ライフサイエンスコーパス: HBV

1 HBV core protein (HBc), encoded by the HBV genome, may p

2 HBV e-antigen (HBeAg), a clinical marker for disease sev

3 HBV entry inhibitors, HBV core inhibitors, HBV cccDNA tr

4 HBV functional cure is sustained hepatitis B surface ant

5 HBV is a major cause of viral hepatitis, liver cirrhosis

6 HBV reactivation of varying severity, even in the settin

7 HBV reactivation was defined as a >1000 IU/mL increase i

8 HBV reactivation with its potential consequences is part

9 HBV replicated unrestricted in HUHEP mice resulting in h

10 HBV uses multiple pathways to harness host innate immuni

11 HBV-coinfected patients were more likely to have signifi

12 HBV-related HCCs expressing increased SALL4 exhibited de

13 HBV-specific T cells lysed HBV-producing hepatoma cells

14 files of 411 patients with HCC (n = 102: 32% HBV, 54% HCV, 14% non-viral) and without HCC (n = 309: 3

15 14% non-viral) and without HCC (n = 309: 39% HBV, 39% HCV, 22% non-viral).

16 n of hepatic and peripheral NK subsets in 43 HBV-LC patients.

17 BV, indicating the requirement of additional HBV-specific factors.

18 discovery of novel antiviral agents against HBV, a group of benzamide (BA) derivatives that signific

19 ggest that the combination of shRNAs against HBV and TGF-beta could be developed into a viable treatm

20 A, viral proteins and DNA knock down agents, HBV release inhibitors, anti-sense nucleosides, exogenou

21 ircular DNA formation, and expression of all HBV markers.

22 This assay was then used to screen all HBV-infected patients identified in a large randomly sel

23 of duck hepatitis B virus (DHBV) cccDNA and HBV nuclear DNA in established cell lines.

24 and Class B in HBV-associated cirrhosis and HBV-associated HCC groups.

25 nomic DNA isolated from HBV-related HCCs and HBV replicating cells, and examined DNA methylation of a

26 The prevalence of HIV, HCV, and HBV among homeless veterans nationally is currently unkn

27 lation prevalence estimates of HIV, HCV, and HBV among homeless veterans nationally.

28 demonstrate high prevalence of HIV, HCV, and HBV among homeless veterans, and reinforce the need for

29 esting rates and prevalence of HIV, HCV, and HBV among homeless veterans.

30 ristics, and the prevalence of HIV, HCV, and HBV among PWID.

31 at particularly high risk for HIV, HCV, and HBV due to a variety of overlapping risk factors, includ

32 e Data from 2015, we evaluated HIV, HCV, and HBV laboratory testing and infection confirmation rates

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

34 iptional regulation, cell proliferation, and HBV-driven tumor growth.IMPORTANCE Hepatitis B virus (HB

35 Co-administration of TGF-beta shRNA and HBV dual-shRNA decreased HBV DNA, HBV RNA, HBsAg, HBeAg,

36 ulation, interferon response stimulation and HBV therapeutic vaccines were reviewed.

37 ed as a selectively active anti-HIV and anti-HBV inhibitor, while being nontoxic to human hepatoblast

38 sitive for HBsAg who were not receiving anti-HBV prophylaxis were enrolled.

39 his is an important new system to study anti-HBV immune responses and screen for combination therapie

40 V-antibody positive, and 9.0% (5.1-13.2) are HBV surface antigen positive; there is substantial geogr

41 o control infections with human hepatitis B (HBV) and C (HCV) viruses.

42 nvestigate the relationships of hepatitis B (HBV) and hepatitis C virus (HCV) infection to age-relate

43 se decreases the decompensation rate in both HBV- and HCV-related cirrhosis.

44 S for any other patient subgroups defined by HBV and HCV.

45 Stratified by HBV coinfection status (hepatitis B surface antigen posi

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

47 evaluation was to identify and characterize HBV reactivation among veterans treated with oral DAA th

48 elopment of antiviral agents against chronic HBV infection.

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

50 ent HBV-specific immune responses in chronic HBV patients and facilitate HBV control.

51 ints for future antiviral therapy in chronic HBV.

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

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

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

55 To investigate whether chronic HBV and HCV infection are associated with increased inci

56 lar carcinoma (HCC) in patients with chronic HBV and HCV infection.

57 interferon alfa-2a in patients with chronic HBV and hepatitis D virus (HDV) co-infection.

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

59 (15%) of the adult participants with chronic HBV infection that were enrolled from January 20, 2011,

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

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

62 ment to eradicate covalently closed circular HBV DNA, and development of immunotherapy for CHB.

