ライフサイエンスコーパス: HBV infection

1 ho were vaccinated before being screened for HBV infection).

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

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

4 une system to efficiently counteract chronic HBV infection.

5 ixture (A + D) were compared for severity of HBV infection.

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

7 ay-even in patients with early stage chronic HBV infection.

8 nucleos(t)ide-analogue treatment in chronic HBV infection.

9 g intrahepatic virological events in chronic HBV infection.

10 No participant had evidence of breakthrough HBV infection.

11 HBsAg used to distinguish those with active HBV infection.

12 nd their possible association with phases of HBV infection.

13 t a role of HNF6 in the gender dimorphism of HBV infection.

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

15 on-related benefit of markedly reduced overt HBV infection.

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

17 possibility of a functional cure of chronic HBV infection.

18 gMDSCs to regulate liver immunopathology in HBV infection.

19 d vanitaracin A, which specifically inhibits HBV infection.

20 dentify factors associated with incidence of HBV infection.

21 d also screen patients with risk factors for HBV infection.

22 ted anti-HBs positive, and 3.4% had an overt HBV infection.

23 nction of cIAPs may promote the clearance of HBV infection.

24 onses in a transgenic mouse model of chronic HBV infection.

25 uld be a new therapeutic approach to chronic HBV infection.

26 patients with lamivudine-resistant, chronic HBV infection.

27 up to protect persons who remain at risk of HBV infection.

28 of clinically significant acute and chronic HBV infection.

29 gh risk for infection should be screened for HBV infection.

30 developed into a viable treatment for human HBV infection.

31 lication and might play a role in persistent HBV infection.

32 e risk for clinical outcomes associated with HBV infection.

33 serum iron marginally increased during acute HBV infection.

34 seful substitute for liver biopsy in chronic HBV infection.

35 oited for development of novel treatments of HBV infection.

36 ficiency mice were used to establish chronic HBV infection.

37 like receptor 7--in chimpanzees with chronic HBV infection.

38 r MDA5 in the innate immune response against HBV infection.

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

40 elopment of antiviral agents against chronic HBV infection.

41 nfection but does not allow establishment of HBV infection.

42 actors are required for the establishment of HBV infection.

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

44 n vivo renders rhesus macaques permissive to HBV infection.

45 regions; and adults seeking protection from HBV infection.

46 to create hepatoma cell lines susceptible to HBV infection.

47 viral replication and the outcome of chronic HBV infection.

48 aspires to global control and elimination of HBV infection.

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

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

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

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

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

54 that result from chronic hepatitis B virus (HBV) infection.

55 rely addressed in chronic hepatitis B virus (HBV) infection.

56 seroconversion in chronic hepatitis B virus (HBV) infection.

57 a highly endemic area for hepatitis B virus (HBV) infection.

58 MSM) are at high risk for hepatitis B virus (HBV) infection.

59 gical screening to detect hepatitis B virus (HBV) infection.

60 in patients with chronic hepatitis B virus (HBV) infection.

61 in patients with chronic hepatitis B virus (HBV) infection.

62 tibody response following hepatitis B virus (HBV) infection.

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

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

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

66 t of treatment of chronic hepatitis B virus (HBV) infections.

67 nted worldwide to prevent hepatitis B virus (HBV) infections.

68 re (20.3% in women, 29.7% in men) and active HBV infection (0.95%).

69 -year survival rate was 37.5% for those with HBV infection, 20.0% for those with HCV infection, 29.5%

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

71 serum samples from 62 patients with chronic HBV infection (50 HBeAg positive).

72 202 patients with chronic hepatitis B virus (HBV) infection, 50% were aged 44-63 years, 57% male, 58%

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

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

75 individuals with chronic hepatitis B viral (HBV) infection acquired the infection around the time of

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

77 Chronic hepatitis B virus (HBV) infection affects 240 million people worldwide and

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

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

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

81 atitis C virus (HCV), and hepatitis B virus (HBV) infections, altered iron balance correlates with mo

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

83 -0.4), and since 1999, prevalence of chronic HBV infection among non-Hispanic blacks has been 2- to 3

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

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

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

87 ow-Smad4 showed significant correlation with HBV infection and a poor overall survival rate.

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

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

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

91 Incidence rates of HBV infection and hepatitis B surface antigen serocleara

92 ound that miR-15b, an important miRNA during HBV infection and hepatocellular carcinoma development,

93 These results suggest that establishment of HBV infection and its replication space is limited by th

94 uce type 1 IFN in response to foreign DNA or HBV infection and mice lacking STING or cyclic guanosine

95 Smac mimetics may have efficacy in treating HBV infection and perhaps, other intracellular infection

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

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

98 inuous monitoring of children with wild-type HBV infection and those with HBsAg-mutant HBV for possib

99 the current strategy prevented 1,006 chronic HBV infections and saved 13,600 QALYs (ICER: $6,957/QALY

100 are a high-risk group for hepatitis B virus (HBV) infection and transmission, but adherence to vaccin

101 rse of the immune-clearance phase in chronic HBV infection, and are predictive of spontaneous HBsAg s

102 al cells (MPCCs) reliably support productive HBV infection, and infection can be enhanced by blocking

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

104 and sequenced from 148 patients with chronic HBV infection, and the human leukocyte antigen (HLA) cla

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

106 reports of hepcidin levels in patients with HBV infections, and the available results are inconsiste

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

108 eatment and prevention of hepatitis B virus (HBV) infection, anti-HBV agents targeting a new molecule

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

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

111 interval [CI], 5.0-6.7), hepatitis B virus (HBV) infection (AOR, 2.40; 95% CI, 2.0-2.9), age (AOR, 1

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

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

114 gen (anti-HBc) and occult hepatitis B virus (HBV) infection are not well known in human immunodeficie

115 s models were used, with an incident case of HBV infection as the outcome variable.

