ライフサイエンスコーパス: HBsAg

1 HBsAg loss has been suggested to be higher in non-endemi

2 HBsAg loss was observed in five (5%) of the 106 HBeAg-ne

3 HBsAg screening was accepted by 5980 (weighted estimate

4 HBsAg was detected in 495 (8.8%, 7.9-9.7) individuals in

5 HBsAg+ prevalence was 0.4% (95% CI, 0.3%-0.5%) in the ge

6 HBsAg-negative, anti-HBc-positive patients had a high ra

7 HBsAg-negative, anti-HBc-positive patients with undetect

8 HBsAg-positive individuals were invited for a comprehens

9 HBsAg-positive women have HBV-DNA load measured.

10 HBsAg-specific antibody-secreting cells (ASCs) response

11 ad (P < .0001), HBeAg/anti-HBe (P < .00001), HBsAg/anti-HBs (P < .00001) than hepatologists but scree

12 alence range, 1.6%-47.5%) and occurred at 11 HBsAg amino acid positions, including 172 and 182, which

13 completed in the alert group compared to 177 HBsAg tests in the control group (p < 0.0001; OR = 2.3;

14 epatitis B surface antigen (HBsAg), with 20% HBsAg loss after long-term follow-up.

15 For both cohorts combined, 389 HBsAg tests were completed in the alert group compared t

16 in the communities, with 402 (81.3%) of 495 HBsAg-positive individuals attending the clinic.

17 For the 515 HBsAg-positive women, median age was 29 years, 92 (17.9%

18 However, only 300 (41.6%) of 721 HBsAg-positive people screened at the blood bank linked

19 A total of 840 HBsAg positive samples was collected and tested for HBV

20 HBcAb+ (33%), HCV+ (18%), liver biopsy (9%), HBsAg+ (6%), neoplastic (6%), or infective risk (5%).Mos

21 Three doses of aluminium-absorbed HBsAg were delivered at 0, 14, and 28days.

22 her investigated as a strategy to accelerate HBsAg loss.

23 Although few patients achieved HBsAg loss, a subgroup of HBeAg-negative patients can ac

24 ients on long-term NA treatment who achieved HBsAg loss and in whom treatment was withdrawn.

25 ients on long-term NA treatment who achieved HBsAg loss and in whom treatment was withdrawn.

26 BsAg-positive compared to those who achieved HBsAg seroclearance (5.5 versus 5.2 kPa, respectively; P

27 Among adult HBsAg carriers, 42% had antibodies to hepatitis delta vi

28 01 administered with hepatitis B surface Ag (HBsAg).

29 ce antigen (HBsAg), and the antibody against HBsAg (anti-HBs).

30 sly described CD4(+) T-cell immunity against HBsAg and polymerase in chimpanzees after vaccination an

31 achieved the primary endpoint and were also HBsAg negative and anti-hepatitis B surface antigen anti

32 Among HBsAg-negative participants, anti-HBc seroprevalence inc

33 o for anti-hepatitis D virus detection among HBsAg-positive patients with liver fibrosis or hepatocel

34 tudies of hepatitis D virus prevalence among HBsAg-positive populations in sub-Saharan Africa.

35 sh the prevalence of hepatitis D virus among HBsAg-positive populations in sub-Saharan Africa.

36 may be considered in pregnant women with an HBsAg level above 4-4.5 log10 IU/mL to interrupt mother-

37 rystal structure of one of the bNAbs with an HBsAg peptide epitope revealed a stabilized hairpin loop

38 g to below 1 IU/mL (P < .001 vs control) and HBsAg seroconversion (P = .046 vs control).

39 mous separation of hepatitis B viral DNA and HBsAg concentrations occurs during the natural history a

40 d, as revealed by the absence of HBV DNA and HBsAg in serum.

41 hese miRNAs were associated with HBV DNA and HBsAg levels.

42 ted with HBeAg status, levels of HBV DNA and HBsAg, and treatment response in CHB patients.

43 NA level of 300 IU/mL predicts HBV flare and HBsAg seroclearance after anti-HCV therapy.

44 her enhanced the prediction of HBV flare and HBsAg seroclearance.