63 okine profiles did not distinguish cirrhotic HBV patients with and without HCC (AUC 0.503) or HCV pat

64 g cell culture systems to study the complete HBV life cycle, including virus spread.

65 In contrast, HBV-infected HIS-HUHEP mice developed chronic hepatitis

66 The 2-year cumulative HBV DNA detectability rate was 40.8%, occurring at a med

67 had a significantly lower 2-year cumulative HBV reactivation rate (5.6% versus 65.0%, P = 0.004).

68 nificantly reduced the amount of cytoplasmic HBV DNA were discovered.

69 TGF-beta shRNA and HBV dual-shRNA decreased HBV DNA, HBV RNA, HBsAg, HBeAg, and liver fibrosis marke

70 em that can be infected with patient-derived HBV without further modifications.

71 At baseline, 9 patients had a detectable HBV viral load, 7 had positive results on hepatitis B su

72 was HBV reactivation, defined as detectable HBV DNA (>/=10 IU/mL).

73 is large population at low risk of diabetes, HBV and HCV infections were associated with diabetes pre

74 shRNA and HBV dual-shRNA decreased HBV DNA, HBV RNA, HBsAg, HBeAg, and liver fibrosis markers in ser

75 d antifibrotic activities of single and dual HBV shRNAs.

76 les in the efficient capsid formation during HBV replication.

77 rus-cell interaction for rendering efficient HBV replication.

78 In contrast, the CTD in empty HBV virions (i.e., enveloped capsids with no RNA or DNA)

79 For secretion of empty HBV virions, which is independent of either viral RNA pa

80 ty of using mRNA electroporation to engineer HBV TCR-redirected T cells in patients with chronic HBV

81 Here, we used our established HBV-persistent mouse line with liver fibrosis to evaluat

82 onses in chronic HBV patients and facilitate HBV control.

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

84 HBeAg-seropositive vaccine failure HBV-carrier children were associated with delayed HBeAg

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

86 001) for HIV, 1.28 (1.16-1.41, p<0.0001) for HBV, and 1.72 (1.67-1.78, p<0.0001) for HCV.

87 To assess for HBV reactivation and hepatitis we identified all hepatit

88 es would help determine the risk factors for HBV-R, define monitoring frequency, and identify patient

89 nce is still the most promising modality for HBV cure in the future.

90 nt cell culture system and animal models for HBV investigation, development of treatment to eradicate

91 table to sorafenib for patients positive for HBV and negative for HCV.

92 a large reservoir of individuals at risk for HBV reactivation in the general population.

93 The population at risk for HBV reactivation includes those who either currently are

94 ematological malignancies remain at risk for HBV reactivation.

95 Because curative and eradicative therapy for HBV is not currently available, there is a large reservo

96 the genomic DNA) versus empty (genome-free) HBV virions.

97 , and identify patients who may benefit from HBV prophylaxis and treatment.

98 -specific and MICA/B-expressing T cells from HBV-infected livers.

99 sequencing PCR of genomic DNA isolated from HBV-related HCCs and HBV replicating cells, and examined

100 f which 230 (0.24%) had HIV, 518 (0.53%) had HBV, and 4476 (4.58%) had HCV.

101 One patient had HBV viremia 16 months post-LT without detectable HBsAg.

102 Mice with high levels of viremia had HBV-infected liver progenitor cells.

103 ied all hepatitis B surface antigen (HBsAg), HBV DNA, and alanine aminotransferase results obtained w

104 Hence, HBV core protein is a dominant antiviral target that may

105 In line with this, a highly HBV permissive cell clone of HepAD38 cells showed a prom

106 ith demonstrable proclivity to transmit HIV, HBV, or HCV needs to be reexamined.

107 developed into a viable treatment for human HBV infection.

108 To achieve functional cure (ie, HBV surface antigen seroclearance) and complete cure (ie

109 -Pugh Class C than in Class A and Class B in HBV-associated cirrhosis and HBV-associated HCC groups.

110 Listing for DC in HBV also decreased in the PI (-17%; P = 0.002) and DAA e

111 tes of decompensation, mortality, and HCC in HBV-, HCV-, and alcohol-related cirrhosis.

112 octadecadienyl carnitine level was higher in HBV-associated cirrhosis group than in other two groups.

113 ion was defined as a >1000 IU/mL increase in HBV DNA or HBsAg detection in a person who was previousl

114 activation, defined as an abrupt increase in HBV replication in patients with inactive or resolved HB

115 demethylation of these CpGs was observed in HBV replicating cells.

