ライフサイエンスコーパス: HBsAg

1 HBsAg genetic diversity was analyzed by population-based

2 HBsAg kinetics of decline paralleled the second phase of

3 HBsAg levels remained elevated despite a significant dec

4 HBsAg screening was accepted by 5980 (weighted estimate

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

6 HBsAg-induced cytokine production by KCs and monocyte-de

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

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

9 HBsAg-positive individuals were invited for a comprehens

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

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

12 epatitis B surface antigen [HBsAg](+) and 10 HBsAg(-)/hepatitis B surface antibody [anti-HBs](+)).

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

14 Of the 13 HBsAg mutations found in these patients, 8 of 13 (M103I-

15 A total of 2,139 HBsAg-seropositive, anti-HCV-seronegative, and treatment

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

17 spital, resulting in the identification of 4 HBsAg-positive and 69 anti-HBc-positive/HBsAg-negative p

18 rveys, the estimated OBI frequency per 10(4) HBsAg-negative subjects declined from 160.7 in unvaccina

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

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

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

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

23 LG can mask immunogenic epitopes, abrogating HBsAg recognition by Abs.

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

25 her investigated as a strategy to accelerate HBsAg loss.

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

27 d HBsAg mutations localized in immune-active HBsAg regions.

28 he natural course of hepatitis B surface Ag (HBsAg) seroconversion in chronic hepatitis B virus (HBV)

29 01 administered with hepatitis B surface Ag (HBsAg).

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

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

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

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

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

35 birth (6.15% versus 31.48%, P = 0.0003) and HBsAg positivity at 6 months old (1.54% versus 10.71%, P

36 were assessed based on levels of HBV DNA and HBsAg and Southern blot analysis.

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

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

39 ell lines reduces replication of HBV DNA and HBsAg production and secretion.

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

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

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

43 ved cell lines producing full-length HBV and HBsAg particles, owing to stable (HepG2215) or transient

44 was developed and fitted to frequent HDV and HBsAg kinetic data from 10 patients during the first 28

45 relationship between serum HBsAg levels and HBsAg-infected cells, IFN's mode of action, and its effe

46 , and a very-low-level viral replication and HBsAg expression is the major mechanism underlying OBI.

47 implications of possible mutations in rt and HBsAg ORFs.

48 vir combination, anti-HBe seroconversion and HBsAg loss were observed, while the titer of HBsAb persi

49 antly, HBeAg loss, HBeAg seroconversion, and HBsAg loss only occurred in patients with stabilized VR.

50 rcinoma, post-LT low anti-HBs, male sex, and HBsAg-positivity in the explant liver tissue.

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

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

53 Hepatitis B surfage Antigen (HBsAg) and anti-HBsAg antibodies (HBsAb) in patients with chronic hepati

54 reatment stopped with loss of HBsAg and anti-HBsAg seroconversion.

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

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

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

58 2000 IU/mL) and hepatitis B surface antigen (HBsAg) (<1000 IU/mL) have been shown to distinguish inac

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

60 nvestigated the hepatitis B surface antigen (HBsAg) and alpha-fetoprotein (AFP) with the lowest conce

61 valence of both hepatitis B surface antigen (HBsAg) and antibodies to HCV (anti-HCV), alone and in co

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

63 ld include both hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (anti-HBc), because

64 interaction of hepatitis B surface antigen (HBsAg) and KCs, and possible functional consequences, we

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

66 Hepatitis B virus surface antigen (HBsAg) became negative in six PEG-IFNa-treated patients

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

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

69 of hepatitis B virus (HBV) surface antigen (HBsAg) clearance and whether their phenotype is related

70 -care tests for hepatitis B surface antigen (HBsAg) could be an ideal tool for a large-scale HBV scre

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

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

73 we investigated hepatitis B surface antigen (HBsAg) genetic features underlying this phenomenon by an

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

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

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

77 e role of serum hepatitis B surface antigen (HBsAg) levels and established models for predicting HBeA

78 A, HBV DNA, and hepatitis B surface antigen (HBsAg) levels as well as presence of HBeAg and hepatitis

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

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

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

82 replication and hepatitis B surface antigen (HBsAg) production in cell lines.

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

84 fits show that hepatitis B surface antigen (HBsAg) remained stable after a short pharmacological del

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

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

87 ss-sectional surveys on HBV surface antigen (HBsAg) seroprevalence were conducted in 1996-2000 and 20

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

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

90 The 90-day hepatitis B surface antigen (HBsAg) testing rate was 28.1% in 15 357 adults.

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

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

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

94 At birth, hepatitis B surface antigen (HBsAg) was detected in 20% and 24% of newborns in the tr

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

96 itis B virus (HBV) DNA, HBV surface antigen (HBsAg), and antibodies to surface (anti-HBs) and core (a

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

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

99 s, quantitative hepatitis B surface antigen (HBsAg), HBeAg levels, HBV genotype, and mutant analysis.

