ライフサイエンスコーパス: HBeAg

1 HBeAg is not required for viral replication but is impli

2 HBeAg loss and seroconversion did not differ between gro

3 HBeAg negativity is thus an ancient HBV infection patter

4 HBeAg seroconversion during childhood predicts a lower r

5 HBeAg seroconversion occurred in 3 patients (5%), all in

6 HBeAg-negative hepatitis subjects carried more A1762T/G1

7 HBeAg-positive immunized children carrying HBsAg-mutant

8 HBeAg-positive patients had higher plasma levels of miR-

9 HBeAg-seropositive vaccine failure HBV-carrier children

10 uently monitored HBV viral load (P < .0001), HBeAg/anti-HBe (P < .00001), HBsAg/anti-HBs (P < .00001)

11 g clearance/loss (RR = 1.9, 95% CI 1.7-3.1), HBeAg seroconversion (RR = 2.1, 95% CI 1.3-3.5), alanine

12 erant phase and were matched for age with 10 HBeAg-positive patients with active disease and 7 HBeAg-

13 Ag loss was observed in five (5%) of the 106 HBeAg-negative patients who entered the TFFU phase, and

14 18 HBeAg-positive patients entered the TFFU phase, of whom

15 t percentages following IFN treatment in 203 HBeAg-positive CHB patients.

16 les, median age 38 years (range: 18-86), 32% HBeAg-positive, median HBV DNA 4.8 log10 IU/ml (undetect

17 copies/mL, respectively, in comparison to 35 HBeAg-positive patients without HBeAg seroconversion (P

18 k 72; 3 HBV e antigen [HBeAg]-positive and 4 HBeAg-negative), 7 matched nonresponders, and 7 healthy

19 3.15), HBV genotype C (hazard ratio = 4.40), HBeAg seroconversion after 18 years of age (hazard ratio

20 HBV DNA undetectability were analyzed in 431 HBeAg-seropositive participants and 1,708 HBeAg-seronega

21 We followed 434 HBeAg-positive chronic HBV-infected patients from a medi

22 genotype (45% genotype D), HBeAg status (47% HBeAg-positive), and duration of lamivudine treatment (m

23 m 62 patients with chronic HBV infection (50 HBeAg positive).

24 DNA suppression (RR = 2.9, 95% CI 1.8-4.6), HBeAg seroconversion (RR = 2.1, 95% CI 1.4-3.3), and hep

25 Wife's HBeAg(+)/HBsAg (+) (AOR = 2.61), HBeAg(-)/HBsAg (+) (AOR = 2.23), positivity of syphilis

26 negative patients were studied: cohort A: 66 HBeAg-negative patients on long-term nucleos(t)ide analo

27 negative patients were studied: Cohort A: 66 HBeAg-negative patients on long-term nucleos(t)ide analo

28 -positive patients with active disease and 7 HBeAg-negative patients with active disease.

29 f nucleos(t)ide-naive patients with CHB (70% HBeAg positive).

30 31 HBeAg-seropositive participants and 1,708 HBeAg-seronegative participants, respectively.

31 We analyzed 803 HBeAg-positive patients treated with PEG-IFN in three gl

32 to reduce severity of liver injury, achieve HBeAg seroconversion, and prevent development of liver f

33 ersus 12 (13%) assigned monotherapy achieved HBeAg seroconversion (P = 0.036).

34 Fifteen patients who achieved HBeAg seroconversion after a mean duration of 19 +/- 14

35 ge of PC, but not BCP, in patients achieving HBeAg seroclearance with HBV DNA < 20,000 IU/mL increase

36 g-mutant HBV may develop hepatitis activity, HBeAg seroconversion, and a low viremic state earlier th

37 (interquartile range 6.14-22.02 years) after HBeAg seroconversion.

38 efore the age of 48 mo and hepatitis B e Ag (HBeAg) seroconversion before the age of 10 y predicted s

39 4.13) and hypertension (OR, 3.27), but also HBeAg positivity (OR, 0.39).

40 essentially structurally identical, although HBeAg from different patients exhibits minor carboxyl-te

41 ncidences of hepatitis B surface antigen and HBeAg seroclearance were 3.2% (n = 5 of 158) and 27.4% (

42 ells, IFN-gamma further suppressed furin and HBeAg expression.

