ライフサイエンスコーパス: HDV

1 HDV enhances liver damage during concomitant infection w

2 HDV genome encodes two forms of hepatitis delta antigen

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

4 HDV is clinically important because although it suppress

5 HDV prevalence declined from 15% in 1988-1989 to 11% in

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

7 HDV RNA is unusual in that it forms an unbranched quasi-

8 HDV virions assembled in PLC/PRF/5 cells were able to in

9 HDV-hepatitis B virus (HBV) dual infection progresses ra

10 HDV-like ribozymes serve several distinct functions in n

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

12 HDV-specific T-cell proliferation and cytokine productio

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

14 s together with double immunostaining of 293-HDV cells, in order to examine the associations between

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

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

17 An HDV antigenomic ribozyme precursor RNA that included the

18 RNAs, as well as the small delta antigen, an HDV-encoded protein known to be essential for replicatio

19 n hepatocytes and to test the efficacy of an HDV-entry inhibitor in vivo.

20 inimal ribonucleoprotein complex requires an HDV unbranched rod RNA of at least about 300 nucleotides

21 The catalytic mechanisms for the CPEB3 and HDV ribozymes appear to be similar, generating cleavage

22 on rates among human CPEB3, chimp CPEB3, and HDV ribozymes.

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

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

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

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

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

28 velope (L) protein on the surface of HBV and HDV particles has many different functions and is requir

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

30 e SVP did not inhibit the ability of HBV and HDV to infect primary human hepatocytes.

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

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

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

34 ly identified bona fide receptor for HBV and HDV.

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

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

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

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

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

40 examine the associations between Pol II and HDV RNAs, as well as the small delta antigen, an HDV-enc

41 rom the United States are >10 years old, and HDV has shown significant temporal variation in other po

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

43 The hepatitis delta virus (HDV) ribozyme and HDV-like ribozymes are self-cleaving RNAs found througho

44 weeks later the animals were sacrificed and HDV replication in normal liver tissues and in center ma

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

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

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

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

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

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

51 atients who had significantly lower baseline HDV RNA levels than nonresponders (2.99 log(10) copies/m

52 11 patients became HDV RNA negative during treatment, with nine remaining H

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

54 ur understanding of the relationship between HDV infection and liver cancer, it was determined whethe

55 e proposed ARMs are not required for binding HDV RNA.

56 ts unambiguously demonstrate that HDAg binds HDV RNA as a multimer and that the HDAg multimer is form

57 consistent with a model in which HDAg binds HDV unbranched rod RNA as multimers of fixed size rather

58 d protein, HDAg-160, that specifically binds HDV unbranched rod RNA with high affinity.

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

60 0.24]), lonafarnib effectiveness in blocking HDV production was greater in group 2 than in group 1 (0

61 ontain the ARMs, was cross-linked to a bound HDV RNA segment in vitro.

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

63 part of antiviral therapies against chronic HDV and HBV, and may help understand the attachment and

64 fficacy of prenylation inhibition in chronic HDV.

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

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

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

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

69 The lack of convenient HDV infection models has hampered the development of eff

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

71 imary human hepatocytes, while Hep3B-derived HDV appeared to be noninfectious.

72 All patients had detectable HDV RNA, and 8 had detectable HBV DNA at baseline.

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

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

75 Drosophila species were also shown to encode HDV-like ribozymes capable of self-cleavage.

76 Surprisingly, HBV-enveloped HDV (hHDV) and wHDV infected PHH with comparable efficie

77 chucks were superinfected with WHV-enveloped HDV (wHDV).

78 presence of replication, deltaAg facilitates HDV RNA transport to the nucleoplasm and helps redirect

79 e than 6000-fold slower than for the fastest HDV ribozyme.

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

81 and no selective therapies are available for HDV infection.

82 binding site was identified as critical for HDV assembly.

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

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

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

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

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

88 e been hampered by a lack of specificity for HDV RNA.

89 e, HBV-positive participants were tested for HDV RNA, HBV DNA, and HCV RNA.

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

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

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

93 ht (32%) of those who were HDAb positive had HDV viremia.

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

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

96 rcludex B, the first entry inhibitor for HBV/HDV.

97 envelope, was applied to prevent de novo HBV/HDV coinfection in vivo.

98 yed to establish a small animal model of HBV/HDV coinfection and superinfection.

99 We established an efficient model of HBV/HDV infection to exploit mechanisms of viral interferenc

100 In the setting of HBV/HDV simultaneous infection, a majority of human hepatocy

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

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

103 ll patients had to have detectable hepatitis HDV RNA and elevated levels of alanine aminotransferase

104 ed virological response should be avoided in HDV infection.

