ライフサイエンスコーパス: HDV

1 HDV controls these relative amounts via differential eff

2 HDV escape from the immune response was associated with

3 HDV genome encodes two forms of hepatitis delta antigen

4 HDV genotype IV (72.2%) was the prevalent genotype circu

5 HDV infection is the only chronic human hepatitis virus

6 HDV is associated with higher health care use and cost b

7 HDV is not related to any known virus, and few details r

8 HDV produces three processed RNAs that accumulate in inf

9 HDV requires a hepatitis B virus (HBV) coinfection to pr

10 HDV RNA viremia is associated with a 3.8-fold higher ris

11 HDV variant peptides were only partially cross-recognize

12 HDV-RNA load (HDVL) should be assessed and monitored in

13 HDV-specific CD8(+) T cells did not express the terminal

14 HDV-specific CD8(+) T cells were as frequent as HBV-spec

15 HDV-specific T-cell proliferation and cytokine productio

16 HDV-specific T-cell responses focused on 3 distinct HDV-

17 s with resolved (n = 12) or chronic (n = 13) HDV infection.

18 Between 2001 and 2014, 2,152 HDV strains were prospectively collected and genotyped i

19 20mer peptides and exogenous interleukin 2, HDV-specific CD4+ and CD8+ T-cell responses of 32 HDV-in

20 ro stimulation with an overlapping set of 21 HDV-specific 20mer peptides and exogenous interleukin 2,

21 pecific CD4+ and CD8+ T-cell responses of 32 HDV-infected patients were analyzed by enzyme-linked imm

22 uencies and phenotypes were determined in 49 HDV-infected patients, 25 individuals with hepatitis B v

23 9, and Feb 28, 2011, we randomly assigned 59 HDV RNA-positive patients to receive peginterferon alfa-

24 A total of 2,727 HDV cases were matched 1:1 by sociodemographic character

25 Little is known about HDV-specific T cells and how they contribute to the anti

26 s essential for HDV and inhibition abrogates HDV production in experimental models.

27 The ex vivo frequency of activated HDV-specific CD8(+) T cells correlated with transaminase

28 The subset of activated HDV-specific CD8(+) T cells targets conserved epitopes a

29 tial outcomes of upcoming antivirals against HDV.

30 f action and efficacy of REP 2139-Ca against HDV in 12 treatment-naive HBV/HDV co-infected patients.

31 tments are only marginally effective against HDV because they fail to inhibit HBsAg production/secret

32 atients; these could be mutations that allow HDV to escape the immune response, resulting in persiste

33 Although HDV-specific CD8(+) T cells are thought to control the v

34 The efficacy of blocking HBsAg and HDV production were 98.2 [94.5-99.9]% and 99.7 [96.0-99.

35 ompanied by rapid declines in both HBsAg and HDV RNA.

36 reproduced the observed decline of HBsAg and HDV, which was simultaneous.

37 ptor-mediated host discrimination of HBV and HDV binding and infection.

38 nd establishes functional control of HBV and HDV co-infection and normalisation of serum aminotransfe

39 w treatment option for patients with HBV and HDV co-infection.

40 ted, and broadly active inhibitor of HBV and HDV entry.

41 le of the human homologue to support HBV and HDV infection.

42 species was cloned and analyzed for HBV and HDV receptor activity in a permissive hepatoma cell line

43 Hepatitis B and D viruses (HBV and HDV) are human pathogens with restricted host ranges and

44 ding of the species specificities of HBV and HDV, and could lead to small animal models for studies o

45 fection, liver infections other than HBV and HDV, or liver cirrhosis.

46 the mechanism of attachment/entry of HBV and HDV.

47 ly identified bona fide receptor for HBV and HDV.

48 approach is a bona fide receptor for HBV and HDV.

49 uman NTCP is a specific receptor for HBV and HDV.

50 es-specific binding and infection by HBV and HDV.

51 ons can equally be observed in HBV, HCV, and HDV infections.

52 t known how the relative amounts of HDAg and HDV RNA affect replication, or whether HDAg synthesis is

53 anti-HDV positive for at least 3 months, and HDV-RNA positive at the local laboratory at the screenin

54 nti-hepatitis D antigen [HDAg] positive, and HDV RNA positive, with serum HBsAg concentrations of mor

55 In conclusion, both HBsAg production and HDV replication are effectively inhibited by REP 2139-Ca

56 uences amplified from HDV seroconverters and HDV-seropositive patients at baseline.