43 for hepatitis B surface antigen (HBsAg) and HBeAg and had high levels of HBV DNA with normal or mini

44 blishment of persistent viral infection, and HBeAg-positive (HBeAg(+)) patients respond less effectiv

45 ants strongly associated with viral load and HBeAg status.

46 ssessing the association between markers and HBeAg seroclearance were calculated using proportional h

47 1 hepatitis B e antigen (HBeAg)-negative and HBeAg-positive patients (129 with HVL) received 48 weeks

48 f alanine aminotransferase normalization and HBeAg seroconversion.

49 ly focus on patients with HBeAg-positive and HBeAg-negative chronic hepatitis, treatment-naive or vir

50 nificantly differ between HBeAg-positive and HBeAg-negative patients.

51 ing and MS results indicated that rHBeAg and HBeAg are essentially structurally identical, although H

52 otential fine differences between rHBeAg and HBeAg, we used these Fabs in microscale immunoaffinity c

53 algorithm selecting HBeAg-positive women and HBeAg-negative women with alanine aminotransferase (ALT)

54 d studied kinetics of hepatitis B e antigen (HBeAg) and hepatitis B surface antigen (HBsAg) levels du

55 eous seroclearance of hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA undetectability a

56 terval [CI] 1.7-3.2), hepatitis B e antigen (HBeAg) clearance/loss (RR = 2.1, 95% CI 1.5-3.1), HBV DN

57 nts were positive for hepatitis B e antigen (HBeAg) in the immune-tolerant phase and were matched for

58 whom, 28.6% were also hepatitis B e antigen (HBeAg) positive.

59 ubjects with maternal hepatitis B e antigen (HBeAg) positivity and who received HBIG off-schedule.

60 Core domains impeding hepatitis B e antigen (HBeAg) production and resembling those observed in HBeAg

61 ir ability to predict hepatitis B e antigen (HBeAg) seroclearance in patients coinfected with human i

62 Their roles in hepatitis B e antigen (HBeAg) seroconversion induced by interferon (IFN) therap

63 ations on spontaneous hepatitis B e antigen (HBeAg) seroconversion, HBV biosynthesis, and the human i

64 enty-two percent were hepatitis B e antigen (HBeAg) seropositive; 20.4% (59/289) had cirrhosis and 10

65 n model included age, gender, HBV e antigen (HBeAg) serostatus, serum levels of HBV DNA, and alanine

66 iRNAs associated with hepatitis B e antigen (HBeAg) status and response to antiviral therapy in patie

67 ad, hepatitis surface (HBsAg) and e antigen (HBeAg) status were obtained at baseline and every 6-12 m

68 were predisposed by maternal HBV e antigen (HBeAg) to support HBV persistence by upregulation of inh

69 were positive for the hepatitis B e antigen (HBeAg) were randomly assigned (2:1) to receive either 25

70 as lack of detectable hepatitis B e antigen (HBeAg) with HBV DNA levels <=1,000 IU/mL 48 weeks after

71 esponse was weaker in hepatitis B e antigen (HBeAg)(+) than HBeAg(-) patients (percent responders: 3%

72 face antigen (HBsAg), hepatitis B e antigen (HBeAg), and cirrhosis.

73 ently associated with hepatitis B e antigen (HBeAg), HAART <2 years, CD4 <200 cells/mm(3), detectable

74 In contrast to hepatitis B e antigen (HBeAg), HBsAg was not a reliable marker of productive sH

75 tis B surface antigen (HBsAg) and e antigen (HBeAg), were tested.

76 ive carrier (IC), and hepatitis B e antigen (HBeAg)-negative (ENEG) hepatitis phases-we performed a s

77 A total of 641 hepatitis B e antigen (HBeAg)-negative and HBeAg-positive patients (129 with HV

78 the difficult-to-cure hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB) is unknown.