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

46 and partner's double positivity of HBeAg and HBsAg was the most significant factor of HBV infection i

47 tis B surface antigen (HBsAg) (anti-HBs) and HBsAg-specific T-cell responses were analyzed.

48 nificantly increased rates of HBsAg loss and HBsAg seroconversion during therapy and functional cure

49 p were present in extracellular vesicles and HBsAg particles derived from hepatoma cells.

50 As are present in extracellular vesicles and HBsAg particles secreted by hepatoma cells.

51 d chimpanzees with protective levels of anti-HBsAg antibodies were rechallenged with HBV after antibo

52 terilizing immunity in individuals with anti-HBsAg antibodies and are consistent with translation of

53 ble data on prevalence of IDU, HIV antibody, HBsAg, and HCV antibody among PWID were selected and, wh

54 n-overlapping epitopes on the HBV S antigen (HBsAg).

55 2000 IU/mL) and hepatitis B surface antigen (HBsAg) (<1000 IU/mL) have been shown to distinguish inac

56 betes comparing hepatitis B surface antigen (HBsAg) (+) to HBsAg (-) participants was 1.17 (95% CI 1.

57 of antibody to hepatitis B surface antigen (HBsAg) (anti-HBs) and HBsAg-specific T-cell responses we

58 kers, including hepatitis B surface antigen (HBsAg) and e antigen (HBeAg), were tested.

59 re positive for hepatitis B surface antigen (HBsAg) and HBeAg and had high levels of HBV DNA with nor

60 ceptor signaling by the HBV surface antigen (HBsAg) attenuates immune responses to facilitate chronic

61 )-seropositive, hepatitis B surface antigen (HBsAg) carrier children, who were followed for at least

62 habitation with hepatitis B surface antigen (HBsAg) carriers, intravenous drug use, and homosexual/bi

63 B viral DNA and hepatitis B surface antigen (HBsAg) concentrations occurs during the natural history

64 o had available hepatitis B surface antigen (HBsAg) data, 123 patients positive for HBsAg who were no

65 (HDV) requires hepatitis B surface antigen (HBsAg) for its assembly and release.

66 ed clearance of hepatitis B surface antigen (HBsAg) from the circulation of chronically infected pati

67 om a single CSP-hepatitis B surface antigen (HBsAg) fusion protein, and this leads to a vaccine compo

68 verse transcriptase and HBV surface antigen (HBsAg) heterogeneity in patients with acute HBV infectio

69 ance pattern of hepatitis B surface antigen (HBsAg) in chronic hepatitis B virus (HBV) infections of

70 e reductions in hepatitis B surface antigen (HBsAg) in control and experimental groups over the first

71 ugh very little hepatitis B surface antigen (HBsAg) is produced.

72 , correlating with high HBV surface antigen (HBsAg) levels.

73 roconversion or hepatitis B surface antigen (HBsAg) loss.

74 r vesicles, and hepatitis B surface antigen (HBsAg) particles of hepatoma cell lines.

75 A total of 42 hepatitis B surface antigen (HBsAg) positive, human immunodeficiency virus and hepati

76 for cancer development and surface antigen (HBsAg) production, but methods to quantify integrations

77 reening using a hepatitis B surface antigen (HBsAg) rapid test and subsequent HBV antiviral therapy v

78 The log-reduction (LR) of surface antigen (HBsAg) reached a maximum value of 1.86 +/- 0.20 (98.6% r

79 ia were offered hepatitis B surface antigen (HBsAg) screening via a point-of-care test.

80 lative rates of hepatitis B surface antigen (HBsAg) seroclearance were 90% and 95% at 1 and 5 years,

81 of normal, and hepatitis B surface antigen (HBsAg) seroclearance.