57 Anti-HDV immunoglobulin G (IgG) was sequentially determined i

58 We studied 136 anti-HDV-positive patients who were followed for at least 6 m

59 e microarray antibody capture assay for anti-HDV immunoglobulin G wherein recombinant HDV delta antig

60 e HBsAg positive for at least 7 months, anti-HDV positive for at least 3 months, and HDV-RNA positive

61 g quantitative fluorescent detection of anti-HDV antibody in small aliquots of patient serum.

62 Routine anti-HDV testing should be considered for HBsAg carriers.

63 ad antibodies to hepatitis delta virus (anti-HDV).

64 ce antigen positive, and 17 (1.5%) were anti-HDV positive.

65 In total, 337 patients with anti-HDV positivity, including 233 patients with HDV RNA vire

66 11 patients became HDV RNA negative during treatment, with nine remaining H

67 ng-term follow-up, with seven patients being HDV RNA-positive at the most recent visit.

68 teraction between HDAg-L and TAP and blocked HDV virion assembly and secretion.

69 0.24]), lonafarnib effectiveness in blocking HDV production was greater in group 2 than in group 1 (0

70 nsion (SHAPE) applied to free and HDAg-bound HDV RNAs indicated that the characteristic secondary str

71 ic CD8(+) T-cell epitopes, and characterized HDV-specific CD8(+) T cells.

72 Chronic HDV infection commonly results in the most rapidly progr

73 fficacy of prenylation inhibition in chronic HDV.

74 Treatment of chronic HDV with lonafarnib significantly reduces virus levels.

75 Our data indicate that in vivo chronic HDV infection can persist in the absence of HBV replicat

76 d DNA samples from 104 patients with chronic HDV and HBV infection at medical centers in Europe and t

77 T cells isolated from patients with chronic HDV and HBV infection recognize HDV epitopes presented b

78 onuclear cells from 28 patients with chronic HDV and HBV infection, identified HDV-specific CD8(+) T-

79 Patients with chronic HDV infection and compensated liver disease who were age

80 patients aged 18 years or older with chronic HDV infection were randomly assigned (3:1 in group 1 and

81 nitiated using in vitro-synthesized circular HDV RNAs, HDV replication was found to depend strongly o

82 +) T cells is functional but unable to clear HDV because of the presence of escape variants.

83 substantial amounts of the pre-S1-containing HDV particles.

84 and also demonstrate that, in this control, HDV behaves similarly to other negative-strand RNA virus

85 Compared with HBV controls, HDV cases had an adjusted incident rate ratio of 1.16 (9

86 /CT was lower than that of (18)F-FDG PET/CT (HDV, 69% [95% CI, 41-89] vs. 94% [95% CI, 70-100] [P = 0

87 CT was higher than that of (18)F-FDG PET/CT (HDV, 96% [95% CI, 87-100] vs. 71% [95% CI, 57-83] [P = 0

88 Accurate assessments of current HDV prevalence have been hampered by the lack of readily

89 pulations and to use this assay to determine HDV prevalence in a population with abnormally high rate

90 A model year 2013 diesel HDV produced approximately 10 times higher PNEFs during

91 cific T-cell responses focused on 3 distinct HDV-specific epitopes that were each detected in 12%-21%

92 We used mathematical modeling to estimate HDV-HBsAg-host parameters and to elucidate the mode of a

93 minal differentiation marker CD57, and fewer HDV-specific than Epstein-Barr virus-specific CD8(+) T c

94 First HDV diagnosis was associated with significant increases

95 n intersubgenotype similarity >90% (>84% for HDV-1) over the whole genome sequence.

96 binding site was identified as critical for HDV assembly.

97 Prenylation is essential for HDV and inhibition abrogates HDV production in experimen

98 rotein form complexes that are essential for HDV replication, and the proper stoichiometry of these c

99 ion of treatments directly targeting HDV for HDV/HBV-infected individuals.

100 r export activity of HDAg-L is important for HDV particle formation.

101 nd protein in cells are indeed important for HDV replication and that the virus does control them.

102 in patients positive and those negative for HDV by PCR.

103 Although HDAg is required for HDV replication, it is not known how the relative amount

104 rged as high-risk groups and a reservoir for HDV infection.

