ライフサイエンスコーパス: HBV

1 HBV cccDNA is converted from viral genomic relaxed circu

2 HBV chronic infection remains the major cause of hepatoc

3 HBV infection (hepatitis B surface antigen) was diagnose

4 HBV infection was defined by positive HBsAg and past exp

5 HBV integration in 50 patients with HBV-related HCC was

6 HBV was found in 69.5% of HCC and 47.2% of cirrhosis cas

7 HBV-DNA and HBV-RNA decreased from baseline in patients

8 HBV-related HCC can be prevented by reducing the exposur

9 black, 93% had HIV RNA<400 copies/mL and 83% HBV DNA<1000 IU/mL.

10 nificantly to broadening the knowledge about HBV composition and should be continued to obtain the mo

11 mising immunotherapeutic tools for achieving HBV functional cure in chronically infected humans.

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

13 In addition, HBV/HIV co-infected females presented at a younger mean

14 immunized twice with a mixture of adjuvanted HBV S and core antigen, followed by a modified Vaccinia

15 mine the protective humoral response against HBV, we cloned and characterized human antibodies specif

16 e development of preventive vaccines against HBV, a therapeutic vaccine inducing an effective antibod

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

18 ng (si)RNAs against the common 3'-end of all HBV transcripts were used to knock down antigen expressi

19 uestions focused on the yield of alternative HBV screening strategies and the accuracy of tools to id

20 on and an undisputed antiviral target for an HBV cure.

21 e with ALT >=40 IU/L, and 144 (28.0%) had an HBV DNA >5.3 log10 IU/mL.

22 Of note, pretreatment with an HBV entry inhibitor attenuated the TLR2-mediated respons

23 there is no evidence for coinfection with an HBV-related hepadnavirus based on virus detection and se

24 , HCV (APC = -0.50% [-0.81% to -0.18%]), and HBV (APC = -1.43% [-1.71% to -0.40%]).

25 functional, HBV-specific CD8(+) T cells, and HBV was eliminated.

26 HBV-DNA and HBV-RNA decreased from baseline in patients receiving al

27 RNA at treatment withdrawal, but HBcrAg and HBV DNA were not detected.

28 Detectable HBcrAg and HBV RNA at the time of treatment withdrawal was only obs

29 erapy, 33% and 30% had detectable HBcrAg and HBV RNA, respectively, despite all being HBV-DNA negativ

30 th NA, 27% and 14% had detectable HBcrAg and HBV RNA.

31 ical biomarkers (HBV DNA, HBsAg, HBcrAg, and HBV RNA) were measured in sequential samples at differen

32 Levels of HBsAg, anti-HBs, and HBV DNA did not differ significantly between the groups

33 AV-Env can redirect T cells from healthy and HBV-infected donors toward hepatocellular carcinoma (HCC

34 ing drugs with dual activity against HIV and HBV exists.

35 ran Africa, the overlap between high HIV and HBV prevalence may increase the incidence of HCC.

36 Antivirals, common to HIV and HBV, suppress HBV DNA levels but do not eradicate virus

37 opulations with high burdens of both HIV and HBV.

38 Here, we compared the phenotypes and HBV-specific response of lymphocytes in CHB patients str

39 Anti-HBV siRNAs and therapeutic vaccines are each being teste

40 tly, knocking out MCPIP1 attenuated the anti-HBV effect of IL-1beta, suggesting that MCPIP1 is requir

41 f siRNAs had reduced levels of HBV antigens, HBV replication, and viremia (1-3 log(10) reduction) com

42 50 cells/mm3, female sex, and lower baseline HBV deoxyribonucleic acid were associated with increased

43 ch is formed by the repair of lesion-bearing HBV relaxed circular DNA delivered by the virions to hep

44 and HBV RNA, respectively, despite all being HBV-DNA negative.

