HHV6 (HR, 0.991; P = .012

13 ins of Epstein-Barr virus (EBV), EBV type 1 (EBV-1) and EBV-2, differ in latency genes, suggesting th

14 Determination of type 1 and type 2 EBV in saliva samples from people from a wide range of g

15 Linkage of Zp and gp350 variants to type 2 EBV is likely to be due to their genes being adjacent to

16 British people carrying predominantly type 2 EBV.

17 lly, we show that BCR signaling can activate EBV lytic induction in freshly isolated B cells from per

18 s showed a coincident expansion of activated EBV-specific CD8(+) T cells, but overall CD8(+) T cell n

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

20 Additional EBV super-enhancer (ESE) targets included MCL1, IRF4, an

21 outcomes of interest were VR of adenovirus, EBV, human herpesvirus 6 (HHV6), cytomegalovirus (CMV),

22 tion (i.e., TNF-alpha and IFN-gamma) against EBV-infected cells, enhancing NK cell activation.

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

24 immunity, especially for protection against EBV and humoral immunity.

25 cells have been reported to respond against EBV-infected B cells in the lytic cycle and to control t

26 cord blood-humanized mouse model that allows EBV-infected B cells to interact with CD4 T cells (the m

27 opulation-wide survey of oral samples for an EBV-like virus in a nonhuman great ape.

28 member of the IL-12 family, consisting of an EBV-induced gene 3 (EBI3) subunit and a P35 subunit.

29 To further examine the presence of EBV or an EBV-like virus in mountain gorillas, we conducted the fi

30 l autoimmune encephalomyelitis model that an EBV-related lymphocryptovirus enables B cells to protect

31 opulation was suspected of infection with an EBV-like virus based on serology and infant histopatholo

32 ein-Barr virus (EBV), EBV type 1 (EBV-1) and EBV-2, differ in latency genes, suggesting that they use

33 for mediating gene silencing of IL-27p28 and EBV-induced gene 3.

34 specific EBV variations with EBV biology and EBV-associated diseases.IMPORTANCE Incidence of diseases

35 l, but the proportions of memory B cells and EBV-specific effector memory CD8(+) T cells were reduced

36 and competing risks, only concurrent CMV and EBV reactivations remained independently associated with

37 Genital replication of CMV and EBV was the most common and was significantly associated

38 sistent shedding was more common for CMV and EBV when compared to other HHVs.

39 libration to international units/ml (CMV and EBV) on variability was also determined.

40 In blood cellular subsets both IL12p35 and EBV-induced gene protein 3 (EBI3) mRNAs were detected on

41 novel cause of combined immunodeficiency and EBV-associated diseases, reminiscent of inherited CD27 d

42 summary, we conclude that the viral load and EBV gp350 diversity during early infection are associate

43 1 (LMP1) (which mimics CD40 signaling), and EBV-encoded nuclear antigen 3A (EBNA3A) and EBNA3C (whic

44 r RUNX3/CBF during B cell transformation and EBV latency that was hitherto unexplored.

45 somal episomes, express 9 latency-associated EBV proteins, and phenotypically resemble antigen-activa

46 Our data suggest that KSHV augments EBV-associated tumorigenesis via stimulation of lytic EB

47 ctly correlated with higher peripheral blood EBV DNA levels during AIM and a greater evolution of div

48 cells, induction of cathepsin G activity by EBV led to total degradation of the immunodominant pepti

49 way for E2F1 activation that is exploited by EBV to promote cell growth and proliferation, offering n

50 on of EBNA3s with RUNX3-a protein induced by EBV during B cell transformation.

51 reat disorders associated with or induced by EBV infection.