105 low-up [PYFU], 16 patients seroconverted for HDV, with an overall incidence rate of 9.07 per 1000 PYF

106 l model was developed and fitted to frequent HDV and HBsAg kinetic data from 10 patients during the f

107 performed using HDV sequences amplified from HDV seroconverters and HDV-seropositive patients at base

108 Some variant peptides in epitopes from HDV were only partially recognized by CD8(+) T cells iso

109 he HDV genus is composed of eight genotypes (HDV-1 to HDV-8) defined by an intergenotype similarity >

110 Patients were excluded if they had HDV superinfection, liver infections other than HBV and

111 sitive on standard western blot or harboring HDV RNA detectable by real-time quantitative PCR.

112 Here, we established HBV and HBV/HDV co-infections and super-infections in self-assemblin

113 suggesting a rapid turnover of HBsAg in HBV/HDV co-infection.

114 139-Ca against HDV in 12 treatment-naive HBV/HDV co-infected patients.

115 n SACC-PHHs, either HBV mono-infected or HBV/HDV co-infected.

116 tem is a versatile platform for studying HBV/HDV co-infections and holds promise for performing chemi

117 ts with chronic hepatitis B and D virus (HBV/HDV) infection, and healthy individuals.

118 hepatitis B, C, and/or D viruses (HBV, HCV, HDV, respectively) on liver decompensation events (ascit

119 One key question is whether and how HDV regulates the relative amounts of viral RNA and prot

120 We aimed to define how HDV escapes the CD8(+) T-cell-mediated response.

121 e results provide a conceptual model for how HDV antigenome RNA production and mRNA transcription are

122 th chronic HDV and HBV infection, identified HDV-specific CD8(+) T-cell epitopes, and characterized H

123 These newly identified HDV epitopes were restricted by relatively infrequent HL

124 e costs ($23,605 vs. $18,228; P < 0.0001) in HDV compared with HBV alone.

125 ed virological response should be avoided in HDV infection.

126 principle contribution of unpaired bases in HDV RNA to HDAg binding is to allow flexibility in the u

127 el in which the internal loops and bulges in HDV RNA contribute flexibility to the quasi-double-stran

128 was observed with no significant changes in HDV level.

129 imary therapeutic endpoint was a decrease in HDV RNA viral titre in serum and the primary safety endp

130 isms were found to correspond to epitopes in HDV that are recognized by CD8(+) T cells; we confirmed

131 We predicted epitopes in HDV that would be recognized by CD8(+) T cells and corre

132 DF resulted in no significant improvement in HDV RNA response rates at the end of treatment.

133 er, a more robust and consistent increase in HDV-specific CD4(+) and CD8(+) T-cell responses was evid

134 ne of the patients with flat second phase in HDV achieved CVR.

135 The observation that a flat second phase in HDV and HBsAg kinetics was associated with failure to ac

136 patients, and searched for polymorphisms in HDV RNA associated with specific HLA class I alleles.

137 We identified 21 polymorphisms in HDV that were significantly associated with specific HLA

138 28.6% experienced a >/=2.0 log reduction in HDV RNA, and 14.3% had undetectable HDV VL within 5 year

139 disease and control of viral replication in HDV infection.

140 y stopping rules during peg-IFN treatment in HDV-infected patients.

141 ith 96 weeks of peginterferon would increase HDV RNA response rates and reduces post-treatment relaps

142 teins capable of the formation of infectious HDV virions.

143 Modeling results provide insights into HDV-host dynamics, the relationship between serum HBsAg

144 with overlapping peptides spanning the large HDV antigen.

145 Late HDV RNA relapses may occur after PEG-IFNa therapy of hep

146 The subset of memory-like HDV-specific CD8(+) T cells is functional but unable to

147 At day 28, compared with placebo, mean log HDV RNA declines from baseline were -0.73 log IU/mL in g

148 gent need to improve methods used to monitor HDV viremia and will be instrumental in achieving that g

149 ed patients demonstrated repeatedly negative HDV PCR results post therapy.

150 Notably, HDV co-infection also did not lead to statistically sign

151 n, yet only minimally affects the ability of HDV to infect and persist.

152 o depend strongly on the relative amounts of HDV RNA and HDAg.

153 ur results show that the relative amounts of HDV RNA and protein in cells are indeed important for HD

154 ced nuclear export of HDAg-L and assembly of HDV virions.