116 to demonstrate the proviral role of PLK1 in HBV biosynthesis and validate PLK1 inhibition a potentia

117 ated RNAi triggers, which together result in HBV gene silencing.

118 e HBV genome, may play a significant role in HBV life cycle.

119 ded X protein (HBx) plays a critical role in HBV-related hepatocarcinoma development.

120 0 shifted A3G's cytosine region selection in HBV DNA and increased A3G's 5' nucleoside preference for

121 rexpression increased SALL4 transcription in HBV replicating cells.

122 A eras (P < 0.001 for all) whereas HCC WL in HBV remained stable (P > 0.05 for all).

123 A interference, HBV cell apoptosis inducers, HBV RNA, viral proteins and DNA knock down agents, HBV r

124 f prevalence of hepatitis B virus infection (HBV) among rural couples was conducted between 2010 and

125 t chronic hepatitis B (CHB) virus infection (HBV) occurred in China.

126 RNA against TGF-beta, though did not inhibit HBV replication alone, enhanced the antiviral and antifi

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

128 HBV entry inhibitors, HBV core inhibitors, HBV cccDNA transcripts RNA interference, HBV cell apopto

129 HBV entry inhibitors, HBV core inhibitors, HBV cccDNA transcripts RNA interfer

130 rs, HBV cccDNA transcripts RNA interference, HBV cell apoptosis inducers, HBV RNA, viral proteins and

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

132 HBV-specific T cells lysed HBV-producing hepatoma cells in vitro.

133 responses against epitopes within all major HBV proteins.

134 PK-JNK pathway was involved in TAK1-mediated HBV suppression.

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

136 g developments targeting different molecular HBV life cycle steps are being pre-clinically tested or

137 screening; its application to the Mongolian HBV surface antigen-positive population reveals an appar

138 version during long-term follow-up, and more HBV genotype C infection and maternal HBsAg seropositivi

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

140 additional applicable studies regarding new HBV antiviral treatment.

141 There was no HBV-related graft loss, and no retransplantation or deat

142 hNTCP confers susceptibility to HDV but not HBV, indicating the requirement of additional HBV-specif

143 hts into the fate of DHBV cccDNA and nuclear HBV DNA under conditions mimicking antiviral therapy.

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

145 ons (about 7.43 million people) and 9.95% of HBV-related deaths (about 0.25 million people) from 1993

146 markers are needed to assess the ability of HBV therapeutics to achieve functional and virologic cur

147 In absence of HBV replication, RNA polymerase II associated with SALL4

148 ti-HBs responses after the administration of HBV vaccination can be useful to distinguish this serolo

149 With the advance of HBV virology, several viral factors have been found to b

150 s is an additional metabolic complication of HBV and HCV infection.

151 rated, and establishes functional control of HBV and HDV co-infection and normalisation of serum amin

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

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

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

155 after allogeneic HSCT, with determinants of HBV reactivation including age >/=50 years and chronic g

156 ine failure subjects who received 3 doses of HBV vaccine in infancy and 251 nonvaccinated subjects.

157 ast 4 weeks corresponding to the duration of HBV mRNA silencing.

158 nfection but does not allow establishment of HBV infection.

159 0 patients treated with DAAs had evidence of HBV reactivation occurring while on DAA treatment.

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

161 One major reason for failure of HBV treatment is the inability to eradicate or inactivat

162 II occupancy of SALL4 gene, as a function of HBV replication.

163 dies were detected by immunocytochemistry of HBV-transfected BHK-21 cells.

164 In vivo, 3 injections of HBV-specific T cells caused progressive viremia reductio

165 Plasma levels of HBV DNA were quantified by PCR reaction, and antigen-spe

166 complete cure additionally includes loss of HBV covalently closed circular DNA.

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

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

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

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

171 n release from the PML-NB in the presence of HBV.

172 omplete viral life cycle, with production of HBV DNA, hepatitis B e (HBe), core (HBc) and surface (HB

173 nti-HBc-positive patients had a high rate of HBV reactivation after allogeneic HSCT, with determinant

174 eased following ART initiation-regardless of HBV status.

175 The FDA identified 29 unique reports of HBV-R in patients receiving DAAs from 22 November 2013 t

176 further investigation because of the risk of HBV reactivation.

177 re still far from achieving seroclearance of HBV surface antigen.

178 echanistic understanding of the stability of HBV cccDNA in the presence of antiviral therapy and duri

179 ulators may disrupt one or multiple steps of HBV replication, depending on their interaction with the

180 ignal enhancement in nucleic acid testing of HBV as compared to the unmodified LFA.

181 usive literature search on new treatments of HBV using the following electronic databases: Pubmed/MED

182 atoma cell lines leads to an upregulation of HBV replication, transcription, and antigen expression.