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

101 c prevalence of hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and cirrhosis.

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

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

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

105 nd enrolled 118 hepatitis B surface antigen (HBsAg)- and hepatitis B e antigen-positive pregnant wome

106 um samples from hepatitis B surface antigen (HBsAg)-negative subjects <18 years enrolled during six s

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

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

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

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

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

112 coexistence of Hepatitis B surfage Antigen (HBsAg) and anti-HBsAg antibodies (HBsAb) in patients wit

113 the detection of Hepatitis B virus antigen (HBsAg) in human blood plasma.

114 NUC treated (36 hepatitis B surface antigen [HBsAg](+) and 10 HBsAg(-)/hepatitis B surface antibody [

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

116 e reactivation can occur in patients who are HBsAg positive/anti-HBc positive or HBsAg negative/anti-

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

118 spots for the reference standard test (AxSYM HBsAg enzyme-linked immunosorbent assay [ELISA]).

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

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

121 Only 8.8% of patients received both HBsAg and hepatitis B surface antibody tests to determin

122 . 3.1% of control patients; P<0.001) carried HBsAg mutations localized in immune-active HBsAg regions

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

124 a" determinant of HBsAg than age-comparable, HBsAg-positive subjects.

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

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

127 Concurrent HBsAg/HBsAb positivity in active CHB is a clinical and v

128 antiviral therapies of a CHB with concurrent HBsAg and HBsAb positivity, and analyse the clinical imp

129 iving a booster at age 10-14 years decreased HBsAg seroprevalence if participants were born to HBsAg-

130 functional interaction with patient-derived HBsAg.

131 viremia 16 months post-LT without detectable HBsAg.

132 months, one TDF-group child newly developed HBsAg positivity, presumably due to postnatal infection

133 version, when compared to levels of HBV DNA, HBsAg, alanine aminotransferase, and HBV genotype, age,

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

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

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

137 screening rate from less than 50% to 94% for HBsAg and from less than 30% to 85% for anti-HBc in pati

138 Clinicians can initiate antivirals for HBsAg-negative/anti-HBc-positive patients anticipating c

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

140 , 85%, 88%, 87.0%, and 92% were negative for HBsAg, respectively, and 95%, 99%, 100%, and 100% had un

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

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

143 00 subjects in total), 293 were positive for HBsAg.

144 trategy: All pregnant women are screened for HBsAg.

145 trategy: All pregnant women are screened for HBsAg.

146 linicians should start antiviral therapy for HBsAg-positive/anti-HBc-positive patients before or cont

147 Experiments with real serum samples from HBsAg-infected patients are presented, demonstrating the

148 Furthermore, HBsAg-exposed macrophages and KC activated natural kille

149 Four HCWs were anti-HBc positive; none had HBsAg.

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

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

152 ]); some of them are already known to hamper HBsAg recognition by humoral response.

153 Ninety-six patients were HBcAb+, HBsAg-.

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

158 mIU/mL and there was a significantly higher HBsAg seroprevalence in the HIV cohort, compared to the

159 evelopment of new therapies that can improve HBsAg clearance and virological cure is warranted.

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

161 ld type for clinically relevant mutations in HBsAg and rt ORFs, successfully treated with a combinati

162 vity is a useful marker for OBI screening in HBsAg-negative subjects, and a very-low-level viral repl

163 Infant HBsAg seropositivity for more than 6 months was defined

164 decreased infant HBV DNA at birth and infant HBsAg positivity at 6 months and ameliorated maternal AL

165 risk (odds ratio 6.82, P = 0.0220) of infant HBsAg positivity.

166 Primary outcome was infant HBsAg at 6 months old.

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

168 omote HBV RNA transcription while inhibiting HBsAg secretion.

169 KCs internalized HBsAg in vitro, which did not change their phenotype, bu

170 Ag, leading to accumulation of intracellular HBsAg; the addition of alisporivir greatly reduced level

171 inoma, body mass index (BMI), HBV DNA level, HBsAg level, liver function test, complete blood count,

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

173 DNA virus with several serological markers: HBsAg and anti-HBs, HBeAg and anti-HBe, and anti-HBc IgM

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 mporaneously with cancer therapy and monitor HBsAg-negative/anti-HBc-positive patients for reactivati

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

186 cated 2.2% (95% confidence [CI]: 0.6-3.8) of HBsAg+ infants from the treated group versus 7.6% (95% C

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

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

189 st innate immune responses in the absence of HBsAg.

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

191 hat NK cells play a role in the clearance of HBsAg during interferon-based combination therapy.

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

193 ne, Vikia, and Espline) for the detection of HBsAg in the field or a laboratory setting in the Gambia

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

195 higher mutation rates in "a" determinant of HBsAg than age-comparable, HBsAg-positive subjects.