116 We defined an incident HBV infection as the presence of any of HBV serological

117 ion and 64 consecutive patients with chronic HBV infection (as control).

118 ves to serology testing for the screening of HBV infection at field level in SSA.

119 1992 from patients with replicative chronic HBV infection at the University of Miami were genotyped

120 Despite an overall decline in HBV infection, attributable to successful vaccination pr

121 viders should screen by testing patients for HBV infection before starting anti-CD20 therapy or hemat

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

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

124 port induction of HBV-specific immunity upon HBV infection, but may also contribute to liver patholog

125 inst lamivudine-resistant hepatitis B virus (HBV) infection, but data to support its clinical efficac

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

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

128 IAPs) impair clearance of hepatitis B virus (HBV) infection by preventing TNF-mediated killing/death

129 Hepatitis B virus (HBV) infection can result in a spectrum of outcomes from

130 e epitopes targeted by patients with chronic HBV infection carrying the relevant HLA class I allele.

131 ti-HBV CTL activity in patients with chronic HBV infection (CHB).

132 In lymphoma patients with resolved HBV infections, chemotherapy-induced HBV reactivation is

133 In acute HBV infection, clearance of HBV may happen between 6 and

134 d total cIAP2 deficiency efficiently control HBV infection compared with WT mice.

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

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

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

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

139 or all sites combined, the incidence rate of HBV infection declined by 19%, but in Tennessee incidenc

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

141 Some patients with acute hepatitis B virus (HBV) infection develop chronic infection.

142 Although HBV infection did not directly affect protein level or p

143 where the prevalence and natural history of HBV infection differ from those of the United States.

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

145 HBV infection evokes significant immune responses even i

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

147 screening guidelines for hepatitis B virus (HBV) infection for asymptomatic, nonpregnant adolescents

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

149 ntification of small molecules that suppress HBV infection from new chemical sources.

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

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

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

153 Chronic hepatitis B virus (HBV) infection has been associated with alterations in l

154 ion, diversity of chronic hepatitis B virus (HBV) infection has changed, affecting disease burden and

155 re settings among persons at sexual risk for HBV infection have been sparse.

156 AART was negatively associated with incident HBV infection (hazard ratio [HR], 0.4; 95% confidence in

157 ivation in lymphoma patients with "resolved" HBV infection (hepatitis B surface antigen [HBsAg] negat

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

159 In HBeAg-positive patients with chronic HBV infection, high viral loads, normal levels of alanin

160 HAART is associated with lower incidence of HBV infection; however, even in the HAART era, incidence

161 nical phases of a chronic hepatitis B virus (HBV) infection-immune tolerant (IT), immune active (IA),

162 The incidence of HBV infection in 5-14-year-old subjects was less than 1

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

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

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

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

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

168 ancy, we investigated the natural history of HBV infection in Greenland by estimating the age-specifi

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

170 e antiretroviral therapy (HAART) on incident HBV infection in HIV-infected and HIV-uninfected MSM are

171 ctively prevent severe acute exacerbation of HBV infection in hospitals among HBV endemic areas.

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

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

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

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

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

177 ssion was used to compare incidence rates of HBV infection in the pre-HAART and HAART eras and to ide

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

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

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

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

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

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

184 Reactivation of hepatitis B viral (HBV) infection in cancer patients undergoing chemotherap

185 However, studies of hepatitis B virus (HBV) infection in chimpanzees have indicated that cytoki

186 kinetics and magnitude of hepatitis B virus (HBV) infection in hepatitis C virus (HCV)-naive and chro

187 The origin of hepatitis B virus (HBV) infection in humans and other primates remains larg

188 in patients with chronic hepatitis B virus (HBV) infection in North America are unknown.