79 al of 1,068 Taiwanese hepatitis B e antigen (HBeAg)-negative HBV carriers with serum HBV DNA level <2

80 Hepatitis B e antigen (HBeAg)-negative hepatitis is a clinical indicator of poo

81 are responsive, with hepatitis B e antigen (HBeAg)-negative patients responding better than HBeAg-po

82 Three cohorts of hepatitis B e antigen (HBeAg)-negative patients were studied: cohort A: 66 HBeA

83 Of the 106 hepatitis B e antigen (HBeAg)-negative patients who entered the TFFU phase, 63

84 (HCC) development in hepatitis B e antigen (HBeAg)-negative patients with an HBV DNA level of <2000

85 og (Nuc) treatment in hepatitis B e antigen (HBeAg)-negative patients with chronic hepatitis B virus

86 Hepatitis B e antigen (HBeAg)-positive adults with HBV DNA > 10(7) IU/mL and al

87 compared between 38 untreated HBV e antigen (HBeAg)-positive children carrying HBsAg-mutant HBV (grou

88 er, randomized trial, hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) patients with

89 Patients were hepatitis B e antigen (HBeAg)-positive or HBeAg-negative, with levels of HBV DN

90 y higher in initially hepatitis B e antigen (HBeAg)-positive patients (62.5%, 53.4%, 51.5%) than HBeA

91 Hepatitis B e antigen (HBeAg)-positive patients achieved a decline of 2.2 log I

92 antiviral therapy for hepatitis B e antigen (HBeAg)-positive patients with high viral load and normal

93 which 43 (61.4%) were hepatitis B e antigen (HBeAg)-positive.

94 ree hundred fifty-six hepatitis B e antigen (HBeAg)-seropositive, hepatitis B surface antigen (HBsAg)

95 The circulating hepatitis B e antigen (HBeAg, p17) is known to manipulate host immune responses

96 serology markers, including HBV "e" antigen (HBeAg), HBV surface antigen (HBsAg), and the antibody ag

97 Maternal hepatitis B e-antigen (HBeAg) and high viral load have been noted to be the mos

98 logic suppression and hepatitis B e-antigen (HBeAg) or hepatitis B surface antigen loss or seroconver

99 HBV e-antigen (HBeAg), a clinical marker for disease severity, is a sol

100 transcription and patient HBV early antigen (HBeAg) status.

101 In addition, hepatitis B early antigen (HBeAg)-positive patients had lower 25(OH)D3 serum levels

102 suffering from Hepatitis B envelope Antigen (HBeAg) positive CHB with concurrent HBsAb positivity.

103 rt, 26.0% were hepatitis B envelope antigen (HBeAg) positive, 43.9% had HBV DNA>/=20,000 IU/mL, and 2

104 Hepatitis B envelope antigen (HBeAg) seroconversion represents an endpoint of treatmen

105 were treatment naive, hepatitis B e antigen [HBeAg] negative, anti-hepatitis D antigen [HDAg] positiv

106 HBsAg clearance by week 72; 3 HBV e antigen [HBeAg]-positive and 4 HBeAg-negative), 7 matched nonresp

107 more decline in hepatitis B surface antigen, HBeAg, and HBV DNA (all P < 0.001).

108 Response was defined as HBeAg loss with HBV DNA <200 IU/mL at week 48.

109 HBV viral load as well as HBeAg and HBsAg levels (P < 0.001), but not leukocyte co

110 associated with altered HBV capsid assembly, HBeAg biosynthesis, and reduced human immune responses f

111 The start of immune-clearance phase, age at HBeAg seroconversion, and serum IL-10 and IL-12 levels a

112 The e antigen of hepatitis B (HBeAg) is positively associated with an increased risk o

113 acquired HBV through sexual exposure, to be HBeAg-positive, to have higher HBV DNA levels, and to be

114 1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg serocon

115 valence did not significantly differ between HBeAg-positive and HBeAg-negative patients.

116 gen (HBsAg) were assessed with an SD BIOLINE HBeAg rapid test and HBV DNA quantification was performe

117 HBeAg, none met the primary endpoint of both HBeAg loss AND HBV DNA <= 1,000 IU/mL 48 weeks post-EOT.

118 Here, to further characterize HBeAg, we used phage display to produce a panel of chime

119 regulatory mechanisms, including circulating HBeAg, but without distinct T-cell-based immune signatur

120 Among treated patients, cirrhosis, HBeAg negative at baseline and failure to remain in viro

121 Although one (4%) participant cleared HBeAg, none met the primary endpoint of both HBeAg loss

122 onths, antiviral therapy improved cumulative HBeAg clearance/loss (RR = 1.9, 95% CI 1.7-3.1), HBeAg s

123 The cumulative HBeAg seroconversion rate was significantly lower in the

124 from Europe), HBV genotype (45% genotype D), HBeAg status (47% HBeAg-positive), and duration of lamiv

125 The P135Q mutants displayed decreased HBeAg secretion and HBV capsid molecular weight, while s

126 arrier children were associated with delayed HBeAg seroconversion during long-term follow-up, and mor

127 y were significantly associated with delayed HBeAg seroconversion.