45 ular changes after the first contact between HBV and primary human hepatocytes (PHH) in vitro and in

46 genetic associations to TDF response between HBV genotypes B and C and lack of a single pattern of mu

47 s of HBV serological/virological biomarkers (HBV DNA, HBsAg, HBcrAg, and HBV RNA) were measured in se

48 treatments for chronic infections with both HBV and HCV should contribute to declines in the rates o

49 Treatment of PHH with both HBV particles and Pam3Cys led to phosphorylation of ERK

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

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

52 partial serological conversion in a chronic HBV mouse model, offering a promising translatable vacci

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

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

55 more than half of HCC patients being chronic HBV carriers, even if underlying mechanisms of tumorigen

56 trials-their combination might cure chronic HBV infection.

57 Long-term viremia in chronic HBV patients occurs either spontaneous in inactive carri

58 The national prevalence of new, chronic HBV diagnoses decreased significantly, from 0.83% in 201

59 nt implications for the treatment of chronic HBV infection.

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

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

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

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

64 is C virus compared to patients with chronic HBV.

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

66 cccDNA in liver biopsies from 56 chronically HBV infected patients after 3 to 5 years of telbivudine

67 absolute copy numbers of total and circular HBV DNA, and calculation of linear HBV DNA.

68 istone deacetylase 1 (HDAC1) to circularized HBV DNA (which resembles covalently closed circular DNA

69 d Nutrition Examination Survey who completed HBV core antibody (anti-HBc) and surface antigen (HBsAg)

70 HBsAg) tests and 47,618 adults who completed HBV surface antibody (anti-HBs) and anti-HBc tests were

71 Consequently, HBV was completely rescued in IFN-gamma-deficient or in

72 The central challenge in curing HBV is eradication of the stable covalently closed circu

73 Current HBV treatments are only marginally effective against HDV

74 Overexpression of MCPIP1 decreased HBV RNA, whereas ablating MCPIP1 in vitro enhanced HBV p

75 HBV reactivation in cohort C had detectable HBV RNA at treatment withdrawal, but HBcrAg and HBV DNA

76 naviral life-cycle were unraveled using duck HBV (DHBV) as a model although DHBV has a capsid protein

77 higher rates of functional cure than during HBV monoinfection treatment.

78 encing at days 8 and 28 on SACC-PHHs, either HBV mono-infected or HBV/HDV co-infected.

79 fully restore T-cell function and eliminate HBV.

80 ad a reduction in intracellular encapsidated HBV DNA (33-64% reduction).

81 vaccine vectors expressing HBV Ags engender HBV-specific CD8(+) T cells unconventionally restricted

82 A, whereas ablating MCPIP1 in vitro enhanced HBV production.

83 cell line to uncover host factors enhancing HBV infection.

84 ined by genetic variations across the entire HBV genome.

85 on-HBV-specific T cells, bypassing exhausted HBV-specific T cells.

86 macaque (RM) CMV vaccine vectors expressing HBV Ags engender HBV-specific CD8(+) T cells unconventio

87 relates with inhibitory receptor expression, HBV-specific CD4(+) T cell responses, and augmentation b

88 Finally, HBV-induced gene expression could be neutralized by TLR2

89 For HBV, HPV16, HPV18 and adeno-associated virus-2 (AAV2), v

90 vel >5.3 log10 IU/mL and 92.7% and 88.1% for HBV DNA >7.3 log10 IU/mL.

91 pecificity of HBeAg were 61.8% and 99.2% for HBV DNA >5.3 log10 IU/mL and 81.3% and 96.7% for HBV DNA

92 ity and specificity were 79.2% and 93.3% for HBV DNA level >5.3 log10 IU/mL and 92.7% and 88.1% for H

93 DNA >5.3 log10 IU/mL and 81.3% and 96.7% for HBV DNA >7.3 log10 IU/mL.

94 iver samples were collected and analyzed for HBV-specific immune responses, liver damage, and viral p

95 sed and the farnesylation motif critical for HBV interaction is absent from a genome region that migh

96 ified CDKN2C as an important host factor for HBV replication.

97 ctively, whereas there were no increases for HBV (P = 0.224) and HCV (P = 0.054).