183 but otherwise exhibit key characteristics of HBVs including genome replication via protein-primed rev

184 sed both A3G cytosine mutation efficiency on HBV DNA and total HBV mutation frequency.

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

186 D virus-negative patients with pretransplant HBV DNA undetectable to 100 IU/mL who received HBIG 5000

187 tegies based on these parameters may prevent HBV reactivation and subsequent complications.

188 e globulin is highly effective in preventing HBV reactivation and graft loss from recurrent hepatitis

189 al therapy is highly effective in preventing HBV recurrence and should be the preferred strategy for

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

191 tly on hepatitis B virus (HBV) reactivation (HBV-R) in patients with HBV-HCV co-infection.

192 viral sequences, we accurately reconstructed HBV haplotypes in a region of 836 bp, which contains the

193 ted hepatocytes, participate in and regulate HBV virion assembly, capsid uncoating, and covalently cl

194 ctivator proteins, which can finely regulate HBV transcription.

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

196 biomarkers in both, low and high-replicative HBV demonstrate modest accuracy for fibrosis diagnosis a

197 -replicative (n = 213) and high-replicative (HBV DNA >/=20,000 IU/mL, n = 153) patients was assessed.

198 ls; furthermore, NKG2D blockade could rescue HBV-specific and MICA/B-expressing T cells from HBV-infe

199 in patients with preexisting LAM resistance HBV.

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

201 d genes (ISGs), ISG20 and tetherin, restrict HBV spread in NTCP-expressing hepatoma cells.

202 tional coactivators failed to support robust HBV replication in the absence of PGC1alpha.

203 red to express a hepatitis B virus-specific (HBV-specific) T cell receptor (TCR) may supplement HBV-s

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

205 ecific) T cell receptor (TCR) may supplement HBV-specific immune responses in chronic HBV patients an

206 unced role of the human homologue to support HBV and HDV infection.

207 Nine patients had suppressed HBV DNA (<10 IU/mL]) at the end of treatment, which was

208 , the proportion of patients with suppressed HBV DNA, and the proportion of patients who maintained t

209 rexpression of TAK1 significantly suppresses HBV replication, while an enzymatically inactive form of

210 superinfection, liver infections other than HBV and HDV, or liver cirrhosis.

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

212 We further found that HBV core interacted with tubulin and co-localized with m

213 HBV core protein (HBc), encoded by the HBV genome, may play a significant role in HBV life cycl

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

215 Here, we report that expression of the HBV entry receptor, human sodium-taurocholate cotranspor

216 reverse transcriptase, which may restore the HBV-specific adaptive immune response.

217 0% prevalence of HDV coinfection among these HBV-infected Mongolian subjects, which may help explain

218 Significantly, BI-2536 administration to HBV-infected humanized liver FRG mice strongly inhibited

219 associated with the progression from CHB to HBV-associated cirrhosis and ultimately to HBV-associate

220 s, and no retransplantation or deaths due to HBV reactivation.

221 fected with HBV or have had past exposure to HBV.

222 n cell clones with diverse permissiveness to HBV replication.

223 plantation, without any mortality related to HBV reactivation.

224 he role of MAIT cells in immune responses to HBV.

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

226 caques, and pigs became fully susceptible to HBV upon hNTCP expression with efficiencies comparable t

227 o HBV-associated cirrhosis and ultimately to HBV-associated HCC.

228 ine mutation efficiency on HBV DNA and total HBV mutation frequency.

229 igen (HBsAg) testing and had an undetectable HBV viral load, and 3 had negative results on HBsAg test

230 lts on HBsAg testing and had an undetectable HBV viral load.

231 n, over 90% of the patients had undetectable HBV DNA, and from 8 years onward, 100% had undetectable

232 tive for HBsAg, all of whom had undetectable HBV DNA.

233 d from 8 years onward, 100% had undetectable HBV DNA.

234 pha, a transcription factor that upregulates HBV transcription.

235 or Myrcludex B binding, taurocholate uptake, HBV covalently closed circular DNA formation, and expres

236 g revealed that HepAD38 cells, a widely-used HBV-inducible cell line, contain cell clones with divers

237 e enhancement was further confirmed by using HBV clinical samples, where we achieved the detection li

238 accine, Triple vaccine, Hepatitis B vaccine (HBV), Polio, Measles, Rubella, Mumps, trivalent MMR vacc

239 Whether chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection promote NHL i

240 Infections with the human hepatitis B virus (HBV) and hepatitis D virus (HDV) depend on species-speci

241 excellent potency against hepatitis B virus (HBV) and varicella-zoster virus (VZV).