52 Despite its ubiquity, infection by EBV is often subclinical; this invariably reflects the n

53 nt differentiation to PCs after infection by EBV, thus favouring long-term latency in MBC and asympto

54 ng the IL1R1 3' untranslated region (UTR) by EBV miR-BHRF1-2-5p was confirmed using 3'-UTR luciferase

55 In the context of cancer, EBV hijacks the exosomal pathway to modulate cell-to-cel

56 lymphoblastoid cell lines (LCLs) that carry EBV DNA as extra-chromosomal episomes, express 9 latency

57 Presence of CMV, EBV, and herpes simplex virus (HSV) were independent pre

58 Expansion of HIV-infected CMV/EBV-specific CD4 + T cells may contribute to maintenance

59 n map of LCL, we constructed a comprehensive EBV regulome encompassing 1,992 viral/cellular genes and

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

61 lymphoma (PEL), and 90% of PELs also contain EBV.

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

63 properly when stimulated with CD70-deficient EBV-infected B cells, whereas expression of CD70 in B ce

64 ver, we recently showed that an LMP1-deleted EBV mutant induces B cell lymphomas in a newly developed

65 ssion correlate with the highly demethylated EBV type III latency program permissive for expression o

66 T-cell samples from mothers but could detect EBV-2 in samples of their breast milk and saliva.

67 We were unable to detect EBV-2 in T-cell samples from mothers but could detect EB

68 We detected EBV-2 in all T-cell samples obtained from EBV-2-infected

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

70 the spatial organization of chromatin during EBV-driven cellular transformation.

71 The 2 strains of Epstein-Barr virus (EBV), EBV type 1 (EBV-1) and EBV-2, differ in latency genes, s

72 All cancers (except EBV-related neoplasia) were recorded.

73 rvations suggest that IR1-and, by extension, EBV-diversifies through both recombination and breakpoin

74 Finally, EBV super-enhancer-targeted IRF2 protected LCLs against

75 For EBV, the gp42 protein assembles into complexes with gHgL

76 ositivity and 25.6% (95% CI: 12.4-38.8%) for EBV DNA positivity; 14.9% (95% CI: 12.4-17.4%) for human

77 ) positivity, 94.7% (95% CI: 90.7-98.8%) for EBV IgG positivity and 25.6% (95% CI: 12.4-38.8%) for EB

78 ere examined for the presence of EBV and for EBV type.

79 This was particularly the case for EBV viral load results.

80 ppression of apoptosis with implications for EBV lymphomagenesis.

81 eratively to demethylate genes important for EBV-driven B-cell growth transformation.

82 ), which represent an experimental model for EBV-associated cancers.

83 l. (2017) develop humanized mouse models for EBV/KSHV co-infection and identify their complementary e

84 ractions isolated from children positive for EBV-1 or EBV-2 and their mothers were examined for the p

85 e B cell receptor signaling, is required for EBV-induced lymphomas in this model.

86 epitope-tagged EBNA3A, EBNA3B or EBNA3C from EBV-recombinants, revealed important principles of EBNA3

87 ed EBV-2 in all T-cell samples obtained from EBV-2-infected children at 12 months of age, with some c

88 evisited this issue, showing that serum from EBV(+) individuals triggered vigorous NK cell degranulat

89 proliferation was normal, in vitro-generated EBV-specific cytotoxic T cell activity was reduced becau

90 pients with negative pretransplant HBc, HCV, EBV, or CMV serology.

91 Like other herpesviruses, EBV has diversified through both coevolution with its ho

92 was higher in patients with persistent high EBV replication (22.4% vs 10.2%, P = 0.005).

93 Persistent high EBV viral load is associated with the occurrence of soli

94 How EBV converts latency type is unclear, although it is kno

95 few models are available for dissecting how EBV causes lymphomas in vivo in the context of a host im

96 These findings help to establish how EBV enlists and manipulates cellular DNA repair factors

97 This work evaluates how EBV's BPLF1 protein and its conserved deubiquitinating a

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

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

100 T2 expression in GC cells may promote type I EBV latency.

101 In this article, we identify EBV-encoded miR-BART16 as a novel viral immune-evasion f

102 tion and suggest that TET2 promotes type III EBV latency in B cells with an ABC or naive phenotype by

103 ibited by ibrutinib or idelalisib.IMPORTANCE EBV establishes viral latency in B cells.