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

99 d previously reported ETV/3TC resistance for HBV using HIV(Y115F/F116Y/Q151M) with F160M/M184V (L180M

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

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

102 ho were vaccinated before being screened for HBV infection.

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

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

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

106 adults aged 18-49 years who were tested for HBV and reported at least 1 of the following infection r

107 emic anticancer therapy should be tested for HBV by 3 tests-hepatitis B surface antigen (HBsAg), hepa

108 We identified 8 871 965 women tested for HBV from 2011-2017.

109 Patients were tested for HBV, hepatitis C virus (HCV) and HIV.

110 could inform immunomodulatory therapies for HBV cure.

111 y of simplified treatment criteria free from HBV DNA and FibroScan (TREAT-B score and simplified WHO

112 red to the simplified WHO criteria free from HBV DNA quantification, TREAT-B is a better alternative

113 d hepatitis B associated glomerulonephritis (HBV-GN) significantly decreased between the two interval

114 proximately 10% of people with HIV also have HBV and are at higher risk of liver disease progression

115 erase (ALT) >=40 IU/L as a predictor of high HBV DNA level.

116 Immune recovery during HIV-HBV treatment with ART may drive higher rates of functio

117 nsferase (ALT) overtime were examined in HIV-HBV coinfection.

118 About 30% with HIV-HBV coinfection had FLD including 10% with steatohepatit

119 on, we isolated >1100 hepatocytes from 5 HIV/HBV coinfected persons with increasing exposure to HBV a

120 HCC is an important complication in the HIV/HBV infected patient.

121 y of TDF binding by RT encoded by intra-host HBV variants that rapidly decline or persist in presence

122 We found that human HBV antibodies are encoded by a diverse set of immunoglo

123 l could be an effective strategy to identify HBV-infected pregnant women at risk of perinatal transmi

124 circulating HBsAg clearance does not improve HBV-specific CD8+ T cell responses in vivo and may have

125 nced fibrosis compared with APRI or FIB-4 in HBV/HIV co-infected adults on combined antiretroviral th

126 o acids, carbohydrates, and organic acids in HBV, but also provided information on venom components f

127 proposed sensor was successfully applied in HBV DNA detection in sera from patients without any ampl

128 ether, our findings define key components in HBV cccDNA formation.

129 nd no evidence of hypoxia gene expression in HBV de novo infection, HBV infected human liver chimeric

130 ion drug use and highlight potential gaps in HBV vaccine protection.

131 116Y/Q151M) with F160M/M184V (L180M/M204V in HBV RT) substituted.

132 MS, were applied to quantify metabolites in HBV samples.

133 A reduction in viral markers was observed in HBV-infected primary human hepatocytes treated with medi

134 allergen Api m 1 (phospholipase A2: PLA2) in HBV.

135 Eight mutants with >70% reduction in HBV RNA and/or HBsAg were selected for chromatin immunop

136 60 and 121-126 may play an important role in HBV transcription regulation, via their impeded interact

137 er risk of liver disease progression than in HBV monoinfection.

138 tibody Bc1.187 suppressed viremia in vivo in HBV mouse models and led to post-therapy control of the

139 ence of viral antigen expression, inadequate HBV-specific immune responses, and treatment regimens th

140 persistent (chronic) HBV infection increased HBV-specific T-cell frequency and resulted in suppressio

141 ersion) is usually associated with increased HBV-specific T cell responsiveness.

142 ified Vaccinia virus Ankara vector to induce HBV-specific B- and T-cell responses.

143 ia gene expression in HBV de novo infection, HBV infected human liver chimeric mice or transgenic mic

144 scriminating between circular and integrated HBV DNA, and to relate the distribution between the two

145 l T cells toward cells containing integrated HBV and cells infected with HBV was assessed using cytok

146 carcinoma (HCC) cells containing integrated HBV DNA resulting in cytokine release, which could be su

147 eric mice or transgenic mice with integrated HBV genome.