242 1) only modestly increase hepatitis B virus (HBV) biosynthesis.

243 the assembly of the T = 4 hepatitis B virus (HBV) capsid in real time.

244 real time the assembly of Hepatitis B Virus (HBV) capsids below the pseudocritical concentration.

245 The hepatitis B virus (HBV) causes acute and chronic liver infection, which may

246 Hepatitis B virus (HBV) chronic infection affects up to 240 million people

247 Hepatitis B virus (HBV) chronically infects 250 million people worldwide, r

248 patients with and without hepatitis B virus (HBV) coinfection on antiretroviral therapy (ART) in Zamb

249 HDV requires a hepatitis B virus (HBV) coinfection to provide HDV with HBV surface antigen

250 s involved.IMPORTANCE The hepatitis B virus (HBV) covalently closed circular (CCC) DNA, by serving as

251 ases as enzymes targeting hepatitis B virus (HBV) DNA in the nucleus thus affecting its persistence.

252 and 100% had undetectable hepatitis B virus (HBV) DNA, respectively.

253 ) patients had detectable hepatitis B virus (HBV) DNA, with a median of 4.5 log copies/mL.

254 The management of hepatitis B virus (HBV) e antigen-positive viremic patients with normal liv

255 Hepatitis B virus (HBV) encodes a multifunction reverse transcriptase or po

256 Reactivation of hepatitis B virus (HBV) has been reported in hepatitis C virus-infected ind

257 n tumor growth.IMPORTANCE Hepatitis B virus (HBV) HBx protein plays a critical role in viral replicat

258 Hepatitis B virus (HBV) immunization has been effectively preventing chroni

259 is for the persistence of hepatitis B virus (HBV) in hepatocytes, even in the presence of available a

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

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

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

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

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

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

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

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

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

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

270 Hepatitis B virus (HBV) is a major global health concern, and the developme

271 Hepatitis B virus (HBV) is endemic in sub-Saharan Africa, and despite the i

272 the associations between hepatitis B virus (HBV) or hepatitis C virus (HCV) infection and the develo

273 ich are related to either hepatitis B virus (HBV) or hepatitis C virus (HCV).

274 ere published recently on hepatitis B virus (HBV) reactivation (HBV-R) in patients with HBV-HCV co-in

275 Hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)

276 nt of prophylaxis against hepatitis B virus (HBV) recurrence in liver transplantation (LT) recipients

277 epatitis C virus (HCV) or hepatitis B virus (HBV) status.

278 P 2139 clears circulating hepatitis B virus (HBV) surface antigen (HBsAg), enhancing the restoration

279 t-listed for LT from HCV, hepatitis B virus (HBV), and nonalcoholic steatohepatitis (NASH) were ident

280 hepatitis C virus (HCV), hepatitis B virus (HBV), NAFLD, and alcoholic liver diseases; (2) performan

281 ther hepatitis A virus or hepatitis B virus (HBV), or a noninfectious cause for their ALF.

282 Hepatitis B virus (HBV)-encoded X protein (HBx) plays a critical role in HB

283 +) homeostasis on chronic hepatitis B virus (HBV)-infected natural killer (NK) and CD8(+) T cells.

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

285 Hepatitis B viruses (HBVs), which are enveloped viruses with reverse-transcri

286 The primary endpoint was HBV reactivation, defined as detectable HBV DNA (>/=10 I

287 To assess whether HBV-R is a safety concern in patients receiving HCV DAAs

288 Among 463 patients analyzed (61 with HBV coinfection), median age was 35 years, 53.7% were wo

289 and donor serology, were not associated with HBV reactivation.

290 virus (HBV) coinfection to provide HDV with HBV surface antigen envelope proteins.

291 Only 3 of the 9 patients identified with HBV reactivation in this cohort exhibited peak alanine a

292 those who either currently are infected with HBV or have had past exposure to HBV.

293 nts receiving ART, chronic co-infection with HBV and HCV is associated with an increased risk for NHL

294 ty capsids through specific interaction with HBV core protein but not other viral and host cellular c

295 In conclusion, patients with HBV or HCV infection, with or without HCC, have distinct

296 (HBV) reactivation (HBV-R) in patients with HBV-HCV co-infection.

297 29 patients with HBV-R receiving HCV DAAs.

298 ly) HBIG in liver transplant recipients with HBV DNA less than 100 IU/mL pre-LT.

299 ies with those of study participants without HBV or HCV infection in the same age range (n=1289).

300 Among participants without HBV or HCV infection, only 6 developed HCC or died from