82 ith hepatitis B virus (HBV) surface antigen (HBsAg) sometimes develop humoral and cellular immunity t

83 tive results on hepatitis B surface antigen (HBsAg) testing and had an undetectable HBV viral load, a

84 t yet completed hepatitis B surface antigen (HBsAg) testing were identified by a novel EHR-based popu

85 ore antibody (anti-HBc) and surface antigen (HBsAg) tests and 47,618 adults who completed HBV surface

86 Using quantitative maternal surface antigen (HBsAg) to predict HBV infection in infants has not been

87 ed to determine hepatitis B surface antigen (HBsAg) turnover rates in chronic hepatitis B (CHB) patie

88 of mice against hepatitis B surface antigen (HBsAg) using a novel real-time controlled jet injector w

89 rum gradient of hepatitis B surface antigen (HBsAg) varies over time after cessation of nucleos(t)ide

90 d prevalence of hepatitis B surface antigen (HBsAg) was 0.36% overall and 3.4% in non-Hispanic Asians

91 ive samples for hepatitis B surface antigen (HBsAg) were assessed with an SD BIOLINE HBeAg rapid test

92 lin G (IgG) and Hepatitis B surface Antigen (HBsAg) were quantitatively analyzed with good reliabilit

93 BV "e" antigen (HBeAg), HBV surface antigen (HBsAg), and the antibody against HBsAg (anti-HBs).

94 rkers including hepatitis B surface antigen (HBsAg), anti-hepatitis B core antibody (anti-HBc), antib

95 were tested for hepatitis B surface antigen (HBsAg), antibody to hepatitis B core antigen (anti-HBc),

96 ing hepatitis B virus (HBV) surface antigen (HBsAg), enhancing the restoration of functional control

97 identified all hepatitis B surface antigen (HBsAg), HBV DNA, and alanine aminotransferase results ob

98 HBV by 3 tests-hepatitis B surface antigen (HBsAg), hepatitis B core antibody (anti-HBc) total immun

99 HBV infection; hepatitis B surface antigen (HBsAg), indicative of chronic (current) infection; and a

100 ts positive for hepatitis B surface antigen (HBsAg), infected with HBV genotypes B or C, and without

101 cy virus (HIV), hepatitis B surface antigen (HBsAg), prevalent hepatic decompensation (HD), hepatocel

102 uent decline in hepatitis B surface antigen (HBsAg), with 20% HBsAg loss after long-term follow-up.

103 reactivation in hepatitis B surface antigen (HBsAg)-negative, antibody to hepatitis B core antigen (a

104 Among HBV surface antigen (HBsAg)-positive HCC cases, 18/66 (27%) were HIV-infected

105 study of 2,562 hepatitis B surface antigen (HBsAg)-positive individuals was conducted to determine t

106 s (HBV) DNA for hepatitis B surface antigen (HBsAg)-positive participants, and antibodies to hepatiti

107 reactivation in hepatitis B surface antigen (HBsAg)-positive patients receiving rituximab-based B-cel

108 treatment, were hepatitis B surface antigen (HBsAg)-positive with hepatitis B virus (HBV) DNA concent

109 nation of hepatitis B virus surface antigen (HBsAg).

110 pression of the hepatitis B surface antigen (HBsAg).

111 re screened for hepatitis B surface antigen (HBsAg).

112 valence of both hepatitis B surface antigen (HBsAg; prevalence of HBV infection) and antibody to hepa

113 ve HBV infection (serum HBV surface antigen; HBsAg), and vaccine-induced HBV immunity (antibody again

114 annon entropy, higher genetic variability at HBsAg amino acid positions 130, 133, and 157 significant

115 Eight occurred in patients known to be HBsAg-positive, and 1 occurred in a patient known to be

116 The ratio between HBsAg and HBV DNA levels in serum correlated with the in

117 The efficacy of blocking HBsAg and HDV production were 98.2 [94.5-99.9]% and 99.7

118 In conclusion, both HBsAg production and HDV replication are effectively inh

119 ve for total anti-HBc, but negative for both HBsAg and anti-HBs, are referred to as anti-HBc alone.

120 -Ca is accompanied by rapid declines in both HBsAg and HDV RNA.

121 e at week 60; another was HBeAg negative but HBsAg positive at week 72, which were their last clinic

122 One child was HBeAg positive but HBsAg negative at week 60; another was HBeAg negative bu

123 terleukin 2, and interleukin 4 production by HBsAg-specific T cells was detected.