128 patients with low viral loads, 280 developed HBeAg-negative hepatitis, with an annual incidence rate

129 8.76-20.59 years), and 75 subjects developed HBeAg seroconversion after antiviral therapy.

130 ed to elucidate the predictors of developing HBeAg-negative hepatitis in chronic HBV-infected subject

131 ed to delineate the predictors of developing HBeAg-negative hepatitis.

132 result in decline and clearance of HBV DNA, HBeAg, and HBsAg.

133 er induction of ISGs in their livers than do HBeAg(-) patients upon IFN-alpha therapy.

134 ess effectively to IFN-alpha therapy than do HBeAg-negative (HBeAg(-)) patients in clinical practice.

135 The weighted probability of durable HBeAg seroconversion was 91.9% and 88.0% at 12 and 24 mo

136 ate their distinct evolution patterns during HBeAg seroconversion.

137 en with severe inflammation that facilitates HBeAg seroconversion in earlier life.

138 and reduced human immune responses following HBeAg seroconversion.

139 from 2.6 for virologic suppression to 17 for HBeAg seroconversion.

140 re 0.85 (0.80-0.90) and 0.78 (0.73-0.83) for HBeAg seroclearance, and 0.77 (0.72-0.82) and 0.73 (0.70

141 ited a 100 times higher binding affinity for HBeAg (K(d) = 0.4 nM) than the unmodified original aptam

142 describe here an affinity binding assay for HBeAg, which takes advantage of G-quadruplex aptamers fo

143 loped an improved sandwich binding assay for HBeAg.

144 icantly greater (P < .001) than the AUCs for HBeAg (0.81 and 0.89 for HBV DNA >5.3 and 7.3, respectiv

145 nzyme-linked immunosorbent assay (ELISA) for HBeAg quantification, which we compared with commerciall

146 DNA level, was found to be a risk factor for HBeAg-negative hepatitis.

147 ble patients were serologically negative for HBeAg and viral DNA at NA cessation.

148 itis B virus (HBV) DNA who were positive for HBeAg and had normal levels of alanine aminotransferase

149 2 x 10(5) IU/mL, the APASL stopping rule for HBeAg-negative CHB patients with proper off-therapy moni

150 Subsequently, 34 baseline samples from HBeAg-positive patients with chronic hepatitis B were an

151 96A were associated with the transition from HBeAg positive to the negative phase of infection.

152 not found in HBeAg-positive patients who had HBeAg seroconversion without HBsAg clearance.

153 n part 2, participants were required to have HBeAg-positive or HBeAg-negative chronic HBV infection,

154 ral serological markers: HBsAg and anti-HBs, HBeAg and anti-HBe, and anti-HBc IgM and IgG.

155 itative hepatitis B surface antigen (HBsAg), HBeAg levels, HBV genotype, and mutant analysis.

156 ual-shRNA decreased HBV DNA, HBV RNA, HBsAg, HBeAg, and liver fibrosis markers in serum and tissues,

157 A low HBsAg/HBeAg ratio by ccHBV-infected HepG2/NTCP cells was attri

158 Importantly, HBeAg loss, HBeAg seroconversion, and HBsAg loss only oc

159 In HBeAg-negative patients with low viral loads and genotyp

160 In HBeAg-positive patients with chronic HBV infection, high

161 In HBeAg-positive patients, baseline qHBcrAg and qAnti-HBc

162 defined by a Metavir fibrosis score >/= 2 in HBeAg-negative CHB patients that had a hepatitis B virus

163 DeltaqHBcrAg was biphasic in HBeAg-positive patients (-0.051 and -0.011 log10 U/mL/mo

164 kers of continued transcription of cccDNA in HBeAg-negative patients despite marked HBV DNA suppressi

165 kers of continued transcription of cccDNA in HBeAg-negative patients despite marked HBV-DNA suppressi

166 These baseline differences were not found in HBeAg-positive patients who had HBeAg seroconversion wit

167 re predictors of HBeAg-negative hepatitis in HBeAg seroconverters (P < 0.05).

168 , which includes integrations, was higher in HBeAg-negative patients than HBeAg-positive.

169 ssion was 65.4%, being numerically higher in HBeAg-positive than HBeAg-negative patients (76.2% versu

170 a strong predictor of response to PEG-IFN in HBeAg-positive CHB.

