ライフサイエンスコーパス: e antigen

1 infected (all in recipients positive for HBV e antigen).

2 ated with a higher prevalence of hepatitis B e antigen.

3 which is proteolytically processed to yield e antigen.

4 s B surface antigen, HBV DNA, or hepatitis B e antigen.

5 ly believed to discriminate between core and e-antigen.

6 antigens and the RHCE gene encodes the c and E antigens.

7 rcentage of cells expressing DEN-2 envelope (E) antigen 7 days after challenge.

8 sponders were still negative for hepatitis B e antigen (94% vs. 40%; P < 0.001) and hepatitis B surfa

9 The primary outcomes were hepatitis B (HB) e antigen (Ag) and HBV-DNA clearance (as measures of eff

10 lanation for the distinction between cAg and e-antigen (an unassembled form of capsid protein) and an

11 The surgeon was positive for hepatitis B e antigen and had a high serum HBV DNA concentration (15

12 d hepatitis B virus DNA testing; hepatitis B e antigen and hepatitis B e antibody were tested <50% of

13 s evidenced by the loss of serum hepatitis B e antigen and hepatitis B virus (HBV) DNA.

14 gic, and functional features between the PAL-E antigen and NRP-1 support our interpretation.

15 (defined by the absence of serum hepatitis B e antigen and serum HBV DNA) at week 52 of treatment.

16 esponded to therapy with loss of hepatitis B e antigen and viral DNA from serum.

17 e-antigen, nor did they discriminate between e-antigen and dimers of dissociated core antigen capsids

18 ercent to 33% experience loss of hepatitis B e antigen, and 53% to 56% have a histologic response.

19 e (ALT) levels, disappearance of hepatitis B e antigen, and improvement in liver histology.

20 Serum levels of HBV surface antigen and HBV e antigen, and numbers of HBV antigen-positive hepatocyt

21 the appearance of antibodies to hepatitis B e antigen (anti-HBe) at the end of PEG-IFN therapy (HBeA

22 ysis of tryptic peptides to identify the PAL-E antigen as a secreted form of vimentin.

23 ral replication (detectable serum HBV-DNA or e antigen) at the time of transplant have a higher rate

24 nd 45 (87%) had detectable serum hepatitis B e antigen before treatment.

25 ne activation and that instantaneous loss of e-antigen by either mechanism is associated with least l

26 ction and propose mechanisms for hepatitis B e-antigen clearance, subsequent emergence of a potent ce

27 We also showed that the PAL-E antigen colocalizes with NRP-1 staining in endothelial

28 was proven by the formation of a 2:1 Fab e6-e-antigen complex.

29 HBV surface antigen and 26 days prior to HBV e antigen detection.

30 pressed ubiquitously, our examination of HLA-E antigen distribution indicated that it is detectable o

31 ent forms of the HBV core antigen (HBcAg) or e antigen (eAg) were found to induce antigen-specific ma

32 The prM/E antigens expressed in lettuce chloroplasts should offe

33 the AUG codon severely impaired hepatitis B e antigen expression (P < 0.001).

34 re promoter mutations diminished hepatitis B e antigen expression in an additive manner.

35 Reduction in hepatitis B e antigen expression may contribute to accelerated seroc

36 was to determine their effect on hepatitis B e antigen expression.

37 hether this double mutation is important for e antigen expression.

38 and -7 (in the residual propeptide) in the "e-antigen" form of the capsid protein and has implicatio

39 tect the presence of the precore protein and e antigen from CID variants.

40 xpression of a model hepatitis B virus (HBV) e antigen fused to an IgG Fc fragment.

41 ansferase levels, HBV DNA level, hepatitis B e antigen (HBeAg) and antibody (anti-HBe), hepatitis B s

42 positive, and 61% had detectable hepatitis B e antigen (HBeAg) and HBV DNA when treatment was begun.

43 TLRs) on spontaneous hepatitis B virus (HBV) e antigen (HBeAg) and hepatitis B s antigen (HBsAg) sero

44 mutants and studied kinetics of hepatitis B e antigen (HBeAg) and hepatitis B surface antigen (HBsAg

45 Spontaneous seroclearance of hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA undete

46 (PD-L)1, and the suppression of hepatitis B e antigen (HBeAg) and surface antigen (HBsAg) biosynthes

47 ous or antiviral therapy-related hepatitis B e antigen (HBeAg) clearance.