148 of mutants had lower levels of intracellular HBV RNA (44-77% reduction) and secretory HBsAg (25-81% r

149 The degree of integration of intrahepatic HBV DNA in the HBeAg-negative stage may be higher than p

150 There is no known HBV resistance to TDF.

151 circular HBV DNA, and calculation of linear HBV DNA.

152 high HBsAg serum levels in patients with low HBV DNA levels.

153 tis D patients did not differ from a matched HBV mono-infected cohort with comparable frequency of li

154 s (range: 18-86), 32% HBeAg-positive, median HBV DNA 4.8 log10 IU/ml (undetectable-8.4), median Fibro

155 hat MCPIP1 is required for IL-1beta-mediated HBV RNA reduction.

156 n the venom of the honey bee Apis mellifera (HBV).

157 or functional cure (HBsAg below 0.05 IU/mL, HBV DNA target not detected, normal level of alanine ami

158 We analysed 400 consecutive treatment-naive HBV-monoinfected patients: 49% males, median age 38 year

159 EP 2139-Ca against HDV in 12 treatment-naive HBV/HDV co-infected patients.

160 infected cells by redirecting endogenous non-HBV-specific T cells, bypassing exhausted HBV-specific T

161 A retrospective analysis of HBV statuses among women of childbearing age nationally

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

163 6 500 (95% CI, 2 952 000-3 284 100) cases of HBV in PLWH, with 73.8% of estimated regional cases from

164 glycoproteins (HBsAg) from memory B cells of HBV vaccinees and controllers.

165 From a cohort of HBV-infected patients in Vietnam, we assessed the propor

166 Concentrations of HBV serological/virological biomarkers (HBV DNA, HBsAg,

167 lay a key role in the spontaneous control of HBV and represent promising immunotherapeutic tools for

168 gens in liver might increase the efficacy of HBV vaccines in mice.

169 as only a minimal effect on the expansion of HBV-specific naive CD8+ T cells undergoing intrahepatic

170 s and increased numbers and functionality of HBV-specific, CD8(+) T cells in mice with low, but not i

171 dence for the clinical benefits and harms of HBV screening vs no screening.

172 come countries hinders the identification of HBV-infected pregnant women at risk of perinatal transmi

173 This study investigated the impact of HBV/HIV co-infection on age at presentation and survival

174 nitially high titers of HBV and knockdown of HBV antigen expression, but not mice with reduced viremi

175 atory cytokine IL-1beta reduced the level of HBV RNA.

176 th low, but not in mice with high, levels of HBV antigen.

177 d whether knocking down expression levels of HBV antigens in liver might increase the efficacy of HBV

178 s injections of siRNAs had reduced levels of HBV antigens, HBV replication, and viremia (1-3 log(10)

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

180 itis B core antigen (anti-HBc; prevalence of HBV exposure).

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

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

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

184 A declining prevalence of HBV seroprotection was evident over time, especially wit

185 Vaccination induced production of HBV-neutralizing antibodies and increased numbers and fu

186 the most comprehensive metabolite profile of HBV.

187 e previously described stealth properties of HBV.

188 Rates of HBV in women born before and after the implementation of

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

190 The seroprevalence of HBV and HCV infection in Malaysia is low and intermediat

191 The epsilon structure of HBV RNA was important for its antiviral activity and cle

192 However, structural studies of HBV RT have been hampered due to its unexpectedly poor s

193 sion level was higher in the liver tissue of HBV-infected patients and mice.

194 Mice with initially high titers of HBV and knockdown of HBV antigen expression, but not mic

195 f HCC recurrence after curative treatment of HBV-related HCC.

196 new insights into a better understanding of HBV rcDNA deproteination and cccDNA biosynthesis.

197 f CDK4/6 associated with the upregulation of HBV transcription enhancers.

198 interferon signaling reversed the effects on HBV replication.

199 investigated the effects of HBx mutations on HBV transcription and the recruitment of HBx, histone ac

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

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

202 28 on SACC-PHHs, either HBV mono-infected or HBV/HDV co-infected.

