ライフサイエンスコーパス: HBV infection

1 iated with a worse clinical outcome of acute HBV infection.

2 a novel target for the treatment of chronic HBV infection.

3 w for timelier diagnosis and intervention of HBV infection.

4 tor Myrcludex B ensured long-term control of HBV infection.

5 developing curative therapeutics of chronic HBV infection.

6 ant insights into the therapeutic control of HBV infection.

7 life-long treatment and there is no cure for HBV infection.

8 itis B surface antigen accurately identifies HBV infection.

9 n clinical trials of agents designed to cure HBV infection.

10 erferon in adults in the IT phase of chronic HBV infection.

11 ffective therapeutic vaccine against chronic HBV infection.

12 ponses which mimic spontaneous resolution of HBV infection.

13 nate cccDNA, which would be required to cure HBV infection.

14 (HBV)infection but might also signify occult HBV infection.

15 elopment of antiviral agents against chronic HBV infection.

16 nfection but does not allow establishment of HBV infection.

17 onal and virologic cure in various phases of HBV infection.

18 cally relevant, pre-clinical animal model of HBV infection.

19 i-hepatitis B to identify those with chronic HBV infection.

20 hat [Mg(2+)]i plays a key role in control of HBV infection.

21 trials-their combination might cure chronic HBV infection.

22 developed into a viable treatment for human HBV infection.

23 -redirected T cells in patients with chronic HBV infection.

24 actors are required for the establishment of HBV infection.

25 n vivo renders rhesus macaques permissive to HBV infection.

26 regions; and adults seeking protection from HBV infection.

27 to create hepatoma cell lines susceptible to HBV infection.

28 viral replication and the outcome of chronic HBV infection.

29 cell line to uncover host factors enhancing HBV infection.

30 aspires to global control and elimination of HBV infection.

31 the weak capacity of this cell type to clear HBV infection.

32 (HBsAg) heterogeneity in patients with acute HBV infection.

33 une system to efficiently counteract chronic HBV infection.

34 ho were vaccinated before being screened for HBV infection.

35 e doses of JNJ-6379 in patients with chronic HBV infection.

36 ely 240 million people living with a chronic HBV infection.

37 nt implications for the treatment of chronic HBV infection.

38 d household contacts of persons with chronic HBV infection.

39 icient immune therapeutic control of chronic HBV infection.

40 of children in the immune-tolerant phase of HBV infection.

41 year) in treatment-naive adults with chronic HBV infection.

42 ve also proved effective in the treatment of HBV infections.

43 egimen for curing chronic hepatitis B virus (HBV) infection.

44 ant (IT) phase of chronic hepatitis B virus (HBV) infection.

45 n associated with chronic hepatitis B virus (HBV) infection.

46 rent or prior exposure to hepatitis B virus (HBV) infection.

47 actors, for patients with hepatitis B virus (HBV) infection.

48 oma with or without hepatitis C or B (HCV or HBV) infection.

49 uce the burden of chronic hepatitis B virus (HBV) infection.

50 poor outcome for chronic hepatitis B viral (HBV) infection.

51 rly promising for chronic hepatitis B virus (HBV) infection.

52 mong SIV children, 26.7% were susceptible to HBV infection, 22.1% had at least one intestinal parasit

53 Sixty-two patients with acute HBV infection (44 with genotype D infection and 18 with

54 Following HBV infection, a complete viral life cycle, with product

55 ns worldwide with chronic hepatitis B virus (HBV) infection, a leading causes of liver cancer.

56 with IDU histories had a previous or ongoing HBV infection: a rate over 4 times higher than the preva

57 It also prevented 9.30% of new HBV infections (about 7.43 million people) and 9.95% of

58 We demonstrated that HBV infection activated cellular PLK1 in PHHs and differ

59 Hepatitis B virus (HBV) infection affects approximately 300 million people

60 Hepatitis B virus (HBV) infection afflicts millions worldwide, causing cirr

61 In a study of men with chronic HBV infection ages 40-65 years in Taiwan, we associated

62 liver tissues from 26 patients with chronic HBV infection (ages, 14-39 y); 9 patients were positive

63 udy of treatment-naive patients with chronic HBV infection, all doses tested of JNJ-6379 were well to