48 nfidence interval [CI] 1.7-3.2), hepatitis B e antigen (HBeAg) clearance/loss (RR = 2.1, 95% CI 1.5-3

49 100 mg/d) in 24 patients who had hepatitis B e antigen (HBeAg) despite 1 to 3 months of prior therapy

50 ong the other 60 patients, 1 showed positive e antigen (HBeAg) early after transplantation, and 2 (1

51 al genome replication and reduce hepatitis B e antigen (HBeAg) expression.

52 a precore/core protein, which is secreted as e antigen (HBeAg) following removal of precore-derived s

53 Secretion of the hepatitis B virus (HBV) e antigen (HBeAg) has been conserved throughout the evol

54 s. 23 percent, P<0.001), loss of hepatitis B e antigen (HBeAg) in serum (32 percent vs. 11 percent, P

55 y); 9 patients were positive for hepatitis B e antigen (HBeAg) in the immune-tolerant phase and were

56 Hepatitis B e antigen (HBeAg) is a secreted version of hepatitis B v

57 The function of the hepatitis B e antigen (HBeAg) is largely unknown because it is not r

58 A predict a higher likelihood of hepatitis B e antigen (HBeAg) loss in patients with chronic hepatiti

59 Undetectable serum HBV DNA and hepatitis B e antigen (HBeAg) loss were significantly more likely at

60 e-third of patients with typical hepatitis B e antigen (HBeAg) positive chronic hepatitis B, but a le

61 CHB, among whom, 28.6% were also hepatitis B e antigen (HBeAg) positive.

62 higher in subjects with maternal hepatitis B e antigen (HBeAg) positivity and who received HBIG off-s

63 epatitis B virus (HBV) genotype, hepatitis B e antigen (HBeAg) presence, persistently high levels of

64 The durability of hepatitis B e antigen (HBeAg) responses after a consolidation period

65 ted death (9.4% vs 0%; P = .03), hepatitis B e antigen (HBeAg) seroconversion (61.5% vs 25.0%, P = .0

66 cts with chronic hepatitis B and hepatitis B e antigen (HBeAg) seroconversion following lamivudine th

67 Their roles in hepatitis B e antigen (HBeAg) seroconversion induced by interferon (

68 It is unclear whether hepatitis B e antigen (HBeAg) seroconversion induced by nucleos(t)id

69 pproved to treat CHB in children.Hepatitis B e antigen (HBeAg) seroconversion is still an important t

70 prolonged viremic phase, delayed hepatitis B e antigen (HBeAg) seroconversion, and an increased incid

71 tion, activity of liver disease, hepatitis B e antigen (HBeAg) seroconversion, and interferon therapy

72 re gene mutations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV biosynthesis, and

73 erferon alfa (IFN-alpha)-related hepatitis B e antigen (HBeAg) seroconversion.

74 In spontaneous hepatitis B e antigen (HBeAg) seroconverters, lower serum HBsAg and

75 Twenty-two percent were hepatitis B e antigen (HBeAg) seropositive; 20.4% (59/289) had cirrh

76 ed with respect to HBV genotype, hepatitis B e antigen (HBeAg) serostatus, and race.

77 k prediction model included age, gender, HBV e antigen (HBeAg) serostatus, serum levels of HBV DNA, a

78 identify miRNAs associated with hepatitis B e antigen (HBeAg) status and response to antiviral thera

79 Hepatitis B e antigen (HBeAg) status and serum hepatitis B virus (HB

80 NA viral load, hepatitis surface (HBsAg) and e antigen (HBeAg) status were obtained at baseline and e

81 t of chronic hepatitis B include hepatitis B e antigen (HBeAg) status, levels of hepatitis B virus (H

82 ages, which were predisposed by maternal HBV e antigen (HBeAg) to support HBV persistence by upregula

83 e the usefulness of quantitative hepatitis B e antigen (HBeAg) values for predicting HBeAg seroconver

84 Circulating hepatitis B e antigen (HBeAg) was found to distinguish the group of

85 f hepatitis B virus core antigen (HBcAg) and e antigen (HBeAg) were analyzed.