171 mma expression in CD3+ CD8+ T lymphocytes in HBeAg-negative subjects compared to the wild-type peptid

172 >18 months, respectively) and monophasic in HBeAg-negative patients.

173 production and resembling those observed in HBeAg-negative human HBV.

174 ar decline in HBV RNA levels was observed in HBeAg-negative patients.

175 suppression may contribute to a reduction in HBeAg/HBsAg biosynthesis.

176 is study aimed to test this stopping rule in HBeAg-negative chronic hepatitis B (CHB) patients treate

177 ges with IFN-induced HBeAg seroconversion in HBeAg-positive CHB patients.

178 nse during polymerase inhibitor treatment in HBeAg-positive patients.

179 0,000 IU/mL) or duration of on-therapy VR in HBeAg-positive patients, but they were significantly hig

180 l responses to HBV, the effect was weaker in HBeAg(+) than HBeAg(-) patients.

181 f PC and BCP mutants can predict IFN-induced HBeAg seroconversion and demonstrate their distinct evol

182 elate their dynamic changes with IFN-induced HBeAg seroconversion in HBeAg-positive CHB patients.

183 Using multivariate analysis, NUC-induced HBeAg seroconversion remained a risk factor of both endp

184 We herein report that the intracellular HBeAg, also known as precore or p22, inhibits the antivi

185 ecular weight, while showing increased 22 kD HBeAg proprotein accumulation in Huh7 cells.

186 birth, length of time in the United Kingdom, HBeAg status, and precore and basal core promoter mutati

187 HBV infection with a detectable viral load, HBeAg seropositivity, and absence of HIV infection.

188 Importantly, HBeAg loss, HBeAg seroconversion, and HBsAg loss only occurred in pa

189 icipants, including the participant who lost HBeAg, and ALT values returned to near baseline levels i

190 Elder age, male, HBeAg, genotype C, and increasing levels of ALT, HBV DNA

191 Having maternal HBeAg positivity is the most important determinant for H

192 ) IU/mL (HBeAg-positive) or 2 x 10(3) IU/mL (HBeAg-negative) and serum alanine aminotransferase conce

193 concentrations of at least 2 x 10(4) IU/mL (HBeAg-positive) or 2 x 10(3) IU/mL (HBeAg-negative) and

194 crAg/qAnti-HBc could be of use in monitoring HBeAg seroclearance.

195 to IFN-alpha therapy than do HBeAg-negative (HBeAg(-)) patients in clinical practice.

196 Analyses of HBeAg in serum samples (concentration ranging from 0.1 t

197 an HBV will allow comparative assessments of HBeAg-mediated HBV pathogenesis, entry, and species barr

198 er-operating characteristic curve (AUROC) of HBeAg-negative, low-replicative (n = 213) and high-repli

199 ession analysis, we found that the chance of HBeAg seroconversion increased by 2.2% (odds ratio [OR]

200 3 cohorts of HBeAg-negative patients were studied: Cohort A: 66 HBeAg

201 ships between HBsAg level and development of HBeAg-negative hepatitis, hepatitis flare, and cirrhosis

202 significant liver histology for diagnosis of HBeAg-negative CHB patients who had indication for liver

203 the function(s) of the intracellular form of HBeAg, previously reported as the precore protein interm

204 f HBV infection, the cumulative incidence of HBeAg seroconversion (P = .0018), and the rate of low se

205 The overall annual incidence of HBeAg-negative hepatitis increased to 2.64% in lamivudin

206 The overall annual incidence of HBeAg-negative hepatitis was 0.37% (95% confidence inter

207 ron for up to 48 weeks rarely led to loss of HBeAg with sustained suppression of HBV DNA levels in ch

208 e HBeAg seroconversion, acting as markers of HBeAg seroconversion (hazard ratios = 2.75 and 4.50; P =

209 Clinical monitoring of HBeAg provides guidance to the treatment of CHB and the

210 couples, and partner's double positivity of HBeAg and HBsAg was the most significant factor of HBV i

211 NA level was the most important predictor of HBeAg seroclearance but serum HBsAg level was the most s

212 eatment was to be the strongest predictor of HBeAg seroconversion, when compared to levels of HBV DNA

213 ion (hazard ratio = 1.42) were predictors of HBeAg-negative hepatitis in HBeAg seroconverters (P < 0.