155 ized the health care use and cost burdens of HDV in the United States using real-world claims data.

156 This comprehensive characterization of HDV T-cell epitopes provides important information that

157 he structural and functional consequences of HDV variability.

158 ovides insight into the genetic diversity of HDV and a clear view of its geographical localization an

159 The net effect of HDV is to make the underlying HBV disease worse, includi

160 pport HDV replication and assembly/egress of HDV virions.

161 re needed to curb the reemerging epidemic of HDV infection in these high-risk groups.

162 to investigate the changing epidemiology of HDV infection among high- and low-risk populations after

163 hanisms of HDAg-L-mediated nuclear export of HDV ribonucleoprotein are not clear.

164 he prevalence, genotype, and risk factors of HDV infection from 2001 through 2012.

165 ns of more than 1000 IU/mL, and a history of HDV infection for 6 months or more before treatment, wer

166 therefore evaluated the long-term impact of HDV viremia on liver-related outcomes in a nationwide co

167 Furthermore, the impact of HDV viremia per se on liver-related outcomes is not real

168 Loss of HDV RNA during follow-up was more frequent in IFNalpha-t

169 The study addresses the unique mechanism of HDV persistence in the absence of ongoing HBV replicatio

170 fic infectivity (SI), which is the number of HDV genomes/cell produced by infection and normalized by

171 linical and virological long-term outcome of HDV-infected patients treated with PEG-IFNa is unknown.

172 of infected PHH, which is the percentage of HDV-infected hepatocytes normalized by the PreS1*-MOI.

173 cs of decline paralleled the second phase of HDV decline consistent with HBsAg-productive-infected ce

174 an apparent approximately 60% prevalence of HDV coinfection among these HBV-infected Mongolian subje

175 rential effects of HDAg on the production of HDV mRNA and antigenome RNA, both of which are synthesiz

176 cells being the main source of production of HDV, with a median t1/2 of 135 days (IQR: 20-460).

177 The prevalence rates of HDV infection were 74.9%, 43.9%, 11.4%, 11.1%, and 4.4%

178 ta demonstrate that formation and release of HDV particles are mediated by TAP and Aly.

179 We analyzed sequences of HDV RNA and HLA class I alleles that present epitope pep

180 tion that will facilitate further studies of HDV immunopathogenesis.

181 ed to explore whether prolonged treatment of HDV with 96 weeks of peginterferon would increase HDV RN

182 A significant increase in the trend of HDV prevalence from 38.5% to 89.8% was observed in HIV-i

183 V replication, advances our understanding of HDV-HBV interactions, and supports the implementation of

184 Durable undetectability of HDV RNA is a valid surrogate endpoint in the treatment o

185 s related to the high genetic variability of HDV and, possibly, to the complex secondary structure of

186 cept study, we aimed to assess the effect on HDV RNA levels, safety, and tolerability of the prenylat

187 RG cells prevented their infection by HBV or HDV.

188 P in mouse, rat, and dog hepatocytes permits HDV infection but does not allow establishment of HBV in

189 o CD8(+) T cells in patients with persistent HDV infection.

190 ays to properly detect or quantify plasmatic HDV RNA.

191 6 vs. $23,605; P < 0.0001) compared with pre-HDV baseline.

192 patitis B virus (HBV) coinfection to provide HDV with HBV surface antigen envelope proteins.

193 Herein, we design double-pseudoknot HDV ribozymes using an inverse RNA folding algorithm and

194 Recent HDV infection was associated with elevated aminotransfer

195 r findings show that the incidence of recent HDV infection in HIV/HBV-coinfected patients increased s

196 idence of and factors associated with recent HDV superinfection among individuals coinfected with hum

197 with chronic HDV and HBV infection recognize HDV epitopes presented by multiple HLA molecules.

198 nti-HDV immunoglobulin G wherein recombinant HDV delta antigen is printed by microarray on slides coa

199 that the main effect of peg-IFN is to reduce HDV production/release with a median effectiveness of 96

200 treatment; seven of these patients remained HDV RNA negative by the end of 1 year follow-up.

201 gative during treatment, with nine remaining HDV RNA negative at the end of treatment; seven of these

202 al therapy among patients with a replicating HDV infection in the Swiss HIV Cohort Study.