86 ection who were positive for the hepatitis B e antigen (HBeAg) were randomly assigned (2:1) to receiv

87 ic T-cell response was weaker in hepatitis B e antigen (HBeAg)(+) than HBeAg(-) patients (percent res

88 atment-experienced children with hepatitis B e antigen (HBeAg)+ CHB were randomized to ADV or placebo

89 titis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and cirrhosis.

90 Hepatitis B e antigen (HBeAg), encoded by the precore RNA, mediates

91 as independently associated with hepatitis B e antigen (HBeAg), HAART <2 years, CD4 <200 cells/mm(3),

92 In contrast to hepatitis B e antigen (HBeAg), HBsAg was not a reliable marker of pr

93 minations were tested for HBsAg, hepatitis B e antigen (HBeAg), serum hepatitis B virus (HBV)-DNA lev

94 ding hepatitis B surface antigen (HBsAg) and e antigen (HBeAg), were tested.

95 (IA), inactive carrier (IC), and hepatitis B e antigen (HBeAg)-negative (ENEG) hepatitis phases-we pe

96 A total of 641 hepatitis B e antigen (HBeAg)-negative and HBeAg-positive patients (

97 ients with the difficult-to-cure hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB) is

98 Hepatitis B e antigen (HBeAg)-negative chronic hepatitis B infection

99 A total of 1,068 Taiwanese hepatitis B e antigen (HBeAg)-negative HBV carriers with serum HBV D

100 Hepatitis B e antigen (HBeAg)-negative hepatitis is a clinical indic

101 total of 243 (69%) patients were hepatitis B e antigen (HBeAg)-negative of whom 15% had clinical cirr

102 r carcinoma (HCC) development in hepatitis B e antigen (HBeAg)-negative patients with an HBV DNA leve

103 (t)ide analog (Nuc) treatment in hepatitis B e antigen (HBeAg)-negative patients with chronic hepatit

104 cleos(t)ide analogue therapy for hepatitis B e antigen (HBeAg)-negative patients with chronic hepatit

105 HBV) DNA of 203 treatment-naive, hepatitis B e antigen (HBeAg)-negative patients with spontaneous HBs

106 ter variants were more common in hepatitis B e antigen (HBeAg)-negative than in HBeAg-positive patien

107 ucleos(t)ide-naive patients with hepatitis B e antigen (HBeAg)-positive (n = 264) or HBeAg-negative (

108 copies/mL, <57 IU/mL) in 91% of hepatitis B e antigen (HBeAg)-positive and -negative patients by Wee

109 Approximately 30% of hepatitis B e antigen (HBeAg)-positive and 40% of HBeAg-negative cas

110 imen of pegylated interferon for hepatitis B e antigen (HBeAg)-positive and HBeAg-negative chronic he

111 tures were compared between 38 untreated HBV e antigen (HBeAg)-positive children carrying HBsAg-mutan

112 , multicenter, randomized trial, hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) pat

113 nterferon (PEG-IFN) treatment of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) res

114 n nucleoside-naive patients with hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB).

115 limited number of patients with hepatitis B e antigen (HBeAg)-positive chronic hepatitis B respond t

116 to be effective in patients with hepatitis B e antigen (HBeAg)-positive chronic hepatitis B, but its

117 une tolerance, immune clearance [hepatitis B e antigen (HBeAg)-positive chronic hepatitis], inactive

118 s given to all 583 children with hepatitis B e antigen (HBeAg)-positive mothers and to 723 of 1773 ch

119 Patients were hepatitis B e antigen (HBeAg)-positive or HBeAg-negative, with level

120 g relatively higher in initially hepatitis B e antigen (HBeAg)-positive patients (62.5%, 53.4%, 51.5%

121 Hepatitis B e antigen (HBeAg)-positive patients achieved a decline o

122 in 14 patients, including 76% of hepatitis B e antigen (HBeAg)-positive patients but only 10% of HBeA

123 Pretransplant HBV E antigen (HBeAG)-positive patients required more HBIG t

124 Fifty-nine hepatitis B e antigen (HBeAg)-positive patients with genotypic evide

125 benefit of antiviral therapy for hepatitis B e antigen (HBeAg)-positive patients with high viral load

126 using nucleoside regimens and in hepatitis B e antigen (HBeAg)-positive patients.

