ライフサイエンスコーパス: HBeAg

1 HBeAg appears to be critical in determining the outcome

2 HBeAg is not required for viral replication but is impli

3 HBeAg loss and seroconversion did not differ between gro

4 HBeAg seroconversion during childhood predicts a lower r

5 HBeAg seroconversion may not always confer favorable out

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

7 HBeAg-negative hepatitis subjects carried more A1762T/G1

8 HBeAg-negative patients who cleared HBsAg had lower base

9 HBeAg-positive immunized children carrying HBsAg-mutant

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

11 HBeAg-seropositive vaccine failure HBV-carrier children

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

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

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

15 atitis B e antigen [HBeAg]-positive, n = 11; HBeAg-negative, n = 29) were virologically characterized

16 performed on 20 chronically HBV-infected (15 HBeAg-positive and 5 HBeAg-negative) patients to assess

17 Out of 16 HBeAg-negative patients with undetectable HBV DNA levels

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

19 We studied 205 HBeAg-positive patients who were treated with PEG-IFN (s

20 TLR9 gene polymorphisms were assessed in 278 HBeAg-positive, chronic HBV-infected patients.

21 Five HBeAg-positive patients (8%) and 3 HBeAg-negative patients (8%) cleared HBsAg.

22 d a cohort observational study, following 33 HBeAg-negative patients with CHB, undetectable serum HBV

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

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

25 3.15), HBV genotype C (hazard ratio = 4.40), HBeAg seroconversion after 18 years of age (hazard ratio

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

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

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

29 ically HBV-infected (15 HBeAg-positive and 5 HBeAg-negative) patients to assess liver inflammation/fi

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

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

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

33 A total of 688 HBeAg-negative patients with baseline serum HBV DNA leve

34 All 7 HBeAg-positive patients with undetectable HBV DNA levels

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

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

37 31 HBeAg-seropositive participants and 1,708 HBeAg-seronegative participants, respectively.

38 Year 4 with rates of ALT normalization 71%, HBeAg seroconversion 57%, and cumulative resistance 0%.

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

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

41 Patients with WT were more likely to achieve HBeAg loss with HBV DNA <10,000 copies/mL (response, 34

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

43 Among WT patients who achieved HBeAg clearance at week 78, 78% had undetectable HBV DNA

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

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

46 In patients achieving HBeAg seroconversion before 30 years of age, NUC-induced

47 For patients achieving HBeAg seroconversion before 30 years of age, the risk of

48 s seroconverters were younger when achieving HBeAg seroconversion.

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

50 impact on the immune active hepatitis after HBeAg seroconversion.

51 Serum HBV-DNA levels at 1 year after HBeAg seroconversion were determined, and their correlat

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

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

54 4.13) and hypertension (OR, 3.27), but also HBeAg positivity (OR, 0.39).

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

56 Among HBeAg-positive patients, a greater proportion given comb

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

58 Screening pregnant women for HBsAg and HBeAg might control mother-to-infant transmission of HBV

59 Rates of HBeAg loss and HBeAg seroconversion were comparable between groups, whe

60 1 hepatitis B e antigen (HBeAg)-negative and HBeAg-positive patients (129 with HVL) received 48 weeks

61 f alanine aminotransferase normalization and HBeAg seroconversion.

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

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

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

65 ontaneous hepatitis B virus (HBV) e antigen (HBeAg) and hepatitis B s antigen (HBsAg) seroconversion

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

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

68 nd the suppression of hepatitis B e antigen (HBeAg) and surface antigen (HBsAg) biosynthesis.

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

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

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

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

73 9.4% vs 0%; P = .03), hepatitis B e antigen (HBeAg) seroconversion (61.5% vs 25.0%, P = .03), and dev

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

75 It is unclear whether hepatitis B e antigen (HBeAg) seroconversion induced by nucleos(t)ide analogues

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

77 In spontaneous hepatitis B e antigen (HBeAg) seroconverters, lower serum HBsAg and HBV DNA lev

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

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

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

81 Hepatitis B e antigen (HBeAg) status and serum hepatitis B virus (HBV) DNA leve

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

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

84 Circulating hepatitis B e antigen (HBeAg) was found to distinguish the group of patients no

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

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

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

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

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

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

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

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

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

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

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

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

97 analogue therapy for hepatitis B e antigen (HBeAg)-negative patients with chronic hepatitis B (CHB).

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

99 203 treatment-naive, hepatitis B e antigen (HBeAg)-negative patients with spontaneous HBsAg seroclea

100 e-naive patients with hepatitis B e antigen (HBeAg)-positive (n = 264) or HBeAg-negative (n = 115) CH

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

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

103 PEG-IFN) treatment of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) results in HBe

104 all 583 children with hepatitis B e antigen (HBeAg)-positive mothers and to 723 of 1773 children with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 hronic liver disease (hepatitis B e antigen [HBeAg]-positive, n = 11; HBeAg-negative, n = 29) were vi

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

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

122 Response was defined as HBeAg loss with the appearance of antibodies to hepatiti

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

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

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

126 ed these 2 cohorts according to their age at HBeAg seroconversion.

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

128 1896A were the most prevalent mutants before HBeAg seroconversion, acting as markers of HBeAg serocon

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

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

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

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

133 The cumulative HBeAg seroconversion rate was significantly lower in the

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

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

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

137 y were significantly associated with delayed HBeAg seroconversion.

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

139 8.76-20.59 years), and 75 subjects developed HBeAg seroconversion after antiviral therapy.

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

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

142 atients with WT had higher baseline HBV DNA, HBeAg, and HBsAg levels than patients with non-WT.