124 sgenic mice that are depleted of circulating HBsAg, via either spontaneous seroconversion or therapeu

125 summary, our results reveal that circulating HBsAg clearance does not improve HBV-specific CD8+ T cel

126 ms the predictability of a one-time combined HBsAg and HBV DNA measurement for future inactive carrie

127 hazard ratio for incident diabetes comparing HBsAg (+) to HbsAg (-) participants was 1.23 (95% CI 1.0

128 Primary outcome of interest comprised HBsAg positivity in couples (both positive: F+M+, only w

129 n genes and recognize various conformational HBsAg epitopes.

130 f combination therapy and virologic control (HBsAg positive, HBV DNA below 2000 IU/mL, normal level o

131 lanine aminotransferase) or functional cure (HBsAg below 0.05 IU/mL, HBV DNA target not detected, nor

132 of phase 3 trials should be functional cure; HBsAg loss in >=30% of patients was suggested as an acce

133 comprehensive measures are needed to detect HBsAg positive patients.NIH Trial Registry Number: NCT04

134 viremia 16 months post-LT without detectable HBsAg.

135 Baseline levels of HBV DNA, HBsAg, and HBcrAg were determined retrospectively and pa

136 serological/virological biomarkers (HBV DNA, HBsAg, HBcrAg, and HBV RNA) were measured in sequential

137 serological/virological biomarkers (HBV DNA, HBsAg, HBcrAg, HBV RNA) were measured in sequential samp

138 tion for chronic hepatitis B, with a durable HBsAg seroclearance rate of 92%, an undetectable HBV DNA

139 Both patients with either HBsAg positivity or viremia had recurrent hepatocellular

140 d rate ratio of 6.97 (95% CI, 5.21-9.33) for HBsAg seroclearance.

141 ne anti-HDV testing should be considered for HBsAg carriers.

142 ction of 1.6 ng/mL for IgG and 1.3 ng/mL for HBsAg were achieved, which were comparable to commercial

143 , 85%, 88%, 87.0%, and 92% were negative for HBsAg, respectively, and 95%, 99%, 100%, and 100% had un

144 The highest LR rate observed for HBsAg was 4.66 +/- 0.19 h(-1) and for HBcAg 0.10 +/- 0.0

145 rom the samples tested, 4% were positive for HBsAg (95% CI 2.7-4.7), 20% were positive for anti-HBc (

146 igen (HBsAg) data, 123 patients positive for HBsAg who were not receiving anti-HBV prophylaxis were e

147 patients remained persistently positive for HBsAg, all of whom had undetectable HBV DNA.

148 trategy: All pregnant women are screened for HBsAg.

149 trategy: All pregnant women are screened for HBsAg.

150 specific to the viral surface glycoproteins (HBsAg) from memory B cells of HBV vaccinees and controll

151 Of these seven patients, none had HBsAg loss or HBV DNA of less than 2000 IU/mL and one (1

152 Six patients had HBsAg levels less than 50 IU/mL by the end of treatment

153 s titres were restricted to patients who had HBsAg levels of less than <1 IU/mL before the introducti

154 Wife's HBeAg(+)/HBsAg (+) (AOR = 2.61), HBeAg(-)/HBsAg (+) (AOR = 2.23),

155 's HBeAg(+)/HBsAg (+) (AOR = 2.61), HBeAg(-)/HBsAg (+) (AOR = 2.23), positivity of syphilis (AOR = 1.

156 n contrast to hepatitis B e antigen (HBeAg), HBsAg was not a reliable marker of productive sHBV infec

157 Findings of chronic HBV (HBsAg-positive) or past HBV (HBsAg-negative and anti-HBc

158 of chronic HBV (HBsAg-positive) or past HBV (HBsAg-negative and anti-HBc-positive) infection require

159 e or refer all patients identified with HBV (HBsAg-positive) for posttest counseling and hepatitis B-

160 e used mathematical modeling to estimate HDV-HBsAg-host parameters and to elucidate the mode of actio

161 ated DNA may explain the persistence of high HBsAg serum levels in patients with low HBV DNA levels.

162 mptoms), correlated with initial decrease in HBsAg, and normalized during therapy and follow-up.

163 s of patients in NAP groups had decreases in HBsAg to below 1 IU/mL (P < .001 vs control) and HBsAg s

164 otal, 8299 API were found to be deficient in HBsAg completion at baseline within our health system.

165 es to hepatitis B core antigen (anti-HBc) in HBsAg-negative participants.