189 espite the high burden of hepatitis B virus (HBV) infection in sub-Saharan Africa, absence of widespr

190 r of persons with chronic hepatitis B virus (HBV) infection in the United States is affected by dimin

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

192 ecent epidemic history of hepatitis B virus (HBV) infections in the United States is complex, as indi

193 nant adolescents and adults at high risk for HBV infection (including those at high risk who were vac

194 Antiviral treatment for chronic HBV infection is associated with improved intermediate o

195 HBV infection is associated with significant morbidity a

196 Acute HBV infection is characterized by complex array of viral

197 Although chronic HBV infection is considered the main risk factor for liv

198 The efficacy of Smac mimetics in treating HBV infection is dependent on their chemistry, host CD4(

199 HBV infection is noncytopathic, and liver injury is most

200 Chronic hepatitis B virus (HBV) infection is a common cause of the development of l

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

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

203 Hepatitis B virus (HBV) infection is a leading cause of death in sub-Sahara

204 Hepatitis B virus (HBV) infection is a major cause of morbidity and mortali

205 Chronic hepatitis B virus (HBV) infection is a major factor in hepatocellular carci

206 Chronic hepatitis B virus (HBV) infection is a major global health burden.

207 Hepatitis B virus (HBV) infection is a major health issue worldwide.

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

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

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

211 Persistent hepatitis B virus (HBV) infection is established by the formation of an int

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

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

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

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

216 Chronic hepatitis B virus (HBV) infection is prevalent, deadly, and seldom cured du

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

218 ive patients with chronic hepatitis B virus (HBV) infection is unknown.

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

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

221 hat the presumed immune tolerance in chronic HBV infections needs to be redefined.

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

223 Occult HBV infection (OBI) is defined by the persistence of HBV

224 Occult hepatitis B virus (HBV) infection (OBI) is defined as low plasma level of H

225 munization affects occult hepatitis B virus (HBV) infection (OBI), serum samples from hepatitis B sur

226 An estimated 20 000 new hepatitis B virus (HBV) infections occur each year in the United States.

227 ,322 person-years of follow-up, 244 incident HBV infections occurred.

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

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

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

231 mouse model to study the effect of maternal HBV infection on HBV persistence in offspring and found

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

233 h most patients serologically resolved acute HBV infection, only 54.1% developed antibody to HBsAg (a

234 V) screening among patients at high risk for HBV infection or HBV reactivation after chemotherapy.

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

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

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

238 ful vaccination programs, a rise in incident HBV infection related to drug use is an increasing conce

239 however, even in the HAART era, incidence of HBV infection remains high among MSM.

240 HBV infection remains highly prevalent in The Gambia.

241 Hepatitis B virus (HBV) infection remains a major health problem worldwide.

242 Chronic hepatitis B viral (HBV) infection remains a significant global health probl

243 Chronic hepatitis B virus (HBV) infection remains the most common risk factor for h

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

245 epatocytes, while species specificity of the HBV infection requires selective downstream events, e.g.

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

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

248 during the primary viremic phases of HCV or HBV infection; serum iron marginally increased during ac

249 reatment of asymptomatic people with chronic HBV infection should reduce the disease burden.

250 ome from countries with a high prevalence of HBV infection, should be screened.

251 Baseline HBV infection status for each veteran was identified fro

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

253 vary dramatically in their permissiveness to HBV infection, suggesting that factors--such as divergen

254 , the only agents available to treat chronic HBV infection target the viral polymerase, and no select

255 In patients with HBeAg-positive HBV infection, tenofovir alafenamide was non-inferior to

256 ng an immunocompetent mouse model of chronic HBV infection that birinapant and other Smac mimetics ar

257 d into hepatocyte-like cells (iHeps) support HBV infection that can also be enhanced by blocking inte

258 (15%) of the adult participants with chronic HBV infection that were enrolled from January 20, 2011,

259 by estimating the age-specific incidence of HBV infection, the proportion of chronic carriers, and t

260 For mothers with chronic hepatitis B virus (HBV) infection, the Centers for Disease Control and Prev

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

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

263 in human primary hepatocytes in response to HBV infection, through retinoic acid-inducible gene-I (R

264 strategy to identify and treat patients with HBV infection to reduce their risk of HBV reactivation.

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

266 the women with isolated anti-HBc and occult HBV infection transmitted HBV to their infants.

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

268 es that enrolled pregnant women with chronic HBV infection treated with antiviral therapy.

269 We followed 215 Japanese patients with acute HBV infection until the clearance of hepatitis B surface

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

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

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

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

274 Vaccination against HBV infection was associated with decreased risk in high

275 HBV infection was delayed and attenuated in the HCV-infe

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

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

278 ng an immunocompetent mouse model of chronic HBV infection, we identified some of the host cellular a

279 Using a mouse model of HBV infection, we sought mechanisms underpinning the age

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

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

282 Those with HBV infection were primarily Asian/Pacific Islanders (63

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

284 endently associated with higher incidence of HBV infection, whereas HBV vaccination was protective (I

285 es that during 2011-2012, there were 847,000 HBV infections (which included ~400,000 non-Hispanic Asi

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

287 dults >/=18 years old diagnosed with chronic HBV infection who received antiviral therapy.

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

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

290 ly diagnosed lymphoma patients with resolved HBV infection who were to receive rituximab-CHOP (cyclop

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

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

293 ssion and reduces MTCT in women with chronic HBV infection with high viral load compared to the use o

294 anti-HBc pattern likely represents resolved HBV infection with low or undetected anti-HBs.

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

296 r with active or resolved hepatitis B virus (HBV) infection with a clinical spectrum that ranges from

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

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 c spread (yes or no), and hepatitis B virus (HBV) infection (yes or no).