104 EBV-induced tumors in this model.IMPORTANCE EBV causes human lymphomas, but few models are available

105 ation of methylated EBV promoters.IMPORTANCE EBV establishes several different types of viral latency

106 imiting downstream LMP1 signaling.IMPORTANCE EBV is a ubiquitous gamma herpesvirus linked to malignan

107 more, LMP1 blocks IRF5-mediated apoptosis in EBV-infected cells.

108 n levels of RNF31 and LMP1 are correlated in EBV-transformed cells.

109 ng protein that is consistently expressed in EBV tumors and is the only viral protein required to mai

110 ORTANCE The EBV protein LMP1 is expressed in EBV-associated epithelial cell diseases, regardless of w

111 sion to be associated with p53 expression in EBV-transformed cells under physiological and DNA damagi

112 ated lytic EBV replication was also found in EBV/KSHV dually infected lymphoproliferative disorders i

113 hough human MOG protein was degraded less in EBV-infected than in uninfected B cells, induction of ca

114 KSHV persisted in EBV-transformed B cells and was associated with lytic EB

115 MP1 promotes efficient lytic reactivation in EBV-infected epithelial cells by enhancing expression of

116 nalyze the sequence of the largest repeat in EBV (IR1).

117 ifically in controlling viral replication in EBV-infected B cells.

118 Knockdown of RNF31 in EBV-transformed IB4 cells by RNA interference negatively

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

120 ptional silencing similar to what is seen in EBV latency type III genomes.

121 Thus, in EBV-infected epithelial cells, LMP1 expression is promot

122 tate (TPA) and sodium butyrate treatment, in EBV-infected epithelial cells by increasing expression o

123 a genome-wide view of sequence variation in EBV isolated from primary NPC biopsy specimens obtained

124 to HN18 had some nonsynonymous variations in EBV genes including genes encoding latent, early lytic,

125 However, during early infection EBV induces rapid B cell proliferation with low levels o

126 During latent infection, EBV encodes latent membrane protein 2A (LMP2A) to promot

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

128 Interestingly, EBV concurrently exists in nearly 70% of PEL cases.

129 l miRNA to regulate internalization of KSHV, EBV, and HSV-2 in hematopoietic and endothelial cells.

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

131 The B lymphotropic EBV is a major risk factor in multiple sclerosis, via as

132 Evidence of elevated lytic EBV replication was also found in EBV/KSHV dually infect

133 ription factors KLF4 and BLIMP1 induce lytic EBV reactivation in epithelial cells by synergistically

134 iated tumorigenesis via stimulation of lytic EBV replication.

135 formed B cells and was associated with lytic EBV gene expression, resulting in increased tumor format

136 but not rapamycin also inhibit BCR-mediated EBV activation.

137 by enhancing EBNA2 activation of methylated EBV promoters.IMPORTANCE EBV establishes several differe

138 Improvements were maintained at 6 months: EBV 56.3% versus SoC 3.2% (P < 0.001), with a mean +/- S

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

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

141 3Kdelta prevents E2F1 activation also in non-EBV-infected cells.

142 Here, we report 18 novel EBV genome sequences from viruses isolated from primary

143 Phylogenetic analysis revealed that all NPC-EBV genomes were distinct from other EBV genomes.

144 d analysis of the large internal repeat 1 of EBV (IR1; also known as the BamW repeats) for more than

145 erse event, occurring in 19 of 65 (29.2%) of EBV subjects.

146 At 3 months, 55.4% of EBV and 6.5% of SoC subjects had an FEV1 improvement of

147 A total of 89.8% of EBV subjects had target lobe volume reduction greater th

148 2A alone has little effect on the ability of EBV to cause lymphomas but delays tumor onset.

149 The ability of EBV to convert human B cells into long-lived lymphoblast

150 A is absolutely essential for the ability of EBV to induce B cell lymphomas in the cord blood-humaniz

151 Analysis of EBV PAR-CLIP miRNA targetome data sets combined with pat

152 IRF5-mediated apoptosis for the benefits of EBV.

153 pathway appears to be a crucial component of EBV-specific T cell immunity and more generally for the

154 on plays an important role in the control of EBV, enhancing NK cell effector functions against infect

155 We report the detection of EBV gp350-specific antibodies capable of neutralizing EB

156 cuss the implications for the development of EBV+ PTLD.