214 ntigen (HBsAg) levels as well as presence of HBeAg and hepatitis B envelope antibody were measured at

215 edicting the 5- and 10-year probabilities of HBeAg seroclearance and HBV DNA undetectability were 0.8

216 add-on therapy led to a higher proportion of HBeAg response, compared to ETV monotherapy.

217 geographic distribution, high proportion of HBeAg, insufficient awareness of HBV status, and low acc

218 o date, the exact nature and quantitation of HBeAg still remain uncertain.

219 The annual incidence rate of HBeAg-negative hepatitis was lowered to 1.1% in patients

220 uppression than TDF alone, although rates of HBeAg seroconversion and hepatitis B surface antigen los

221 ls <200 IU/mL, the adjusted hazard ratios of HBeAg-negative hepatitis were 2.4 (95% confidence interv

222 DeltaqAnti-HBc was monophasic regardless of HBeAg status.

223 on during childhood predicts a lower risk of HBeAg-negative hepatitis in later life.

224 Sensitivity and specificity of HBeAg were 61.8% and 99.2% for HBV DNA >5.3 log10 IU/mL

225 e used in the pretreatment stratification of HBeAg-negative patients chronically infected by genotype

226 patients achieved HBsAg loss, a subgroup of HBeAg-negative patients can achieve a low-replicative st

227 significant liver fibrosis for treatment of HBeAg-negative CHB patients that had indication for live

228 Validities of HBeAg and of the algorithm to identify HBV DNA >2 thresh

229 The impact of the most prevalent mutant on HBeAg biosynthesis was assessed by Western blotting and

230 One hundred and one HBeAg-negative patients (92% genotype D) with compensate

231 nly), and HBV infection (+HBsAg, HBV DNA, or HBeAg).

232 ants were required to have HBeAg-positive or HBeAg-negative chronic HBV infection, with serum HBV DNA

233 re hepatitis B e antigen (HBeAg)-positive or HBeAg-negative, with levels of HBV DNA >/=3 log10 IU/mL

234 sistent viral infection, and HBeAg-positive (HBeAg(+)) patients respond less effectively to IFN-alpha

235 important host and virus factors can predict HBeAg seroclearance and HBV DNA undetectability.

236 levels and established models for predicting HBeAg seroclearance and HBV DNA undetectability.

237 or treatment might be helpful for predicting HBeAg seroconversion.

238 offs with the highest accuracy in predicting HBeAg seroclearance at 36 months were qHBcrAg <6.5 log10

239 cificity (Sp) of marker levels in predicting HBeAg seroclearance were assessed using time-dependent r

240 cale immunoaffinity chromatography to purify HBeAg from individual patient plasmas.

241 l <1,500 IU/mL at week 12 achieved response (HBeAg loss with HBV DNA <2,000 IU/mL at 6 months posttre

242 mtricitabine) and with undetectable HIV RNA, HBeAg, CD4 <200 mm(3), and reporting <95% adherence rema

243 is an important factor driving CHB patient's HBeAg status.

244 Wife's HBeAg(+)/HBsAg (+) (AOR = 2.61), HBeAg(-)/HBsAg (+) (AOR

245 cytosolic p22 protein, but not the secreted HBeAg, significantly reduces interferon-stimulated respo

246 uates the validity of an algorithm selecting HBeAg-positive women and HBeAg-negative women with alani

247 Spontaneous HBeAg seroclearance and HBV DNA undetectability were ana

248 Spontaneous HBeAg seroconversion occurred in 359 subjects at a media

249 ng the inflammatory phase before spontaneous HBeAg seroconversion.

250 ism were associated with earlier spontaneous HBeAg seroconversion.

251 onfidence internal 0.35-0.39) in spontaneous HBeAg seroconverters.

252 A total of 2165 Taiwanese HBeAg-negative noncirrhotic patients were followed for 1

253 positive patients (62.5%, 53.4%, 51.5%) than HBeAg-negative patients (43.7%, 31.3%, 30.1%) (P = 0.064

254 Ag)-negative patients responding better than HBeAg-positive patients.

255 HBV, the effect was weaker in HBeAg(+) than HBeAg(-) patients.

256 ker in hepatitis B e antigen (HBeAg)(+) than HBeAg(-) patients (percent responders: 3% vs 23%; P = .0

257 atients had lower 25(OH)D3 serum levels than HBeAg-negative patients (P = 0.0013).