166 f antiviral genes was exclusively induced in HBsAg-deficient mice.

167 Infant HBsAg seropositivity for more than 6 months was defined

168 s were identified as currently HBV infected (HBsAg positive) or exposed (HBcAb positive).

169 ionship between the prevalence of infection (HBsAg) and exposure (anti-HBc) (R2 = 0.45, p < 0.001).

170 eveal that these mutations did not influence HBsAg secretion or infectivity.

171 ive against HDV because they fail to inhibit HBsAg production/secretion.

172 omote HBV RNA transcription while inhibiting HBsAg secretion.

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

174 failure, genotype C infection, and maternal HBsAg positivity were significantly associated with dela

175 d more HBV genotype C infection and maternal HBsAg seropositivity.

176 Estimated rates of infection at maternal HBsAg levels of 4, 4.5, and 5 log10 IU/mL were 2.4% (95%

177 justment for the other risk factor, maternal HBsAg level was significantly associated with risk of in

178 6 mother-infant pairs with positive maternal HBsAg under current immunoprophylaxis.

179 Quantitative maternal HBsAg predicts infection in infants as well as maternal

180 redicting infection by quantitative maternal HBsAg was comparable to that by maternal viral load (0.8

181 Results showed that maternal HBsAg was positively correlated with maternal viral load

182 33.7% vs 13.4%, P < .0001), and the maternal HBsAg-positive rate was higher (97.1% vs 66.4%, P < .000

183 nic infection in infants at various maternal HBsAg levels were estimated using a multivariate logisti

184 Modeling HBsAg kinetics during REP 2139-Ca monotherapy indicates

185 Thus, human neutralizing HBsAg antibodies appear to play a key role in the sponta

186 We retrospectively analyzed 77 noncirrhotic HBsAg carriers with hematological cancer who received ri

187 Virus still occurs in approximately 2-5% of HBsAg positive mothers.

188 ion of anti-HBc positivity in the absence of HBsAg in organ transplant donors and in candidate patien

189 Our data demonstrate that in the absence of HBsAg, hepatic HBV replication leads to Tlr3-dependent i

190 st innate immune responses in the absence of HBsAg.

191 on the mode of liver damage; in the case of HBsAg-driven hepatocarcinogenesis, NF-kappaB in hepatocy

192 ccurately reproduced the observed decline of HBsAg and HDV, which was simultaneous.

193 orresponding absolute DNA level or degree of HBsAg and HBV DNA decline.

194 80), but there was no increased detection of HBsAg positivity from the alert (15 versus 13 respective

195 idence of exposure to HBV, with detection of HBsAg used to distinguish those with active HBV infectio

196 evaluated the putative modulatory effects of HBsAg.We observed that gene expression of NUC-treated pa

197 Eradication of HBsAg as a therapeutic goal might facilitate the inducti

198 The extent of HBsAg amino acid variability was measured by Shannon ent

199 consisted of prevalence and risk factors of HBsAg positivity among husbands or wives.

200 The serum gradient of HBsAg measured throughout the off-therapy observation is

201 of age in NF-kappaB-deficient hepatocytes of HBsAg-expressing mice.

202 The pooled annual incidence of HBsAg loss was 1.17% (95% CI 0.94-1.41, I(2)=97%).

203 od to estimate the age-specific incidence of HBsAg seroclearance at a population-level and evaluate i

204 ered before hospital discharge to infants of HBsAg-negative women.

205 Infants of HBsAg-positive women receive HepB and HBIG </=12 hours o

206 HBIG are administered at birth to infants of HBsAg-positive women, and HepB is administered before ho

207 were positively correlated with the level of HBsAg decline at week 48.

208 The serum level of HBsAg was associated with virological (P < 0.001) and cl

209 Levels of HBsAg, anti-HBs, and HBV DNA did not differ significantl

210 ver, we developed a model that low levels of HBsAg, HBcAb, and albumin and high fibrosis values predi

211 The mean (standard deviation) half-life of HBsAg in blood was 6.7 (5.5) days, which reflects recent

212 Spontaneous loss of HBsAg (known as functional cure) in patients with chroni

213 ctional cure is defined as sustained loss of HBsAg and several therapeutic strategies are in clinical

214 The one-time baseline measurement of HBsAg <1000 IU/mL and HBV DNA <2000 IU/mL distinguished

215 of MB provided quantitative measurements of HBsAg with a linear concentration range of 0.3-1000 pgmL

216 (34.9%) patients had a favorable outcome of HBsAg seroclearance.