127 Among hepatitis B e antigen (HBeAg)-positive samples, median titers were 4

128 dy compared rates of spontaneous hepatitis B e antigen (HBeAg)-positive to -negative seroconversion i

129 ruited, of which 43 (61.4%) were hepatitis B e antigen (HBeAg)-positive.

130 Three hundred fifty-six hepatitis B e antigen (HBeAg)-seropositive, hepatitis B surface anti

131 ted nonstructural protein called hepatitis B e antigen (HBeAg).

132 ein is secreted from the cell as hepatitis B e antigen (HBeAg).

133 Maternal hepatitis B e-antigen (HBeAg) and high viral load have been noted to

134 HBV e-antigen (HBeAg), a clinical marker for disease severit

135 ction as assembled capsids; and the sentinel e-antigen (HBeAg), a non-particulate form.

136 vely referred to as core antigen (HBcAg) and e-antigen (HBeAg), share a sequence of 149 residues but

137 the most frequent cause of hepatitis B virus e-antigen (HBeAg)-negative chronic hepatitis B virus (HB

138 years, who were treatment naive, hepatitis B e antigen [HBeAg] negative, anti-hepatitis D antigen [HD

139 ions, HBV viral level, change in hepatitis B e antigen [HBeAg] status, genotype, HBV mutations, nonal

140 the secreted nonparticulate form (hepatitis e antigen [HBeAg]).

141 duals with HBsAg clearance by week 72; 3 HBV e antigen [HBeAg]-positive and 4 HBeAg-negative), 7 matc

142 constructs containing wild-type (hepatitis B e antigen [HBeAg]-positive) and precore mutant (HBeAg-ne

143 ency virus or hepatitis B virus (hepatitis B e antigen [HBeAg]-positive) led the Centers for Disease

144 V-related chronic liver disease (hepatitis B e antigen [HBeAg]-positive, n = 11; HBeAg-negative, n =

145 Hepatitis B virus "e-antigen" (HBeAg) is thought to be a soluble dimeric pr

146 initially positive patients lost hepatitis B e antigen; hepatitis B surface antigen was undetectable

147 hematical models for the role of hepatitis B e-antigen in creating immunological tolerance during hep

148 , however, is incorrect, because recombinant e-antigen is a stable dimer and its apparent monovalency

149 The e-antigen is often considered to be a monomeric protein

150 pproaches for the isolation of the authentic e-antigen, its biological assay, and its stabilization a

151 -2 positions moderately reduced hepatitis B e antigen levels (P < 0.001) to an extent comparable to

152 r HBV DNA levels, lower rates of hepatitis B e antigen loss, increased cirrhosis and liver-related mo

153 t for mechanisms responsible for hepatitis B e-antigen loss, such as seroconversion and virus mutatio

154 IP-10 or CXCL10) and hepatitis B surface and e antigens might induce these defective pDC functions.

155 positive, and of these, 103/140 (73.6%) were e-antigen negative and 118/140 (84.3%) showed an HBV DNA

156 74-0102 and GS-US-174-0103), 375 hepatitis B e antigen-negative (HBeAg(-) ) patients and 266 HBeAg(+)

157 We analyzed data from 347 hepatitis B e antigen-negative and 238 hepatitis B e antigen positiv

158 K-cell phenotype and function in hepatitis B e antigen-negative chronic HBV patients either untreated

159 Hepatitis B e antigen-negative chronic hepatitis B (e-CHB) has been

160 es in noncirrhotic patients with hepatitis B e antigen-negative chronic hepatitis B.

161 ive mothers and 0.04 (CI, 0.001 to 0.24) for e antigen-negative mothers.

162 ctive HBV carriers, or untreated hepatitis B e antigen-negative patients with chronic infections.