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

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

107 was observed with no significant changes in HDV level.

108 No significant decline in HDV RNA, ALT, or quantitative HBsAg levels was observed.

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

110 The temporal increase in HDV prevalence among those with chronic HBV infection is

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

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

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

114 28.6% experienced a >/=2.0 log reduction in HDV RNA, and 14.3% had undetectable HDV VL within 5 year

115 disease and control of viral replication in HDV infection.

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

117 teins capable of the formation of infectious HDV virions.

118 h the ability of full-length HDAg to inhibit HDV RNA editing in cells, an activity that involves RNA

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

120 with overlapping peptides spanning the large HDV antigen.

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

122 was expressed in the absence of full-length HDV RNAs, it colocalized with nucleolin, a predominant n

123 Rather, a minimum-length HDV RNA unbranched rod approximately 311 nt was essentia

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

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

126 nd absence of replicating and nonreplicating HDV RNAs.

127 Following expression of nonreplicating HDV RNAs, deltaAg moved to the nucleoplasm, but nucleoli

128 Notably, HDV superinfection led to a median 0.6log reduction of H

129 The demonstrated ability of HDV to infect already formed HCCs may facilitate develop

130 ominantly to the nucleolus in the absence of HDV genome replication while in the presence of replicat

131 ng protein essential for the accumulation of HDV RNA-directed RNA transcripts.

132 lly to nucleic acids has impeded analysis of HDV RNA protein complexes and conclusive determination o

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

134 he structural and functional consequences of HDV variability.

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

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

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

138 he mechanisms of (i) attachment and entry of HDV and HBV and (ii) transmission of HDV infection/disea

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

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

141 B, efficiently hindered the establishment of HDV infection in vivo.

142 Establishment of HDV infection was highly efficient in both HBV-infected

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

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

145 There are eight reported genotypes of HDV with unexplained variations in their geographical di

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

147 ocalization was insensitive to inhibitors of HDV replication, suggesting that the majority of deltaAg

148 Based on accumulation levels of HDV RNAs and numbers of infected cells, the efficiency o

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

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

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

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

153 The molecular pathogenesis of HDV infection remains poorly understood.

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

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

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

157 The prevalence of HDV is declining in some endemic areas but increasing in

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

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

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

161 approximately 400-nucleotide (nt) segment of HDV unbranched rod RNA.

162 Binding occurred with several segments of HDV RNA, although with various affinities and efficienci

163 these data is that host range specificity of HDV is determined entirely by pre-S1 and that the WHV an

164 between the unbranched rodlike structure of HDV RNA and hepatitis delta antigen (HDAg), a basic, dis

165 the R2 ribozyme from D. simulans to that of HDV was a result of convergent evolution, not common des

166 ntry of HDV and HBV and (ii) transmission of HDV infection/disease.

167 Treatment of HDV is with pegylated interferon alfa; however, response

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

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

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

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

172 d understanding of the molecular virology of HDV will identify novel therapeutic targets for this mos

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

174 rom liver cell lines that produced SVP only, HDV plus SVP, and HBV plus SVP.

175 The SVP made in the absence of HBV or HDV were further examined by electron microscopy.

176 RG cells prevented their infection by HBV or HDV.

177 In some organisms HDV-like and hammerhead ribozymes appear to be dedicated

178 controls the 524 HIV-monoinfected patients, HDV coinfection (adjusted hazard ratio [AHR], 7.5; 95% c

179 ately 5 innersphere Mg2+...-O2P contacts per HDV molecule when the crystal is exposed to a solution c

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

181 Plasma HDV and HBV loads and HBV surface antigen (HBsAg) levels

182 ays to properly detect or quantify plasmatic HDV RNA.

183 transcription and accumulation of processed HDV RNA species.

184 HV) are superinfected with HDV, they produce HDV with a WHV envelope, wHDV.

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

186 Recent HDV infection was associated with elevated aminotransfer

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

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

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

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

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

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

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

194 is delta antigen (HDAg) in cells replicating HDV.

195 deltaAg was expressed along with replicating HDV RNA, it was found predominantly in the nucleoplasm a

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

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

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

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

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

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

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

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

204 HBV spreading was completed, confirming that HDV can replicate intrahepatically also in the absence o

205 Our results indicate that HDV-like ribozymes are abundant in nature and suggest th

206 not statistically significant suggests that HDV may hinder HBV replication.

207 The HDV ribozyme self-cleaves by a chemical mechanism involv

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

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

210 tigen (HBsAg) levels were determined for the HDV seroconverters.