157 is was achieved through target enrichment of EBV DNA by hybridization, followed by next-generation se

158 The incidence of EBV+ PTLD is variable depending on the organ transplante

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

160 hermore, we demonstrate that (independent of EBV) TET2 is turned off in normal and malignant germinal

161 d, consistent with their impaired killing of EBV-infected cells.

162 Manipulation of EBV BHRF1-2 miRNA activity in latently infected B cells

163 hus, our results reveal a novel mechanism of EBV in diverting the functions of MYC in malignant trans

164 ir mothers were examined for the presence of EBV and for EBV type.

165 To further examine the presence of EBV or an EBV-like virus in mountain gorillas, we conduc

166 roenvironment and enhance the progression of EBV-associated cancers.

167 ive DNA demethylation, is a key regulator of EBV latency type DNA methylation patterning.

168 stent KSHV infection in vivo and the role of EBV co-infection in PEL development have been hampered b

169 a mutation in the main laboratory strain of EBV that impairs virus function, and we suggest that tum

170 tes NFkappaB and is critical for survival of EBV-immortalized B cells.

171 genesis, which would impact the treatment of EBV-associated cancer.IMPORTANCE Nasopharyngeal carcinom

172 al to understand the highly tuned tropism of EBV for epithelial cells and B lymphocytes and may resul

173 Here, we review the virology of EBV, mechanisms underlying disease pathogenesis in PIDs,

174 lticenter 2:1 randomized controlled trial of EBVs plus standard of care or standard of care alone (So

175 because we observed only minimal effects on EBV-specific CD8 T cells, suggesting that responding cel

176 gations into the impact of valganciclovir on EBV-associated diseases are needed.

177 P2A may be sufficient to promote early-onset EBV-induced tumors in this model.IMPORTANCE EBV causes h

178 isolated from children positive for EBV-1 or EBV-2 and their mothers were examined for the presence o

179 luated the effects of valganciclovir on oral EBV shedding in a randomized, double-blind, placebo-cont

180 all NPC-EBV genomes were distinct from other EBV genomes.

181 eveloped cytomegalovirus and BK and 2 others EBV and BK viremia.

182 Heterodimeric IL-27 (p28/EBV-induced gene 3) is an important member of the IL-6/I

183 the possibility that, like papillomaviruses, EBV has evolved to take advantage of epithelial differen

184 usceptible to viral infections, particularly EBV, suggesting that these patients have defective funct

185 .001) were more likely to develop persistent EBV viremia.

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

187 phosphoprotein-65, tetanus toxoid precursor, EBV nuclear Ag 2, or HIV gag protein.

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

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

190 enes relevant to these diseases and proposed EBV vaccines.

191 The diversity of the latency protein EBV nuclear antigen leader protein (EBNA-LP) resides pre

192 Finally, the prototype EBV strain B95-8 contains four nonconsensus variants wit

193 we report a patient suffering from recurrent EBV-induced B cell proliferations including Hodgkin's ly

194 to 5-hydroxymethylcytosine (5hmC), regulates EBV latency type in B cells by enhancing the ability of

195 to 5-hydroxymethylcytosine (5hmC), regulates EBV latency type in B cells.

196 months of age, with some children retaining EBV-2-positive T cells through 24 months of age, suggest

197 In some EBV-associated cancers, p53 tends to be wild type and ov

198 ive analysis so far of variation in specific EBV genes relevant to these diseases and proposed EBV va

199 directed analysis of association of specific EBV variations with EBV biology and EBV-associated disea

200 mation and provide a rationale for targeting EBV's roles in cell cycle modulation.