163 However, when we evaluated hepatitis B e antigen-negative patients with levels of HBV DNA <2000

164 Among hepatitis B e antigen-negative patients with low viral loads, HCC ri

165 In HBV e antigen-negative patients, a lower baseline plasma HBV

166 continuing antiviral therapy in hepatitis B e antigen-negative patients, monotherapy versus adding a

167 The e antigen-negative variant of HBV associated with the G1

168 x mAbs did not discriminate between core and e-antigen, nor did they discriminate between e-antigen a

169 t's antibody reacted preferentially with the e antigen of the Rh system.

170 lization impaired the upregulation of I-Ad/I-Ed antigens on macrophages from infected mice.

171 higher rates of seroconversion (hepatitis B e antigen or hepatitis B surface antigen) compared to si

172 mutation suppresses but does not abolish the e antigen phenotype.

173 tis B e antigen-negative and 238 hepatitis B e antigen positive patients receiving tenofovir disoprox

174 icantly higher in those who were hepatitis B e antigen positive, suggesting that antiviral therapy th

175 hepatitis B surface antigen and hepatitis B e antigen positive; 4 had cirrhosis.

176 t baseline, 91% of patients were hepatitis B e antigen-positive and 85% had prior exposure to HBV the

177 100 births were 3.37 (CI, 2.08 to 5.14) for e antigen-positive mothers and 0.04 (CI, 0.001 to 0.24)

178 2009 to March 2011, we enrolled hepatitis B e antigen-positive mothers with HBV DNA >6 log10 copies/

179 peripartum antivirals (to 80% of hepatitis B e antigen-positive mothers), and population-wide testing

180 continuing antiviral therapy in hepatitis B e antigen-positive patients who seroconverted from hepat

181 easily detectable in the acute, hepatitis B e antigen-positive phase of infection, suggesting that t

182 s B surface antigen (HBsAg)- and hepatitis B e antigen-positive pregnant women with HBV DNA >/=7.5 lo

183 The management of hepatitis B virus (HBV) e antigen-positive viremic patients with normal liver fu

184 Maternal hepatitis B e antigen positivity but not hepatitis B immunoglobulin

185 n of K562 clones expressing D and G or c and E antigens, respectively.

186 The structure of recombinant e-antigen (rHBeAg) was recently determined, yet to date,

187 with YMDD variants, experienced hepatitis B e antigen seroconversion while on lamivudine therapy or

188 f interferon alfa-2b can achieve hepatitis B e antigen seroconversion, normalization of aminotransfer

189 ggest that in addition to immunoglobulin (Ig)E, antigen-specific IgG also contributes to the pathogen

190 or beta epitope (in a prior nomenclature for e-antigen specificity).

191 A negative e antigen status or a viral load less than 5 x 107 IU/mL

192 markers of HBV disease activity (hepatitis B e antigen status or HBV DNA level) are associated with H

193 HCC risk include their sex, age, hepatitis B e antigen status, HBV genotype, and levels of alanine am

194 based on age, viral levels, and hepatitis B e antigen status, these clinical and biochemical paramet

195 loads less than 5 x 107 IU/mL, regardless of e antigen status.

196 xpressing two configurations of dengue virus E antigen (subviral particles [prME] and soluble E dimer

197 tate its persistence, and use maternal viral e antigen to educate immunity of the offspring to suppor

198 patients who seroconverted from hepatitis B e antigen to hepatitis B e antibody and about the safety

199 her rates of seroconversion from hepatitis B e antigen to hepatitis B e antibody, normalization of al

200 accelerated seroconversion from hepatitis B e antigen to its antibody in black South Africans infect

201 e antigen variants with reduced hepatitis B e antigen translation by a ribosomal leaky scanning mech

202 have identified a novel class of hepatitis B e antigen variants with reduced hepatitis B e antigen tr

203 dimers of the same genotype, and hepatitis B e antigen was quantified from culture medium of transfec

204 Epitope valency of the e-antigen was also studied, using a sandwich SPR assay w

205 so studied, using a sandwich SPR assay where e-antigen was captured with one mAb and probed with a se

206 ore RNA and, consequently, the expression of e antigen were reduced.

207 Both c and E antigens were expressed after transduction of K562 cel

208 The precore RNA codes for the secreted e antigen, while the core RNA codes for the major core p