64 The high burden of HBV infection among African immigrants in the United Sta

65 nclusion: This study revealed disparities of HBV infection among ethnic/racial groups and between U.S

66 nclusion: This study revealed disparities of HBV infection among ethnic/racial groups and between U.S

67 -0.4), and since 1999, prevalence of chronic HBV infection among non-Hispanic blacks has been 2- to 3

68 positivity, indicating a previous or ongoing HBV infection, among adults aged 20-59 years with an inj

69 ) positivity, indicating previous or ongoing HBV infection, among adults aged 20-59 years with inject

70 r disease, of whom 9.6% (n = 88) had current HBV infection and 73.9% (n = 679) had exposure.

71 ent-naive patients (1339 [2.6%] with chronic HBV infection and 7506 [14.3%] with HCV infection) were

72 ent-naive patients (1339 [2.6%] with chronic HBV infection and 7506 [14.3%] with HCV infection) were

73 treated at 35 centers in France, with HCV or HBV infection and biopsy-proven cirrhosis, Child-Pugh A

74 d in patients with partial immune control of HBV infection and can remain in the liver after the reso

75 fficacy in adults in the IT phase of chronic HBV infection and cannot be recommended.

76 help us learn more about the pathogenesis of HBV infection and develop therapeutic agents to reduce i

77 HBsAg loss in adults with untreated chronic HBV infection and examined the effect of regional endemi

78 ersons had significantly lower prevalence of HBV infection and exposure as well as higher prevalence

79 igate the relationship between prevalence of HBV infection and exposure in Africa, undertaking a syst

80 herapy is a promising means to treat chronic HBV infection and HBV-associated hepatocellular carcinom

81 antiviral and antitumoral strategies against HBV infection and HBV-mediated carcinogenesis.

82 for the exit of Sp110 from the PML-NB during HBV infection and HBx recruitment on the promoter of the

83 ign of novel, epigenetic therapies to combat HBV infection and poor prognosis HBV-associated liver ca

84 responses that prevent the establishment of HBV infection and reduce viral proteins in the serum and

85 g the hepatocyte: the only target cell where HBV infection and replication take place.

86 HBV infection models to evaluate a role for HBV infection and the viral regulatory protein HBx to dr

87 into HBV-infected, humanized mice controlled HBV infection and virological markers declined 4-5 log o

88 aptive immune responses to acute and chronic HBV infections and responses to antiviral therapy.

89 n naturally clear chronic hepatitis B virus (HBV) infection and acquire protection from reinfection a

90 itis B surface antigen (HBsAg; prevalence of HBV infection) and antibody to hepatitis B core antigen

91 atients with HCV infection, 98 patients with HBV infection, and 8 patients with both); 80 of these pa

92 s the key strategy for global elimination of HBV infection, and has been highly effective in reducing

93 the genetic variants associated with HCV and HBV infection, and how these variants affect specific ex

94 en serum hepcidin and progression of chronic HBV infection, and may shed a new light on the developme

95 in children in the immune-tolerant phase of HBV infection, and treatment was associated with frequen

96 he mcHBV-GLuc cccDNA model is independent of HBV infection, and will be valuable for investigating HB

97 HCV) infection, 17.9% had hepatitis B virus (HBV) infection, and 2.2% had both.

98 63.5% were susceptible to hepatitis B virus (HBV) infection, and 31.0% had at least one intestinal pa

99 ffective cure for chronic hepatitis B virus (HBV) infection, antibodies are protective and correlate

100 In children with chronic HBV infection, antivirals compared to no antiviral thera

101 High AST completely mediated the HBV infection-any cataract association.

102 ng the window phase, and resolved or chronic HBV infection are all possible and only distinguishable

103 y about 24%-45% of US adults at high risk of HBV infection are protected.

104 These in vivo macaque HBV infections are characterized by longitudinal HBV DNA

105 hanisms of action against hepatitis B virus (HBV) infection are being explored with the goal of achie

106 Therapies for chronic hepatitis B virus (HBV) infection are urgently needed because of viral inte

107 volunteers and in participants with chronic HBV infection, assessed in all treated participants.