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

202 as a model for KSHV infection and find that EBV/KSHV dual infection enhanced KSHV persistence and tu

203 We hypothesized that EBV genomic variations might contribute to the pathogene

204 We previously reported that EBV-2 infects T cells in vitro.

205 Here, we show that EBV BHRF1-2 miRNAs block NF-kappaB activation following

206 ord blood-humanized mouse model to show that EBV can cooperate with human CD4 T cells to cause B cell

207 We show that EBV-specific T lymphocytes did not expand properly when

208 We review the strategies that EBV uses to subvert and evade host immunity and discuss

209 These data suggest that EBV-2 uses T cells as an additional latency reservoir bu

210 ls through 24 months of age, suggesting that EBV-2 persists in T cells.

211 The EBV genetic variants identified here provide a basis for

212 The EBV oncoprotein latent membrane protein 1 (LMP1) functio

213 The EBV oncoprotein LMP1 constitutively activates NFkappaB a

214 The EBV surface protein gp350 is a major target for antibodi

215 o activate Z and R expression.IMPORTANCE The EBV protein LMP1 is expressed in EBV-associated epitheli

216 BNA1 allows the long-term persistence of the EBV genome are currently unclear.

217 Sequence analysis of the EBV genome is unusually challenging because of the large

218 egulated in a fashion similar to that of the EBV genome.

219 s a cofactor of EBNA2 and coregulator of the EBV type III latency program and DNA methylation state.I

220 In this overview, we review the EBV life cycle and discuss our current understanding of

221 The heterodimeric gH/gL complex binds to the EBV epithelial cell receptor or gp42, which binds to the

222 sertions, and 154 deletions, compared to the EBV reference genome.

223 Here we examined whether the EBV LMP2A protein, which mimics constitutively active B

224 These EBV genomes harbored 20,570 variations totally, includin

225 host dependency factors resulting from these EBV+, B cell-transformed cell states, we performed paral

226 However, in these EBV-associated cancers, only NPC exhibits remarkable eth

227 s, and further, Pol eta was found to bind to EBV DNA, suggesting that it may allow for bypass of dama

228 with sex, HLA type, or previous exposure to EBV or cytomegalovirus.

229 er the recipient has preexisting immunity to EBV but can be as high as 20%.

230 enes essential for LCL growth were linked to EBV enhancers.

231 Humans respond to EBV in two alternative ways.

232 s to both forms of innate immune response to EBV having benefit for human survival.

233 rent understanding of the immune response to EBV in healthy, immunocompetent individuals, in transpla

234 via FcgammaR-IIIA (CD16) in the response to EBV.

235 gene transcripts are regulated similarly to EBV type III latency genes and that TET2 protein is a co

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

237 liferation, offering new strategies to treat EBV-carrying cancers.

238 cells by synergistically activating the two EBV immediate early promoters (Zp and Rp).

239 findings provide novel mechanisms underlying EBV-mediated oncogenesis and may have a broad impact on

240 ed trials of the Zephyr endobronchial valve (EBV) treatment have demonstrated benefit in severe heter

241 fic for control viruses, Epstein-Barr virus (EBV) and cytomegalovirus (CMV), and compared to bulk mem

242 The human tumor viruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) es

243 uman B cells infected by Epstein-Barr virus (EBV) become activated, grow, and proliferate.

244 Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma (BL) and immunosupp

245 Epstein-Barr virus (EBV) causes infectious mononucleosis and can lead to lym

246 Epstein-Barr virus (EBV) encodes >44 viral microRNAs (miRNAs) that are diffe

247 Epstein-Barr virus (EBV) entry into epithelial cells is mediated by the cons

248 Epstein-Barr virus (EBV) establishes a stable latent infection that can pers

249 The Epstein-Barr virus (EBV) gp350 glycoprotein interacts with the cellular rece

250 n and persistence of the Epstein-Barr virus (EBV) have long been difficult to resolve.