258 , was higher in HBeAg-negative patients than HBeAg-positive.

259 ng numerically higher in HBeAg-positive than HBeAg-negative patients (76.2% versus 56.7%, P = 0.130).

260 ncing and in situ hybridization suggest that HBeAg-negative shrew HBVs cause intense hepatotropic mon

261 ALT) level, the maximal ALT level during the HBeAg-positive phase of HBV infection, the cumulative in

262 Peripheral MAIT cells of patients in the HBeAg-negative phase were least activated.

263 f integration of intrahepatic HBV DNA in the HBeAg-negative stage may be higher than previously antic

264 ent with the hypothesis that mutation of the HBeAg open reading frame is an important factor driving

265 In line with this, HBeAg(+) patients exhibit weaker induction of ISGs in th

266 -5p, miR-193b-3p, and miR-194-5p compared to HBeAg-negative patients, and levels of these miRNAs were

267 tio = 2.46), and lamivudine therapy prior to HBeAg seroconversion (hazard ratio = 1.42) were predicto

268 An algorithm using HBeAg and ALT level could be an effective strategy to id

269 ring patients who were HBeAg-positive versus HBeAg-negative, were genotype B versus C, and had detect

270 e but HBsAg negative at week 60; another was HBeAg negative but HBsAg positive at week 72, which were

271 One child was HBeAg positive but HBsAg negative at week 60; another wa

272 The primary endpoint was HBeAg loss and HBV DNA <= 1,000 IU/mL 48 weeks after end

273 (17.9%) were HBeAg positive, 47 (9.1%) were HBeAg negative with ALT >=40 IU/L, and 144 (28.0%) had a

274 /mL (range, 4.11-10.06), and 49 (20.4%) were HBeAg-positive.

275 en, median age was 29 years, 92 (17.9%) were HBeAg positive, 47 (9.1%) were HBeAg negative with ALT >

276 d with HBV genotypes B and C (93%), 99% were HBeAg positive with a mean baseline level of HBV DNA of

277 rence found when comparing patients who were HBeAg-positive versus HBeAg-negative, were genotype B ve

278 a decline of 2.2 log IU/mL in HBsAg, whereas HBeAg-negative patients only achieved a decline of 0.6 l

279 verified with seroconversion panels, the WHO HBeAg standard, rHBeAg, and patient plasma samples.

280 Comparing HBeA-positive (67/133, 50%) with HBeAg-negative subjects, 64/67 (96%) vs 35/66 (55%) show

281 Ag and qAnti-HBc levels were associated with HBeAg seroclearance (adjusted HR, 0.48/log10 U/mL [95% c

282 percentage was significantly associated with HBeAg seroconversion with HBV DNA < 2,000 IU/mL (OR = 1.

283 g the inflammatory phase was associated with HBeAg seroconversion.

284 e identified miRNAs that are associated with HBeAg status, levels of HBV DNA and HBsAg, and treatment

285 Interestingly, patients with HBeAg seroconversion who had a high PC mutant percentage

286 n 105 centres in 17 countries, patients with HBeAg-negative chronic HBV were randomly assigned (2:1)

287 In patients with HBeAg-negative chronic HBV, the efficacy of tenofovir al

288 and safety of the two drugs in patients with HBeAg-negative chronic hepatitis B virus (HBV) infection

289 higher chances of off-NA VR in patients with HBeAg-negative chronic hepatitis B.

290 cure should initially focus on patients with HBeAg-positive and HBeAg-negative chronic hepatitis, tre

291 and safety of the two drugs in patients with HBeAg-positive chronic hepatitis B virus (HBV) infection

292 In patients with HBeAg-positive HBV infection, tenofovir alafenamide was

293 monitored in the management of patients with HBeAg-seronegative chronic hepatitis B.

294 altered polarization upon restimulation with HBeAg.

295 ey were significantly higher in studies with HBeAg-negative patients and on-therapy VR > 24 than </=

296 le patients were aged at least 18 years with HBeAg-negative chronic HBV infection (with plasma HBV DN

297 also evaluated in subjects with and without HBeAg-negative hepatitis.

298 arison to 35 HBeAg-positive patients without HBeAg seroconversion (P < 0.001 for months 3 and 6).

299 A2131C HBV gene mutations than those without HBeAg-negative hepatitis.

300 ned a risk factor of both endpoints in young HBeAg seroconverters.