203 distribution between the two forms to other HBV markers.

204 ociated virus that transferred an overlength HBV genome-and expressed HB surface antigen at levels re

205 tion of entecavir, developed polyfunctional, HBV-specific CD8(+) T cells, and HBV was eliminated.

206 erapy and virologic control (HBsAg positive, HBV DNA below 2000 IU/mL, normal level of alanine aminot

207 ine serum levels of the ISG CXCL10 predicted HBV reactivation in a cohort of coinfected people taking

208 Pretreatment HBV DNA >=2000 IU/mL is associated with increased risk o

209 tein-1-induced protein 1 (MCPIP1) can reduce HBV RNA in hepatocytes.

210 previously undiscovered clinically relevant HBV host factor, allowing the development of improved in

211 ale C57BL/6 mice that persistently replicate HBV (genotype D, serotype ayw)-either from a transgene o

212 and new agents, could characterize residual HBV-RNA transcription from cccDNA and assist drug develo

213 system is a versatile platform for studying HBV/HDV co-infections and holds promise for performing c

214 Antivirals, common to HIV and HBV, suppress HBV DNA levels but do not eradicate virus because the tr

215 et irradiation of viral particles suppressed HBV infectivity but not the induction of cytokines in PH

216 ational guidelines based on reference tests (HBV DNA quantification and FibroScan); and the accuracy

217 higher health care use and cost burden than HBV alone, underscoring the need for improved screening

218 nted at a younger mean age (36.8 years) than HBV mono-infected women (50.5 years) (p = 0.09).

219 The HBV capsid assembly reaction can result in a heterogeneo

220 The HBV vaccine is effective in decreasing infections, but s

221 The HBV-induced gene expression profile was similar to that

222 the typical linearization breakpoint in the HBV genome allowed for quantification of the absolute co

223 as a cause of morbidity and mortality in the HBV/HIV co-infected patient population.

224 tems for drug discovery and the study of the HBV life cycle.

225 t targeted 3 non-overlapping epitopes on the HBV S antigen (HBsAg).

226 iated with few specific mutations in RT, the HBV on-TDF persistence is defined by genetic variations

227 We find that the HBV post-transcriptional regulatory element (PRE), speci

228 tence, which are differentially available to HBV strains.

229 r recurrence-free survival rates compared to HBV and HCV-HCC cases.

230 ly higher in the NAFLD-HCC cases compared to HBV-HCC (HR = 0.35, 95% CI 0.15-0.80) and HCV-HCC (HR =

231 infected persons with increasing exposure to HBV antivirals (HB1-HB5; no exposure to >7 years exposur

232 can be prevented by reducing the exposure to HBV by vaccination or by treatment of CHB infection.

233 The exposure of PHH to HBV particles resulted in nuclear translocation of NFkap

234 ths (LC and cirrhosis deaths were related to HBV [39% and 29%], HCV [29% and 26%], ALD [16% and 25%],

235 tor attenuated the TLR2-mediated response to HBV, suggesting a receptor binding-related mechanism.

236 To examine the human antibody response to HBV, we screened 124 vaccinated and 20 infected, spontan

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

238 Most adults were susceptible to HBV.

239 We estimated the prevalence of total HBV core antibody (anti-HBc) positivity, indicating a pr

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

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

242 re and after the implementation of universal HBV vaccination recommendations were determined.

243 developed experimental systems where various HBV relaxed-circular-DNA substrates are repaired to form

244 Honeybee (Apis mellifera) venom (HBV) has been a subject of extensive proteomics research

245 Hepatitis B virus (HBV) and hepatitis C virus (HCV) remain, at present, the

246 tailing in transcripts of hepatitis B virus (HBV) and human cytomegalovirus (HCMV), generated via a s

247 Epstein-Barr virus (EBV), hepatitis B virus (HBV) and human papilloma virus (HPV; for example, HPV16

248 Patients co-infected with hepatitis B virus (HBV) and the human immunodeficiency virus (HIV) are at r

249 unodeficiency virus (HIV)-hepatitis B virus (HBV) coinfected adults starting tenofovir-based antiretr