217 AOR = 1.46) were significantly predictors of HBsAg positivity in husbands.

218 Prevalence and predictors of HBsAg positivity in wives had similar results.

219 In The Gambia, where the prevalence of HBsAg is 8.8% in people older than 30 years, adult scree

220 nkage into care, and the small proportion of HBsAg carriers who need treatment suggest that large-sca

221 The low and homogeneous rate of HBsAg loss highlights the need for new therapeutics aime

222 matically determined a pooled annual rate of HBsAg loss in adults with untreated chronic HBV infectio

223 We assessed rate of HBsAg loss, and stratified results by whether the underl

224 to estimate the age-specific annual rate of HBsAg seroclearance.

225 ability and significantly increased rates of HBsAg loss and HBsAg seroconversion during therapy and f

226 r, correlating with a 2.7 log10 reduction of HBsAg.

227 fe (1.3 days) suggesting a rapid turnover of HBsAg in HBV/HDV co-infection.

228 BV viral load, and 3 had negative results on HBsAg testing and had an undetectable HBV viral load.

229 Clearances of intrahepatic cccDNA and/or HBsAg are critical endpoints for future antiviral therap

230 utants with >70% reduction in HBV RNA and/or HBsAg were selected for chromatin immunoprecipitation an

231 Upon HBcAg(core) or HBsAg(env)-stimulation, 85% and 60% of HBs(lo) patients

232 ined as a >1000 IU/mL increase in HBV DNA or HBsAg detection in a person who was previously negative.

233 e higher in responders (combined response or HBsAg loss) compared to nonresponders.

234 Overall HBsAg seroprevalence was 7.8% (95% confidence interval [

235 eting 48 weeks of follow-up) with persistent HBsAg seroconversion.

236 y accumulation of HBV envelope polypeptides, HBsAg transgenic mice, which show no HBV-specific immune

237 HBV infection was defined by positive HBsAg and past exposure by positive anti-HBc.

238 between anti-HBs levels and cells producing HBsAg-specific interferon gamma and interleukin 2 (T-hel

239 Maternal viral load and quantitative HBsAg were measured in the peripartum period.

240 elation between our multiplexed quantitative HBsAg results and the qualitative results obtained using

241 lity of one-time measurement of quantitative HBsAg and HBV DNA levels for inactive carrier status and

242 er and supports strategies aimed at reducing HBsAg production in CHB patients.

243 ts completed the TDF + pegIFN + NAP regimen, HBsAg levels were 0.05 IU/mL or lower in 24/40 participa

244 ce in liver stiffness for those who remained HBsAg-positive compared to those who achieved HBsAg sero

245 d HBV dual-shRNA decreased HBV DNA, HBV RNA, HBsAg, HBeAg, and liver fibrosis markers in serum and ti

246 lar HBV RNA (44-77% reduction) and secretory HBsAg (25-81% reduction), and 12 mutants had a reduction

247 However, a causative link between serum HBsAg levels and impairment of intrahepatic CD8+ T cells

248 phocytes in CHB patients stratified by serum HBsAg levels <500 (HBs(lo)) or >50,000 IU/ml (HBs(hi)) u

249 Median serum HBsAg half-life (t(1/2)) was estimated as 1.3 [0.9-1.8]

250 ces of recurrence, defined by positive serum HBsAg, of 2.9% (upper 95% confidence interval, 19%).

251 ery 4 weeks for changes in qualitative serum HBsAg, HBV DNA, and alanine aminotransferase (ALT) conce

252 t designed to pharmacologically reduce serum HBsAg, break immune tolerance, and increase functional c

253 Surprisingly, we found that serum HBsAg clearance has only a minimal effect on the expansi

254 Thus, serum HBsAg correlates with inhibitory receptor expression, HB

255 DC, monocytes and CD8+ T cells, while serum HBsAg levels had little effect.

256 ] positive, and HDV RNA positive, with serum HBsAg concentrations of more than 1000 IU/mL, and a hist

257 cluded the proportion of patients with serum HBsAg less than 50 IU/mL, the proportion of patients wit

258 ng REP 2139-Ca monotherapy indicates a short HBsAg half-life (1.3 days) suggesting a rapid turnover o

259 Spontaneous HBsAg loss occurred in 3837 (7.8%) of 48 972 patients, w

260 onic HBV infection that achieved spontaneous HBsAg loss, published up to Oct 1, 2018.

