ライフサイエンスコーパス: HEV

1 HEV antigen levels were measured with the Wantai enzyme-

2 HEV circulates as quasi-enveloped virions in the blood t

3 HEV comprises four genotypes with different geographic d

4 HEV genotype 3 (gt3) infections were cleared from liver

5 HEV is a highly relevant model to study these questions.

6 HEV is endemic in France and hyperendemic in some areas;

7 HEV ORF3 shares several structural features with class I

8 HEV RNA detection by real-time polymerase chain reaction

9 HEV RNA was detected, indicating subclinical infections

10 HEV RNA, HEV-specific T-cell responses, IgG anti-HEV ant

11 HEV-specific interferon-gamma-producing T cells were 2-f

12 HEV-specific T-cell responses were detected in 41/44 imm

13 HEV-specific T-cell responses were elevated in reinfecte

14 HEVs and HRVs may contribute to the development of AOM i

15 ormational antigenic sites of the genotype 1 HEV p239 antigen, and cross-react with other genotypes.

16 petent patients with acute HEV infection, 18 HEV-exposed immunosuppressed organ-transplant recipients

17 ransmission of hepatitis E virus genotype 3 (HEV G3) has become recognized as an emerging problem in

18 ver transplant recipients, without achieving HEV sustained virological response, and may induce a bio

19 Neutrophil transmigration across HEVs is faster than across conventional postcapillary ve

20 ORF2 Ag can be used as a marker of active HEV infection and for assessment of the effect of antivi

21 Acute HEV infection is very rare in adult Americans with ALF (

22 Acute HEV infection was frequently associated with GBS in our

23 Acute HEV infection was independently associated with piglet s

24 is not yet documented, and diagnosing acute HEV infection can be a challenge.

25 and discuss difficulties in diagnosing acute HEV infection.

26 and 5 healthy patients recovered from acute HEV infection were analyzed for anti-HEV IgG and for ant

27 Health England has monitored cases of acute HEV infection in England and Wales since 2003.

28 assays for HEV, indicating a possible acute HEV infection.

29 tients (6%) in our cohort had probable acute HEV infection.

30 o that in healthy patients with recent acute HEV infection.

31 ding 44 immune-competent patients with acute HEV infection, 18 HEV-exposed immunosuppressed organ-tra

32 V Ag remained detectable for >100 days after HEV RNA clearance in ribavirin-treated patients with chr

33 osbuvir has shown antiviral activity against HEV in vitro but clinical utility in vivo is unknown.

34 vir may have some antiviral activity against HEV when added to ribavirin.

35 romising trivalent vaccine candidate against HEV, RV, and AstV, which is worth for further developmen

36 type I IFN-mediated antiviral effect against HEV remains unclear.

37 lated interferon-alpha (pegIFNalpha) against HEV infections in humanized mice and modelled intrahepat

38 are important factors for protection against HEV reinfection.

39 ificantly higher neutralizing titers against HEV infection in cell culture, as well as significantly

40 All HEV isolates were genotype 3a.

41 Viral titers could be further enhanced by an HEV variant harboring a mutation in the RNA-dependent RN

42 viral diarrhea virus construct containing an HEV RNA insert (SynTura HEV) was developed, value assign

43 tural and biophysical characterization of an HEV nonstructural protein using a construct that has par

44 ter dramatically decreases replication of an HEV subgenomic replicon.

45 major blood-borne RNA viruses - HIV, HCV and HEV.

46 HRV and HEV showed higher population-attributable risk percentag

47 , 24, and 36 months and screened for HRV and HEV using real-time reverse-transcription quantitative p

48 f the possibility of disease reemergence and HEV viral transmission in LT patients.

49 Anti-HEV Ag-specific ELISA revealed significantly higher HEV

50 Anti-HEV Ag-specific ELISA was less sensitive than real-time

51 Anti-HEV IgG was detected in 38.8% of patients.

52 Recently, an anti-HEV antigen (Ag)-specific enzyme-linked immunosorbent as

53 garded as a self-limiting infection and anti-HEV antibodies seem to protect against reinfection, its

54 ent therapy were tested for HEV RNA and anti-HEV immunoglobulin G (IgG).

55 epatitis C therapy in patients carrying anti-HEV immunoglobulin G antibodies, raising 2 major questio

56 mmunoglobulin products tested contained anti-HEV capable of neutralizing HEV antigen.