108 und antiviral therapy for hepatitis B virus (HBV) infection associated with improved intermediate out

109 mples from 104 patients with chronic HDV and HBV infection at medical centers in Europe and the Middl

110 ive patients with chronic hepatitis B virus (HBV) infection but not in treatment-experienced patients

111 te, resolved, and chronic hepatitis B virus (HBV)infection but might also signify occult HBV infectio

112 th agencies have set the goal of eliminating HBV infection by 2030.

113 ing the restoration of functional control of HBV infection by immunotherapy.

114 and the therapeutic implications for chronic HBV infection by learning from the epigenetic therapies

115 t immune defenses against hepatitis B virus (HBV) infection by the viral proteins is speculated to ca

116 Hepatitis B virus (HBV) infection can be prevented through vaccination.

117 patitis C virus (HCV) and hepatitis B virus (HBV) infections can lead to cirrhosis, end-stage liver d

118 ioral risk factors would identify nearly all HBV infection cases.

119 In HIS-HUHEP mice, HBV infection completes a full life cycle and recapitula

120 eutic ARC-520 for chronic hepatitis B virus (HBV) infection consists of a melittin-derived peptide co

121 herapy.IMPORTANCE Chronic hepatitis B virus (HBV) infection continues to be a major global health con

122 treatment interventions, hepatitis B virus (HBV) infection continues to cause nearly 1 million death

123 cuses on the immune active phases of chronic HBV infection; decision-making in other commonly encount

124 l rates of newly diagnosed acute and chronic HBV infection declined or were stable overall, but incre

125 l rates of newly diagnosed acute and chronic HBV infections declined or were stable overall, but incr

126 the huge global burden of hepatitis B virus (HBV) infection depends on improved insights into virus e

127 on of HBV remains the major cause of chronic HBV infection despite immunization.

128 y evaluated as a population intervention for HBV infection, despite high-profile data supporting its

129 Previous animal models mimicking chronic HBV infection do not faithfully reflect disease progress

130 Screening for hepatitis B virus (HBV) infection during pregnancy identifies women whose i

131 Treating HBV infection, either with IFN or NUCs, substantially re

132 s in the United States remain susceptible to HBV infection, especially MSMs, IDUs, diabetics, HCV pat

133 We aimed to determine the prevalence of HBV infection, exposure, self-reported vaccination, vacc

134 ies for prevention and management of chronic HBV infection for African Americans.

135 tis B Research Network enrolls patients with HBV infection from 21 clinical sites in the United State

136 ollow-up study of 2666 patients with chronic HBV infection (genotypes B or C), level of HBcrAg is an

137 re goal of treatment is to eradicate chronic HBV infection globally.

138 Patients with HBV infection had to be receiving effective antiviral th

139 The overall prevalence of chronic HBV infection has remained constant since 1999: 0.3% (95

140 Hepatitis B virus (HBV) infection has a global reach with high prevalence i

141 Almost all adults with acute HBV infection have a rapid immune response to the virus,

142 al infant HBV vaccination, rates of maternal HBV infection have increased annually by 5.5% since 1998

143 g age in the US, but changes in hepatitis B (HBV) infection have not been studied.

144 ed States, but changes in hepatitis B virus (HBV) infections have not been studied.

145 HBV infection (HBs antigen) had to be diagnosed with ser

146 HBV infection (hepatitis B surface antigen) was diagnose

147 e antigen (anti-HBc), indicative of previous HBV infection; hepatitis B surface antigen (HBsAg), indi

148 In patients with chronic HBV infection, high levels of virus antigens might preve

149 cells from 28 patients with chronic HDV and HBV infection, identified HDV-specific CD8(+) T-cell epi

150 The USPSTF recommends screening for HBV infection in adolescents and adults at increased ris

151 s with moderate certainty that screening for HBV infection in adolescents and adults at increased ris

152 y, natural history, and treatment of chronic HBV infection in adolescents and children, and we highli

153 ldren, and we highlight key differences from HBV infection in adults.

154 fection worldwide, but little is known about HBV infection in African-born persons in the United Stat

155 The estimated global prevalence of HBV infection in children aged 5 years or younger is 1.3

156 to investigate the natural course of chronic HBV infection in children with vaccine failure and compa

157 tiviral therapy in the management of chronic HBV infection in children.