203 sing in vitro-synthesized circular HDV RNAs, HDV replication was found to depend strongly on the rela

204 The assembled virions bore the same HDV ribonucleoprotein and differed only by the HBV varia

205 ers in Europe and the Middle East, sequenced HDV, typed human leukocyte antigen (HLA) class I alleles

206 Median serum HDV half-life (t1/2 ) was estimated as 2.9 days (IQR: 1.

207 V) co-infection should be undetectable serum HDV RNA 6 months after stopping treatment.

208 ly with overall clinical events, while serum HDV RNA positivity at baseline did not correlate with an

209 pegylated interferon alpha (PEG-IFNa) showed HDV RNA negativity rates of 25-30% 24 weeks after therap

210 Both cell lines were able to support HDV replication and assembly/egress of HDV virions.

211 pecific trend of D > B > E > A in supporting HDV infectivity.

212 lementation of treatments directly targeting HDV for HDV/HBV-infected individuals.

213 Out of these, nine individuals tested HDV RNA-positive at least once during further long-term

214 Sixteen patients tested HDV RNA-negative 6 months after PEG-IFNa treatment who w

215 ncommon HLA class I alleles, indicating that HDV evolves, at the population level, to evade recogniti

216 The HDV genome and antigenome RNAs form ribonucleoprotein co

217 The HDV group had significantly higher prevalence of substan

218 The HDV-infected cell loss was estimated to be 0.052 [0.035-

219 [SE 0.06] vs 0.739 [0.05], p<0.001), and the HDV half-life was 1.62 days (0.07).

220 ch regulation might be important because the HDV RNA and protein form complexes that are essential fo

221 ents in development, designed to disrupt the HDV life cycle, that might benefit patients with this de

222 HIV/HBV-coinfected patients to estimate the HDV incidence between 1992 and 2012.

223 A residue Y (position 374) in the HDV binding site was identified as critical for HDV asse

224 We identified polymorphisms in the HDV proteome that associate with HLA class I alleles.

225 llowing for in-depth characterization of the HDV genotypes and subgenotypes.

226 the dynamics and catalytic mechanism of the HDV ribozyme and demonstrate the power of new techniques

227 cis-acting C75U-inhibited structures of the HDV ribozyme.

228 We analyzed the role of the HDV RNA sequence and secondary structure in the formatio

229 Approximately half of the HDV-specific CD8(+) T cells had a memory-like PD1(+)CD12

230 This study confirms that the HDV genus is composed of eight genotypes (HDV-1 to HDV-8

231 nferred from structure, and suggest that the HDV ribozyme transition state resembles the cleavage pro

232 med in vitro revealed complexes in which the HDV RNA is substantially condensed by bending or wrappin

233 Thereafter, HDV declined in a biphasic manner, where a rapid first p

234 hat CD8(+) T cells in culture targeted these HDV epitopes.

235 nus is composed of eight genotypes (HDV-1 to HDV-8) defined by an intergenotype similarity >85% or >8

236 In contrast to HDV, a large delta antigen is not expressed and the farn

237 tocytes with hNTCP confers susceptibility to HDV but not HBV, indicating the requirement of additiona

238 The total HDV yields varied within a 122-fold range.

239 On treatment HDV RNA suppression associated with normalization of ALT

240 ical response (CVR), defined as undetectable HDV 6 months after treatment stopped with loss of HBsAg

241 ction in HDV RNA, and 14.3% had undetectable HDV VL within 5 years.

242 the percentage of patients with undetectable HDV RNA at the end of treatment assessed by intention to

243 Phylogenetic analysis was performed using HDV sequences amplified from HDV seroconverters and HDV-

244 racin A was observed with hepatitis D virus (HDV) but not hepatitis C virus.

245 No hepatitis D virus (HDV) cases were detected.

246 nt for phase 3 trials for hepatitis D virus (HDV) co-infection should be undetectable serum HDV RNA 6

247 ents with chronic HBV and hepatitis D virus (HDV) co-infection.

248 patitis B virus (HBV) and hepatitis D virus (HDV) depend on species-specific host factors like the re

249 Hepatitis D virus (HDV) infection affects 15-20 million individuals worldwi

250 The emergence of hepatitis D virus (HDV) infection in the era of widespread HBV vaccination

251 patitis B virus (HBV) and hepatitis D virus (HDV) infections, we still do not completely understand h

252 Hepatitis D virus (HDV) requires hepatitis B surface antigen (HBsAg) for it

253 rate (TDF) would increase hepatitis D virus (HDV) RNA suppression is unknown.