261 Globally, spontaneous HBsAg loss occurs infrequently (about 1% per year) in tr

262 Strikingly, HBsAg-specific memory B cells from natural controllers m

263 condary endpoints included overall survival, HBsAg positivity, and changes in liver biochemistry and

264 chievable and should be defined as sustained HBsAg loss in addition to undetectable HBV DNA 6 months

265 For HBV 'functional cure', sustained HBsAg loss with undetectable HBV DNA after completion of

266 emonstrated validity in predicting sustained HBsAg loss was considered the most appropriate criterion

267 hin muscle and s.c. afferent lymph, and that HBsAg-AS01 uniquely induces the selective migration of A

268 Moreover, our model estimated that HBsAg seroclearance resulted in 23.38% of the decrease o

269 d on our findings it cannot be excluded that HBsAg may act locally in the infected liver or affects p

270 We hypothesize that HBsAg is a major HBV-mediated evasion mechanism controll

271 We show that HBsAg-AS01 induces a distinct immunogenic cellular signa

272 The HBsAg seroclearance occurred predominantly in the early

273 We found that the HBsAg seroclearance in chronic HBV infections of China a

274 S,S, only a minimal antibody response to the HBsAg carrier was induced.

275 = 140) were followed every 3 months through HBsAg quantification.

276 Antibodies to HBsAg were detected only in mice injected with antigen w

277 infection, only 54.1% developed antibody to HBsAg (anti-HBs).

278 HBsAg status, serial changes in antibody to HBsAg levels, and donor serology, were not associated wi

279 hanges in liver biochemistry and antibody to HBsAg levels.

280 l parameters, including baseline antibody to HBsAg status, serial changes in antibody to HBsAg levels

281 g hepatitis B surface antigen (HBsAg) (+) to HBsAg (-) participants was 1.17 (95% CI 1.06-1.31; P = 0

282 resulted in 23.38% of the decrease of total HBsAg prevalence for population aged 1-59 years in 2006.

283 However, little is known about pre-treatment HBsAg levels as an indicator of HBV immune potential.

284 The association of time-varying HBsAg levels with relapses was assessed through a time-d

285 The association between the time-varying HBsAg serum gradient and risk of relapse has not been el

286 Individually, 6.1% were HBsAg positive with a higher rate seen in husbands (7.0%

287 rs (range 18 to 90 years), 68/106 (64%) were HBsAg-positive, and 22/100 (22%) were HIV infected.

288 allogeneic HSCT recipients, 85 (28.7%) were HBsAg-negative, anti-HBc-positive, of whom 62 were recru

289 All patients were HBsAg positive for at least 7 months, anti-HDV positive

290 compared to 3/34 (9%) among those that were HBsAg-negative (p = 0.04).

291 to serum anti-HBs trough level) if they were HBsAg- and HBV-DNA negative at time of switch.

292 nvHCC was diagnosed when HBsAg and anti-HCVAb was negative.

293 In sub-Saharan Africa, where HBsAg prevalence is higher than 8%, hepatitis D virus mi

294 Among the patients (n = 19) whose HBsAg levels ever dropped below 10 IU/mL, only one and t

295 percent of the unvaccinated households with HBsAg carriers were aware of their risk.

296 h HBsAg <100 IU/ml compared to patients with HBsAg >5,000 IU/ml.

297 gher fold change in ASCs among patients with HBsAg <100 IU/ml compared to patients with HBsAg >5,000

298 ohort of 49 anti-HDAg-positive patients with HBsAg persistence for at least 6 months.

299 l and sustained undetectable HBV DNA without HBsAg loss after stopping treatment an intermediate goal

300 ression (undetectable serum HBV DNA) without HBsAg loss, 6 months after discontinuation of treatment