158 and HBsAg was the most significant factor of HBV infection in couples.

159 Ntcp is the key host factor limiting HBV infection in cynomolgus and rhesus macaques and in p

160 verall age-standardized prevalence of active HBV infection in Hispanic/Latino adults (0.29%) was no d

161 maternal surface antigen (HBsAg) to predict HBV infection in infants has not been investigated.

162 is vector in the prevention and treatment of HBV infection in mouse models.

163 ted to estimate the prevalence and burden of HBV infection in PLWH at global, regional, and national

164 This study suggests a high burden of HBV infection in PLWH, with disparities according to reg

165 This study suggests a high burden of HBV infection in PLWH, with disparities according to reg

166 The USPSTF recommends screening for HBV infection in pregnant women at their first prenatal

167 re is convincing evidence that screening for HBV infection in pregnant women provides substantial ben

168 erapy in patients with immune active chronic HBV infection in reducing the risk of cirrhosis, decompe

169 Other tests have been developed to detect HBV infection in resource-limited settings.

170 show a high burden and discordant pattern of HBV infection in rural couples, and partner's double pos

171 ll risk among patients with current or prior HBV infection in the context of DAA treatment is unknown

172 sibility of a screen-and-treat programme for HBV infection in The Gambia, west Africa, and estimated

173 , on macaque primary hepatocytes facilitates HBV infection in vitro, where all replicative intermedia

174 gs as immunocompetent animal models to study HBV infection in vivo, immunological responses against t

175 ntiviral effect of PLK1 inhibitor BI-2536 on HBV infection in vivo.

176 tical to identify those at risk of acquiring HBV infections in order to target testing and vaccinatio

177 th HBeAg-negative chronic hepatitis B virus (HBV) infection in a non-inferiority study.

178 th HBeAg-positive chronic hepatitis B virus (HBV) infection in a non-inferiority study.

179 lack of models that mimic hepatitis B virus (HBV) infection in a physiologically relevant context has

180 age-dependent outcomes of hepatitis B virus (HBV) infection in humans, we previously established an a

181 mate the global burden of hepatitis B virus (HBV) infection in people living with human immunodeficie

182 lence and distribution of hepatitis B virus (HBV) infection in U.S. Hispanics/Latinos.

183 se in the number of acute hepatitis B virus (HBV) infections in the United States.

184 adolescents and adults at increased risk for HBV infection, including those who were vaccinated befor

185 fection on the basis of persistent (chronic) HBV infection increased HBV-specific T-cell frequency an

186 Chronic HBV infection increases long-term morbidity and mortalit

187 Chronic HBV infection is a major cause of liver disease and canc

188 be a target of antiviral therapy.IMPORTANCE HBV infection is a worldwide health problem, but the mec

189 Acute HBV infection is characterized by complex array of viral

190 of high-risk groups, diagnosing and treating HBV infection is likely to be of most impact in driving

191 HBV infection is noncytopathic, and liver injury is most

192 lable antiviral therapeutics to cure chronic HBV infection is their inability to eradicate or inactiv

193 Chronic hepatitis B virus (HBV) infection is a global public health challenge on th

194 Chronic hepatitis B virus (HBV) infection is a global public health issue.

195 Chronic hepatitis B virus (HBV) infection is a global public health problem.

196 Hepatitis B virus (HBV) infection is a major cause of acute and chronic liv

197 Chronic hepatitis B virus (HBV) infection is a major public health problem that aff

198 Chronic hepatitis B virus (HBV) infection is a major risk factor for developing hep

199 Chronic hepatitis B virus (HBV) infection is a major risk factor for hepatocellular

200 Chronic hepatitis B virus (HBV) infection is a risk factor for hepatocellular carci

201 Hepatitis B virus (HBV) infection is a serious public health problem, which

202 Chronic hepatitis B virus (HBV) infection is estimated to affect >350 million peopl

203 Chronic Hepatitis B Virus (HBV) infection is generally not curable with current ant

204 Hepatitis B virus (HBV) infection is more common in African Americans than

205 Chronic hepatitis B virus (HBV) infection is partly responsible for hepatitis, fatt

206 A hallmark of chronic hepatitis B virus (HBV) infection is the functional impairment and depletio

207 immunopathogenesis studies in children with HBV infection; long-term follow-up of children on nucleo