57 Past exposure to HEV with detectable anti-HEV IgG was significantly more common in the ALF patient

58 Subjects with a detectable anti-HEV IgM also underwent testing for HEV RNA.

59 d 70 demonstrated repeatedly detectable anti-HEV IgM, but all were HEV-RNA negative and had other put

60 m acute HEV infection were analyzed for anti-HEV IgG and for antibody reacting with HEV antigen.

61 M was higher in donors living in a high anti-HEV IgG seroprevalence area (1.9% versus 0.7%, P < 0.001

62 infusion therapy demonstrated a higher anti-HEV IgG level and neutralizing activity, compared with s

63 fection or shed virus in feces, and IgG anti-HEV antibody levels were unchanged (P = .017).

64 RNA, HEV-specific T-cell responses, IgG anti-HEV antibody, and the IgG anti-HEV avidity index were te

65 ses, IgG anti-HEV antibody, and the IgG anti-HEV avidity index were tested.

66 y HEV RNA in stool, and increase in IgG anti-HEV levels between 63- and 285-fold (P = .003).

67 Four animals with baseline IgG anti-HEV levels from 1.5 to 13.4 World Health Organization (W

68 Eight animals with baseline IgG anti-HEV levels from 2.8 to 90.7 WHO U/mL did not develop inf

69 The performance of anti-HEV Ag-ELISA was compared with that of real-time PCR, us

70 The presence of anti-HEV IgG was associated with increasing age (P < 0.001) a

71 The frequency of anti-HEV IgM was higher in donors living in a high anti-HEV I

72 d assays to determine the prevalence of anti-HEV immunoglobulin G (IgG) and IgM among 10,569 French b

73 afforded by the ubiquitous presence of anti-HEV in immunoglobulin replacement products.

74 The anti-HEV Ag-specific ELISA is less sensitive than HEV RNA rea

75 virus (anti-HAV) and hepatitis E virus (anti-HEV) was 65.2% (95% CI, 64.2%-66.1%) and 33.3% (95% CI,

76 n, 294 (43.4%) of the ALF patients were anti-HEV IgG positive with the seroprevalence being highest i

77 AV seroprevalence had decreased whereas anti-HEV seroprevalence had risen.

78 n can indicate the presence of an associated HEV infection.

79 Although mostly asymptomatic, HEV G3 infection has a range of outcomes, including mild

80 an promote ap237 adsorption as well as avian HEV adsorption and infection of the cells.

81 reports about the interaction between avian HEV and host cells.

82 standing about the interaction between avian HEV and its host cells.

83 ment to and infection of host cells by avian HEV are significantly reduced.

84 nhibitors, attachment and infection by avian HEV significantly decreased.

85 rresponded with that in tissues during avian HEV infection.

86 w insight to understand the process of avian HEV infection of host cells.IMPORTANCE The process of vi

87 t time that OATP1A2 interacts with the avian HEV capsid protein and can influence viral infection in

88 in chicken liver cells by a truncated avian HEV capsid protein (ap237) in which the host protein OAT

89 ed to interact with ap237, a truncated avian HEV capsid protein spanning amino acids 313 to 549, by a

90 n different tissues is consistent with avian HEV infection in vivo Finally, when the functions of OAT

91 U/mL evidenced reinfection as determined by HEV RNA in stool, and increase in IgG anti-HEV levels be

92 is report demonstrates that ISG15 induced by HEV replication in Huh7-S10-3 human liver cells plays an

93 found the patient to be infected by camelid HEV.

94 oped a cell culture system and characterized HEV particles; we identified 3 ORF2 capsid proteins (ORF

95 plant recipient with cirrhosis after chronic HEV infection.

96 ting acute viral hepatitis, although chronic HEV infection has recently become a significant clinical

97 pecificity to distinguish acute from chronic HEV infection.

98 However, chronic HEV infection has recently become a significant clinical

99 ve a regression of liver fibrosis in chronic HEV patients.

100 uccessfully developed a pig model of chronic HEV infection and examined immune correlates leading to

101 aid in delineating the mechanisms of chronic HEV infection and in developing effective therapeutics a

102 , this is the first reported case of chronic HEV infection in an HIV(+) U.S. individual.

103 may facilitate the establishment of chronic HEV infection.

104 years later, developed biopsy-proven chronic HEV infection.

105 erferon (IFN) has been used to treat chronic HEV infection in solid-organ transplant patients with so

106 rin is highly efficient for treating chronic HEV infection in SOT recipients and shows that the predo

107 Data from 255 SOT recipients with chronic HEV infection from 30 European centers were analyzed.

108 gan transplant (SOT) recipients with chronic HEV infection treated with ribavirin monotherapy (N = 25

109 organ-transplant recipients (8 with chronic HEV), and 27 healthy volunteers.