250 lack of activity against hepatitis B virus (HBV) could limit their global impact, particularly in po

251 Hepatitis B virus (HBV) covalently closed circular (ccc)DNA is the key geno

252 The biosynthesis of hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) requires th

253 The paucity of hepatitis B virus (HBV) DNA measurement in low-/middle-income countries hin

254 he persistent form of the hepatitis B virus (HBV) genome in viral infection and an undisputed antivir

255 data exist as to whether hepatitis B virus (HBV) has the ability to induce innate immune responses.

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

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

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

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

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

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

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

263 63.5% were susceptible to hepatitis B virus (HBV) infection, and 31.0% had at least one intestinal pa

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

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

266 nerated from junctions of hepatitis B virus (HBV) integration in the HCC chromosome, as a circulating

267 Hepatitis B virus (HBV) is a leading cause of liver disease.

268 Hepatitis B virus (HBV) is a leading cause of liver failure and hepatocellu

269 Hepatitis B virus (HBV) is a major health problem worldwide, with approxima

270 e as a satellite virus of hepatitis B virus (HBV) is a singular case in animal virology for which no

271 Hepatitis B virus (HBV) is an important but difficult to study human pathog

272 sub-Saharan Africa, where hepatitis B virus (HBV) is an important risk factor.

273 Hepatitis B virus (HBV) is the leading cause of hepatocellular carcinoma (H

274 Hepatitis B virus (HBV) is the major causative factor of chronic viral hepa

275 ailure) for patients with Hepatitis B Virus (HBV) related acute-on-chronic liver failure (ACLF).

276 Hepatitis B virus (HBV) remains a major global health problem with 257 mill

277 ite an effective vaccine, hepatitis B virus (HBV) remains a major public health threat since chronic

278 bly modulator that blocks hepatitis B virus (HBV) replication, was well tolerated and demonstrated do

279 evaluated the ability of hepatitis B virus (HBV) RNA and hepatitis B core-related antigen (HBcrAg) a

280 longed infection with the hepatitis B virus (HBV), which can substantially increase the risk of devel

281 firm advanced fibrosis in hepatitis B virus (HBV)-human immunodeficiency virus (HIV) co-infected pati

282 to augment the endogenous hepatitis B virus (HBV)-specific T cell response in CHB patients have demon

283 th chronic infection with hepatitis B virus (HBV).

284 ient-years was 49.3 among hepatitis B virus (HBV)/hepatitis C virus (HCV) coinfected and 18.2 among H

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

286 of perinatal transmission in countries where HBV DNA quantification is not routinely available.

287 uppressive effects of TH2 cytokines, whereas HBV coinfection did not alter schistosome pathogenicity.

288 n immunodeficiency virus type-1 (HIV-1) with HBV-associated amino acid substitutions Y115F/F116Y/Q151

289 on Survey to examine factors associated with HBV exposure among participants who reported ever using

290 9-153.38) were significantly associated with HBV exposure.

291 odeficient (SCID)/beige mice challenged with HBV in vivo, immune induction could only marginally be s

292 s. $18,228; P < 0.0001) in HDV compared with HBV alone.

293 Compared with HBV controls, HDV cases had an adjusted incident rate ra

294 terval [CI] 1.5-2.7) and to be infected with HBV (PR: 4.6; 95% CI 3.6-6.0) than Iraqi adults.

295 n-positive HCC cells and cells infected with HBV in vitro, causing a reduction of hepatitis B e antig

296 ining integrated HBV and cells infected with HBV was assessed using cytokine secretion assays and ima

297 Only those patients with HBV reactivation in cohort C had detectable HBV RNA at t

298 774 patients with HBV related ACLF defined in the CANONIC study were analy

299 the tumor load in majority of patients with HBV-related HCC and aided in monitoring residual tumor a

300 HBV integration in 50 patients with HBV-related HCC was determined by the Hybridization capt