208 ecular explanation for why immunotherapy for HBV infection may require combinations of complementary

209 cation in patients with inactive or resolved HBV infection, may result in clinically significant hepa

210 In both models of HBV infection, mice that express hepatocyte-specific sma

211 is end, we employed physiologically relevant HBV infection models of primary human hepatocytes (PHHs)

212 of CHB patient liver parenchyma and in vitro HBV infection models shows a nonuniform distribution of

213 e used state-of-the-art in vitro and in vivo HBV infection models to evaluate a role for HBV infectio

214 In 3 studies of patients with resolved HBV infection, none received HBV prophylaxis and reactiv

215 of a seronegative occult hepatitis B virus (HBV) infection (OBI) in a successfully vaccinated infant

216 the complex epigenetic landscape of chronic HBV infection observed in vivo and demonstrate that fine

217 Persons born in regions with a prevalence of HBV infection of 2% or greater, such as countries in Afr

218 ative sample showed a prevalence of maternal HBV infection of 85.8 cases per 100 000 deliveries from

219 so disrupted cccDNA synthesis during de novo HBV infection of HepG2 cells expressing sodium taurochol

220 ound that the HBsAg seroclearance in chronic HBV infections of China aged 1-59 years occurred at an a

221 ntigen (HBsAg) in chronic hepatitis B virus (HBV) infections of China remains unclear.

222 Chronic hepatitis B virus (HBV) infection often develop into cirrhosis, and both ar

223 gh AST significantly mediates the effects of HBV infections on any cataract outcome, but the associat

224 to other causes, such as hepatitis B virus (HBV) infection or alcohol, remains unknown.

225 from patients in different stages of chronic HBV infection, our work shows that the profile of histon

226 BV infection, S mansoni infection influenced HBV infection outcomes in a phase-dependent manner.

227 HBeAg negativity is thus an ancient HBV infection pattern, whereas Ntcp usage for entry is n

228 Hepatitis B virus (HBV) infection persists because the virus-specific immun

229 National HBV infection prevalence in persons who inject drugs rem

230 The national HBV infection prevalence in persons who inject drugs rem

231 mined reactivation in patients with resolved HBV infection receiving chemotherapy for hematologic mal

232 isolated from patients with chronic HDV and HBV infection recognize HDV epitopes presented by multip

233 inical courses of chronic hepatitis B virus (HBV) infection reflect the complex host-virus interactio

234 of chronic hepatitis B.IMPORTANCE Persistent HBV infection relies on stable maintenance and proper fu

235 Acute hepatitis B virus (HBV) infection remains a frequent cause of acute liver f

236 Hepatitis B virus (HBV) infection remains a major global health problem, ex

237 h immune-tolerant chronic hepatitis B virus (HBV) infection remains unknown.

238 Hepatitis B virus (HBV) infection represents a significant public health bu

239 a large proportion of patients with chronic HBV infection require antiviral therapy in Vietnam.

240 Chronic hepatitis B virus (HBV) infections result in 887,000 deaths annually.

241 HDV) superinfection of patients with chronic HBV infection results in rapid progression to liver cirr

242 70 liver biopsies from patients with chronic HBV infection revealed that the fraction of linear HBV D

243 ological evidence of vaccine protection from HBV infection rose from 57.8 (95% CI: 55.4-60.1) million

244 was not affected by either acute or chronic HBV infection, S mansoni infection influenced HBV infect

245 (serum HBV core antibody; anti-HBc), active HBV infection (serum HBV surface antigen; HBsAg), and va

246 (SDGs) for elimination of hepatitis B virus (HBV) infection set ambitious targets for 2030.