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

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

145 ate their distinct evolution patterns during HBeAg seroconversion.

146 at TLR9 rs5743836 promoter predicted earlier HBeAg seroconversion (hazard ratios [HRs], 2.45 and 3.65

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

148 Five HBeAg-positive patients (8%) and 3 HBeAg-negative patien

149 and reduced human immune responses following HBeAg seroconversion.

150 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

151 nnual incidence rates were 4.4% and 1.9% for HBeAg-negative hepatitis and hepatitis flare, respective

152 6 and 12 correlated with CD4 cell count for HBeAg-positive patients.

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

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

155 th HBV DNA <10,000 copies/mL) to PEG-IFN for HBeAg-positive CHB.

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

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

158 2 x 10(5) IU/mL, the APASL stopping rule for HBeAg-negative CHB patients with proper off-therapy moni

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

160 1 and PD-L1 mRNA levels in liver tissue from HBeAg-positive patients.

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

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

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

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

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

166 experience acute exacerbations of hepatitis, HBeAg seroconversion, lamivudine resistance, and liver d

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

168 In HBeAg-negative patients with CHB, it is safe and effecti

169 In HBeAg-negative patients with HBV genotype B or C infecti

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

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

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

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

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

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

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

177 s known about their impacts on HBsAg loss in HBeAg-negative patients with limited viral replication.

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

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

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

181 ositive chronic hepatitis B (CHB) results in HBeAg loss in 30% of patients, but clearance of hepatiti

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

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

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

185 0,000 IU/mL) or duration of on-therapy VR in HBeAg-positive patients, but they were significantly hig

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

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

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

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

190 NUC-induced HBeAg seroconverters may not have durable response after

191 A total of 148 noncirrhotic NUC-induced HBeAg seroconverters were consecutively enrolled.

192 of follow-up for spontaneous and NUC-induced HBeAg seroconverters, respectively.

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

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

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

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

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

198 were compared with 203 age- and sex-matched HBeAg-negative controls.

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

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

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

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

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

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

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

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

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

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

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

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

214 associated with an increased probability of HBeAg seroconversion during long-term follow-up (adjuste

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

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

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

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

219 Rates of HBeAg loss and HBeAg seroconversion were comparable betw

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

221 We compared the rates of HBeAg seroreversion and HBV reactivation between these 2

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

223 nversion before 30 years of age, the risk of HBeAg seroreversion and HBV reactivation is higher in NU

224 oconversion correlate with increased risk of HBeAg-negative hepatitis and hepatitis flare.

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

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

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

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

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

230 is B e antigen (HBeAg)-positive (n = 264) or HBeAg-negative (n = 115) CHB.

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

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

233 HBV-DNA levels >/=2000 IU/mL at 1 year post HBeAg seroconversion correlate with increased risk of HB

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

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

236 or treatment might be helpful for predicting HBeAg seroconversion.

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

238 down in HepG2.2.15 cells also down-regulated HBeAg and HBsAg biosynthesis.

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

240 baseline is a strong predictor of response (HBeAg loss with HBV DNA <10,000 copies/mL) to PEG-IFN fo

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

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

243 Spontaneous HBeAg seroclearance and HBV DNA undetectability were ana

244 Spontaneous HBeAg seroconversion occurred in 359 subjects at a media

245 A total of 390 spontaneous HBeAg seroconverters with a long-term follow-up were enr

246 load on long-term outcomes after spontaneous HBeAg seroconversion remains unclear.

247 ng the inflammatory phase before spontaneous HBeAg seroconversion.

248 subjects, 204 (73.4%) developed spontaneous HBeAg seroconversion, 21 (7.6%) developed spontaneous HB

249 ism were associated with earlier spontaneous HBeAg seroconversion.

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

251 ical control of 407 noncirrhotic spontaneous HBeAg seroconverters was also recruited.

252 nosis that is similar to that of spontaneous HBeAg seroconversion.

253 NUC-induced seroconverters than spontaneous HBeAg seroconverters.

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

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

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

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

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

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

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

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

262 ed to a significant decrease in HBsAg in the HBeAg-positive population.

263 en (anti-HBe) at the end of PEG-IFN therapy (HBeAg seroconversion), along with HBeAg seroconversion a

264 rapy could provide an incremental benefit to HBeAg-positive patients with baseline levels of HBV DNA

265 Administration of HBIG to infants born to HBeAg-negative mothers did not appear to reduce the rate

266 29%; P = .65) were noted in children born to HBeAg-negative mothers who were or were not given HBIG.

267 Children born to HBeAg-positive mothers are at greatest risk for chronic

268 -5p, miR-193b-3p, and miR-194-5p compared to HBeAg-negative patients, and levels of these miRNAs were

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

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

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

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

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

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

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

276 N therapy (HBeAg seroconversion), along with HBeAg seroconversion and hepatitis B surface antigen cle

277 B genotype was significantly associated with HBeAg seroconversion at the end of treatment (P < .001);

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

279 g the inflammatory phase was associated with HBeAg seroconversion.

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

281 NA levels were independently associated with HBeAg-negative hepatitis flare, which confirmed their im

282 16.76%) and HBsAg (9.26%) than children with HBeAg-negative mothers (1.58% and 0.29%, respectively; P

283 ive mothers and to 723 of 1773 children with HBeAg-negative mothers.

284 ficantly greater percentage of children with HBeAg-positive mothers tested positive for antibodies ag

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

291 rologic response to PEG-IFN in patients with HBeAg-positive chronic hepatitis B.

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 C-induced seroconverters had a higher 2-year HBeAg seroreversion rate than spontaneous seroconverters

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