254 Hepatitis D virus (HDV) superinfection in patients with hepatitis B virus (

255 Hepatitis D virus (HDV) superinfection of patients with chronic HBV infecti

256 ocess of entry of HBV and hepatitis D virus (HDV).

257 the early kinetics of hepatitis delta virus (HDV) and hepatitis B surface antigen (HBsAg) during inte

258 garding the extent of hepatitis delta virus (HDV) associated health care burden in the United States

259 Hepatitis delta virus (HDV) causes the most severe form of human viral hepatiti

260 nd antigenome RNAs of hepatitis delta virus (HDV) form characteristic unbranched, quasi-double-strand

261 Therapies for chronic hepatitis delta virus (HDV) infection are unsatisfactory.

262 Chronic hepatitis delta virus (HDV) infection causes severe liver disease which often l

263 Hepatitis delta virus (HDV) infection is associated with fast progression to li

264 Hepatitis delta virus (HDV) infection of humans was first reported in 1977, and

265 Hepatitis delta virus (HDV) is a human hepatitis-causing RNA virus, unrelated t

266 Hepatitis delta virus (HDV) is a satellite of hepatitis B virus that increases

267 tween them.IMPORTANCE Hepatitis delta virus (HDV) is a satellite of hepatitis B virus that increases

268 Hepatitis delta virus (HDV) is a satellite virus of hepatitis B virus (HBV).

269 Hepatitis delta virus (HDV) is responsible for the most severe form of acute an

270 Hepatitis delta virus (HDV) is the most severe form of viral hepatitis.

271 The hepatitis delta virus (HDV) ribozyme catalyzes a self-cleavage reaction using a

272 In the case of the hepatitis delta virus (HDV) ribozyme, there are three high-resolution crystal s

273 hepatitis B virus and hepatitis delta virus (HDV) viral loads (VL) during tenofovir-containing antire

274 Infection by the hepatitis delta virus (HDV), a satellite of the hepatitis B virus (HBV), increa

275 atitis B virus (HBV), hepatitis delta virus (HDV), requires only the envelope proteins from HBV in or

276 We show that large hepatitis delta virus (HDV)-like ribozymes are activated by peripheral domains

277 nd specificity of the hepatitis delta virus (HDV)-specific T-cell response in patients at different s

278 are co-infected with hepatitis delta virus (HDV).

279 treatment option for hepatitis delta virus (HDV).

280 both within the irradiated high-dose volume (HDV) and on a patient basis.

281 ntrol the virus, little is known about which HDV epitopes are targeted by virus-specific CD8(+) T cel

282 Using a novel transfection system in which HDV replication is initiated using in vitro-synthesized

283 ly-developed World Health Organization (WHO) HDV international standard (WHO-HDV-IS), the first inter

284 zation (WHO) HDV international standard (WHO-HDV-IS), the first international external quality contro

285 Panel B, composed of dilutions of the WHO-HDV-IS, allowed the conversion of results from copies/mL

286 age were significant factors associated with HDV infection.

287 HLA class I alleles were not associated with HDV sequence polymorphisms.

288 )T-bet(low) phenotype, which associated with HDV sequence variants with reduced HLA binding and reduc

289 afarnib serum concentrations correlated with HDV RNA change (r(2)=0.78, p<0.0001).

290 Infection with HDV can be an acute or chronic process that occurs only

291 with HDV peptides correlated inversely with HDV titer.

292 us-specific T-cell immunity in patients with HDV infection, the largest to date, revealed premature a

293 -HDV positivity, including 233 patients with HDV RNA viremia and 91 without HDV viremia at baseline,

294 -fold higher, respectively, in patients with HDV viremia compared with those without viremia, althoug

295 Among patients with HDV viremia with no baseline cirrhosis, the cumulative r

296 prognosis was rather poor for patients with HDV viremia without cirrhosis at baseline, but it was ne

297 Of the 12 patients with HDV viremia, 2 were infected with genotype 2 and 10 with

298 n of interferon gamma after stimulation with HDV peptides correlated inversely with HDV titer.

299 We associated these with HDV sequence variations and clinical features of patient

300 patients with HDV RNA viremia and 91 without HDV viremia at baseline, were retrospectively studied, w