247 in patients with chronic hepatitis B virus (HBV) infection significantly reduces liver-related compl

248 Baseline HBV infection status for each veteran was identified fro

249 cine failure with chronic hepatitis B virus (HBV) infection still develops in children after universa

250 t recapitulated in existing models for acute HBV infection, suggesting a role for inflammatory mediat

251 porting proportions of patients with chronic HBV infection that achieved spontaneous HBsAg loss, publ

252 (15%) of the adult participants with chronic HBV infection that were enrolled from January 20, 2011,

253 mmend vaccination of adults at high risk for HBV infection, the prevalence of undetectable immunity (

254 Among adults at high risk for HBV infection, the prevalence of undetectable immunity d

255 aque hepatocytes renders them susceptible to HBV infection, thereby establishing a physiologically re

256 atocytes hampers efficient innate control of HBV infection; this may explain why HBV has adapted to s

257 TANCE The inability of patients with chronic HBV infection to clear HBV is associated with defective

258 blishing a physiologically relevant model of HBV infection to study immune clearance and test therape

259 of-the-art models for both acute and chronic HBV infection to study the pathogen-crosstalk during the

260 t enrolled children (<18 years) with chronic HBV infection treated with antiviral therapy.

261 ion of anticancer therapy.Patients with past HBV infection undergoing anticancer therapies associated

262 ic T cell receptor (TCR) may achieve cure of HBV infection upon adoptive transfer.

263 humanized liver FRG mice strongly inhibited HBV infection, validating PLK1 as an antiviral target in

264 Current barriers to eradication of incident HBV infections via MTCT include underutilization of immu

265 ectly evaluated the effects of screening for HBV infection vs no screening on clinical outcomes such

266 The prevalence of active HBV infection was 0.29% (95% confidence interval: 0.19-0

267 al time after HCC diagnosis for persons with HBV infection was 22.3 months, compared with 13.1 months

268 The pooled prevalence of HBV infection was 8.4% (95% confidence interval [CI], 7.

269 The pooled prevalence of HBV infection was 8.4% (95% confidence interval: 7.9-8.8

270 Antiviral therapy for HBV infection was associated with improved intermediate

271 HBV infection was defined by positive HBsAg and past exp

272 The prevalence of HBV infection was determined by serological testing and

273 Prevalence of HBV infection was highest in non-Hispanic Asians in both

274 Prevalence of HBV infection was highest in non-Hispanic Asians in both

275 Genotype C HBV infection was more frequent in the vaccine failure g

276 No significant change in the prevalence of HBV infection was observed between 1999 and 2016 (P = 0.

277 Nationally, the annual rate of acute HBV infections was stable, but increased in Kentucky, Al

278 Nationally, the annual rate of acute HBV infections was stable, but rates increased in Kentuc

279 tios (ORs) for nuclear and any cataract with HBV infection were 1.09 [95% confidence interval (95CI)

280 Most of the children with chronic HBV infection were in the immune-tolerant phase.

281 .01) were less likely to be associated with HBV infection, whereas having a mother with hepatitis wa

282 an 260 million people worldwide have chronic HBV infection, which causes 0.8 million deaths a year.

283 f new therapies for the treatment of chronic HBV infection, which has so far been very challenging.

284 cleos(t)ide analogs in patients with chronic HBV infection, which is under way.

285 here is no cure for individuals with chronic HBV infection, which they acquire during early life.

286 lts with IDU history had previous or ongoing HBV infection, which was over four times higher than the

287 ansplanted for terminal liver disease due to HBV infection who were HBV DNA-negative at transplant we

288 on alfa-2a (pegIFN) in patients with chronic HBV infection who were negative for hepatitis B e antige

289 Patients with chronic HBV infection who were positive for the hepatitis B e an

290 Patients with resolved hepatitis B virus (HBV) infection who are treated for hematological maligna

291 tion has been effectively preventing chronic HBV infection with >90% efficacy in countries with unive

292 were associated with diabetes prevalence and HBV infection with the risk of incident diabetes.

293 t least 18 years with HBeAg-negative chronic HBV infection (with plasma HBV DNA concentrations of >20

294 ave HBeAg-positive or HBeAg-negative chronic HBV infection, with serum HBV DNA concentrations of at l

295 antigen-positive or -negative (74%) chronic HBV infection without cirrhosis.

296 n poorly documented in patients with chronic HBV infection worldwide, especially in low-and-middle-in

297 ntribute markedly to the goal of eliminating HBV infection worldwide.

298 V) remains the major risk factor for chronic HBV infection worldwide.

299 highest rates of chronic hepatitis B virus (HBV) infection worldwide, but little is known about HBV

300 and this stimulation significantly inhibits HBV infection, yet only minimally affects the ability of