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

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

213 HDAg multimerization in the formation of the HDV ribonucleoprotein complex (RNP).

214 In the structures of the HDV ribozyme a cytosine nucleobase resides at the active

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

216 tallized and determined the structure of the HDV ribozyme bound to an inhibitor RNA containing a deox

217 sitions in and around the active site of the HDV ribozyme were identical in R2.

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

219 ild-type and 7-deazaguanosine mutants of the HDV ribozyme.

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

221 critical determinant of the structure of the HDV RNP.

222 condary structure that closely resembles the HDV ribozyme.

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

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

225 Thus, the HDV ribozyme may use a combination of metal ion Lewis ac

226 inding of Mg(2+) and Co(NH(3))(6)(3+) to the HDV ribozyme is studied by Raman microscopic analysis of

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

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

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

230 M II in HDAg-160 did not diminish binding to HDV unbranched rodlike RNA.

231 binds with high affinity and specificity to HDV RNA segments in vitro.

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

233 Cells of WHV-induced HCCs are susceptible to HDV infection in vivo, and therefore express functional

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

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

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

237 The primary end point of undetectable HDV RNA at the end of treatment was achieved in 3 patien

238 ry end point was achievement of undetectable HDV RNA at the end of treatment.

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

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

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

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

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

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

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

246 Superinfection with hepatitis D virus (HDV) may increase the risk for hepatitis flares and chro

247 Hepatitis D virus (HDV) requires hepatitis B surface antigen (HBsAg) to pro

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

249 Hepatitis delta virus (HDV) and cytoplasmic polyadenylation element-binding pro

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

251 Hepatitis delta virus (HDV) assembly also uses the envelope proteins of HBV to

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

253 The two ribozymes of hepatitis delta virus (HDV) cleave faster in divalent metal ions than in monova

254 Hepatitis delta virus (HDV) encodes one protein, hepatitis delta antigen (delta

255 ving ribozymes of the hepatitis delta virus (HDV) family for processing their 5' termini.

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

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

258 otypes A to I support hepatitis delta virus (HDV) infectivity.

259 Hepatitis delta virus (HDV) is a natural subviral agent of human hepatitis B vi

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

261 Hepatitis delta virus (HDV) is a small, defective RNA virus that can infect onl

262 Hepatitis delta virus (HDV) is a subviral pathogen that increases the severity

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

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

265 Most hepatitis delta virus (HDV) prevalence estimates from the United States are >10

266 Hepatitis delta virus (HDV) replication and packaging require interactions betw

267 The hepatitis delta virus (HDV) ribozyme and HDV-like ribozymes are self-cleaving R

268 ydrate in crystals of hepatitis delta virus (HDV) ribozyme and to follow the effects of magnesium hyd

269 While the hepatitis delta virus (HDV) ribozyme can undergo self-cleavage in the presence

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

271 The hepatitis delta virus (HDV) ribozyme is a self-cleaving RNA enzyme essential fo

272 d in structure to the hepatitis delta virus (HDV) ribozyme occurs in a number of mammals, including c

273 The hepatitis delta virus (HDV) ribozyme uses the nucleobase C75 and a hydrated Mg(

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

275 imilar to that of the hepatitis delta virus (HDV) ribozyme.

276 Hepatitis delta virus (HDV) RNA forms an unbranched rod structure that is assoc

277 tigenomic sequence of hepatitis delta virus (HDV) RNA is 33-nt downstream of the poly(A) site for the

278 tis B virus (HBV) and hepatitis delta virus (HDV) share the HBV envelope proteins.

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

280 tly available against hepatitis delta virus (HDV), a defective virus leading to the most severe form

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

282 hepatocytes either by hepatitis delta virus (HDV), a subviral agent that uses HBV envelope proteins,

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

284 be circumvented with hepatitis delta virus (HDV), which needs the HBV large envelope protein only fo

285 observed for HBV and hepatitis delta virus (HDV), which shares the same L, M, and S.

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

287 treatment option for hepatitis delta virus (HDV).

288 and liver cancer, it was determined whether HDV could infect in vivo the cells of hepadnavirus-induc

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

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

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

292 Characteristics associated with HDV exposure and viremia were identified.

293 hanism of liver pathogenesis associated with HDV infection.

294 age were significant factors associated with HDV infection.

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

296 cted to identify the associated factors with HDV seroconversion.

297 th HBV-infected and naive chimeric mice with HDV titers rising up to 1 x 10E9 copies/mL.

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

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

300 hepatitis virus (WHV) are superinfected with HDV, they produce HDV with a WHV envelope, wHDV.