196 the NTx group (P50.001) and no difference of HBsAg+ rate between infants in the LdT and LAM groups(1.

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

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

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

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

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

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

208 ion of alisporivir greatly reduced levels of HBsAg in these cells.

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

210 months after treatment stopped with loss of HBsAg and anti-HBsAg seroconversion.

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

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

213 heterosexuals, and the general population of HBsAg-positive subjects, respectively.

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

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

216 th chronic HBV were analyzed for presence of HBsAg and their phenotype, and compared with KCs in cont

217 The prevalence of HBsAg in patients with psoriasis is lower than that obse

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

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

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

221 ficantly higher incidence of reappearance of HBsAg after HBV reactivation (100% vs. 28.5%; P=0.003).

222 ological breakthrough (i.e., reappearance of HBsAg) is the most important predictor of HBV-related he

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

224 n of CYPA significantly reduced secretion of HBsAg, leading to accumulation of intracellular HBsAg; t

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

226 stimated efficacy of catch-up vaccination on HBsAg seroprevalence in early adulthood was 21% (95% CI

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

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

229 ion was not related to sex, HBV genotype, or HBsAg a determinant mutation.

230 who are HBsAg positive/anti-HBc positive or HBsAg negative/anti-HBc positive.

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

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

233 of 4 HBsAg-positive and 69 anti-HBc-positive/HBsAg-negative patients, two of them with positive viral

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

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

236 as the proportion of patients with recurrent HBsAg-positivity.

237 linear range, reflecting clinically relevant HBsAg concentrations.

238 of 7 patients carrying these sites remained HBsAg negative despite HBV reactivation.

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

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

241 antly reduced levels of HBV DNA and secreted HBsAg.

242 Serum HBsAg levels should be monitored in the management of pa

243 ost dynamics, the relationship between serum HBsAg levels and HBsAg-infected cells, IFN's mode of act

244 t predictor of HBeAg seroclearance but serum HBsAg level was the most significant predictor of HBV DN

245 itis C virus infection, HIV infection, serum HBsAg level >==250 IU/mL, duration of drug use, and olde

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

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

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

249 , and 6.08 (3.19-11.61) for those with serum HBsAg levels of 1,000-9,999, 100-999, and <100 IU/mL, re

250 ersistence of HBV in the liver without serum HBsAg and HBVDNA.

251 Spontaneous HBsAg seroconversion was not related to sex, HBV genotyp

252 Both were predictors of spontaneous HBsAg seroconversion and HBV recovery (odds ratios 4.0 a

253 infection, and are predictive of spontaneous HBsAg seroconversion and HBV recovery.

254 The clinical course of spontaneous HBsAg seroconversion was assessed in 296 chronically HBV

255 before the age of 10 y predicted spontaneous HBsAg seroconversion in chronically HBV-infected patient

256 Serum HBV-DNA viral load, hepatitis surface (HBsAg) and e antigen (HBeAg) status were obtained at bas

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

258 Among 1117 subjects, 133 (12%) tested HBsAg-positive.

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

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

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

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

263 The HBsAg a determinant sequence of chronically HBV-infected

264 The HBsAg seroclearance occurred predominantly in the early

265 e absence of amino acid substitutions in the HBsAg sequences of the Hepatitis B Virus (HBV) genome ab

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

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

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

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

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

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

272 hanges in liver biochemistry and antibody to HBsAg levels.

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

274 seroprevalence if participants were born to HBsAg-positive mothers (hazard ratio [HR] = 0.68, 95% CI

275 should be considered in individuals born to HBsAg-positive mothers and who have completed the HBV ne

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

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

278 viewpoint, involving a strategy of universal HBsAg and selective anti-HBc testing.

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

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

281 No patient was HBsAg positive, none of them underwent pre-emptive thera

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

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

284 Intrahepatic KCs were HBsAg positive and more activated than those from contro

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

286 In the HIV cohort born after 1987 who were HBsAg negative, over half (52.9%) had antibody to hepati

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

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

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

290 tween patients with chronic hepatitis B with HBsAg clearance and nonresponders suggest that NK cells

291 edge, the first case described of a CHB with HBsAg/HBsAb positivity, wild type for clinically relevan

292 second phase of HDV decline consistent with HBsAg-productive-infected cells being the main source of

293 une-suppressive therapy, and correlates with HBsAg mutations endowed with enhanced capability to evad

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

295 in 7 responders (defined as individuals with HBsAg clearance by week 72; 3 HBV e antigen [HBeAg]-posi

296 Compared to individuals with HBsAg levels >/= 10,000 IU/mL, the multivariate-adjusted

297 KCs directly interact with HBsAg in vivo and in vitro.

298 yte-derived macrophages also interacted with HBsAg, leading to activation and cytokine production.

299 cally HBV-infected subjects with and without HBsAg seroconversion was also analyzed.

300 atients who had HBeAg seroconversion without HBsAg clearance.