251 % (95% CI: 0.7-4.7%) for Epstein-Barr virus (EBV) immunoglobulin M (IgM) positivity, 94.7% (95% CI: 9

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

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

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

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

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

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

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

259 Epstein-Barr virus (EBV) infects greater than 90% of humans, is recognized a

260 omosome (BAC).IMPORTANCE Epstein-Barr virus (EBV) infects the majority of the world population but ca

261 Epstein-Barr virus (EBV) is a common human pathogen that infects over 95% of

262 Epstein-Barr virus (EBV) is a human herpes virus that infects >90% of indivi

263 Epstein-Barr virus (EBV) is a ubiquitous human gammaherpesvirus that establi

264 Epstein-Barr virus (EBV) is associated with multiple human malignancies.

265 host control.IMPORTANCE Epstein-Barr virus (EBV) is transmitted orally, replicates in the throat, an

266 Epstein-Barr virus (EBV) is typically acquired asymptomatically in childhood

267 ylation state.IMPORTANCE Epstein-Barr virus (EBV) latency and carcinogenesis involve the selective ep

268 Epstein-Barr virus (EBV) latency and its associated carcinogenesis are regul

269 we provide evidence that Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) promotes IRF4 phos

270 Epstein-Barr virus (EBV) latently infects normal B cells and contributes to

271 Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mon

272 rted that posttransplant Epstein-Barr virus (EBV) replication is frequent and indicates overimmunosup

273 nlarged set of about 200 Epstein-Barr virus (EBV) strains, including many primary isolates, have been

274 Epstein-Barr virus (EBV) transforms B cells to continuously proliferating ly

275 ytomegalovirus (CMV) and Epstein-Barr virus (EBV) were the most commonly detected HHV in semen of HIV

276 common viral pathogens: Epstein-Barr virus (EBV), adenovirus (AdV), cytomegalovirus (CMV), BK virus

277 lated DNA viruses: KSHV, Epstein-Barr virus (EBV), and herpes simplexvirus-2 (HSV-2).

278 -1 and the related virus Epstein-Barr virus (EBV), as well as influenza A virus (IAV).

279 f cytomegalovirus (CMV), Epstein-Barr virus (EBV), BK virus (BKV), adenovirus (ADV), and human herpes

280 The 2 strains of Epstein-Barr virus (EBV), EBV type 1 (EBV-1) and EBV-2, differ in latency ge

281 h cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), herpes simplex virus

282 ans become infected with Epstein-Barr virus (EBV), which then persists for life.

283 Epstein-Barr virus (EBV)-associated diseases of epithelial cells, including

284 y-ala repeat sequence of Epstein-Barr virus (EBV)-encoded EBNA1, results in PI3Kdelta-dependent induc

285 e protein 1 (LMP1) is an Epstein-Barr virus (EBV)-encoded oncoprotein that is packaged into small ext

286 tion, can be detected in Epstein-Barr virus (EBV)-positive tumors, and manipulate several biological

287 tomegalovirus (CMV)- and Epstein-Barr virus (EBV)-responsive CD4+ T cells following chemotherapy.

288 ften associated with the Epstein Barr virus (EBV).

289 s closely related to the Epstein-Barr virus (EBV).

290 hepatitis C virus [HCV], Epstein-Barr virus [EBV], or cytomegalovirus [CMV]) in KTR on sirolimus (SRL

291 lpha-mediated programmed cell death, whereas EBV-induced BATF/IRF4 were critical for BIM suppression

292 ver, cellular factors that determine whether EBV enters the highly transforming type III latency, ver

293 c approach uncovered key mechanisms by which EBV oncoproteins activate the PI3K/AKT pathway and evade

294 The results suggest a mechanism by which EBV recruits cellular repair factors, such as Pol eta, t

295 ate to become memory B cells (MBC), in which EBV persistence is established.

296 erplasia (PRLH), a condition associated with EBV in HIV-infected children.

297 RTANCE Incidence of diseases associated with EBV varies greatly in different parts of the world.

298 ciclovir reduced the proportion of days with EBV detected from 61.3% to 17.8% (relative risk, 0.28; 9

299 In vitro, about 20 days after infection with EBV lacking functional EBNA3A and EBNA3C, cells develop

300 Three patients presented with EBV-associated Hodgkin's lymphoma and hypogammaglobuline

301 association of specific EBV variations with EBV biology and EBV-associated diseases.IMPORTANCE Incid