110 e in ribavirin-treated patients with chronic HEV.

111 lyses were performed to compare the clinical HEV strains.

112 nses were detected in 41/44 immune-competent HEV exposed volunteers (median magnitude: 397 spot-formi

113 In conclusion, HEV gt1 and gt3 infections do not elicit innate intrahep

114 In this context, HEV infection frequently evolves to chronic infection wi

115 he assay successfully amplified 16 different HEV sequences with significant nucleotide mismatching in

116 type I IFN-mediated antiviral effect during HEV replication.

117 ential immunomodulatory role of ISG15 during HEV replication.

118 IFN-stimulated gene expression levels during HEV replication.

119 High hepatitis E (HEV) seroprevalence has been reported in the general pop

120 an rhinoviruses (HRVs), human enteroviruses (HEVs) and human parechoviruses (HPeVs) have been linked

121 he index cases, veterinary and environmental HEV strains were identical.

122 clinical status, serologies and serum/feces HEV RNA every 4 months.

123 r operator characteristic curve of 0.86) for HEV exposure at 0.3 IU/mL.

124 showed positive reactivity on IgM assays for HEV, indicating a possible acute HEV infection.

125 y 2 billion people live in areas endemic for HEV and are at risk of infection.

126 e absence of a robust cell culture model for HEV infection, the analysis of the viral life cycle, the

127 in plasma from mice that tested negative for HEV RNA in plasma but positive for HEV RNA in stool and

128 n of a WHO international reference panel for HEV genotypes (code 8578/13) showed viral load results f

129 ative for HEV RNA in plasma but positive for HEV RNA in stool and was detected after viral clearance

130 In a subgroup, polymerase chain reaction for HEV was performed.

131 rganization (WHO) international standard for HEV RNA (code 6329/10), and used to prepare working assa

132 and men enrolled in U.S. cohort studies for HEV viremia using a high-throughput nucleic acid testing

133 globulin replacement therapy were tested for HEV RNA and anti-HEV immunoglobulin G (IgG).

134 Given that antibody testing for HEV infection is not routinely obtained, we hypothesized

135 able anti-HEV IgM also underwent testing for HEV RNA.

136 The MIF and FRVs for HEVs and PHEVs mostly lie between those for ICEVs and BE

137 mens and suspensions of fecal specimens from HEV-infected and ribavirin-treated humanized mice were a

138 g was detected in both plasma and stool from HEV-infected mice, and levels increased over time.

139 liver cells) and in vivo (liver tissues from HEV-infected pigs); however, ISG15 is not required for v

140 We performed studies with gt3 HEV cell culture-produced particles and patient blood an

141 common fecal-oral route, causing hepatitis (HEV) and gastroenteritis (RV and AstV) respectively in h

142 equine encephalitis virus), and Hepeviridae (HEV), indicating that it might be a significant tropism

143 specific ELISA revealed significantly higher HEV Ag in chronically infected individuals as compared t

144 s macaques were reinoculated with homologous HEV genotype 1 (gt1, Sar-55) and followed for 115 days.

145 were collected monthly and analyzed for HRV, HEV, and HPeV.

146 nables model specific assessments for ICEVs, HEVs, PHEVs, and BEVs required to determine the optimal

147 re significantly higher in immunocompromised HEV-infected pigs.

148 ous particles, but are the major antigens in HEV-infected patient sera.

149 al clearance by pegIFNalpha was confirmed in HEV gt1, but not in Hepatitis B Virus infected animals.

150 logical relevance of ORF2 N-glycosylation in HEV lifecycle remain to be elucidated.

151 A polymerase mutations do not play a role in HEV clearance.

152 pletion affected LN structure with increased HEVs, upregulated chemokines, and cell adhesion molecule

153 Hepatitis E virus infection (HEV) is an emerging problem in developed countries.

154 le in replication and assembly of infectious HEV particles.

155 nt media conditions to produce intracellular HEV cell culture-derived particles (HEVcc) with viral ti

156 n efficient cell culture system and isolated HEV particles that were infectious in vitro and in vivo.

157 gle-host viruses, using 244 near-full-length HEV genomes.

158 ost T-cell responses against the full-length HEV virus and assessed a novel "Quantiferon" assay for t

159 The 4 reinfected animals showed a lower HEV-IgG avidity index (average 35.5%) than the 8 protect

160 While most often clinically mild, HEV can be severe or fatal in certain demographics, such

161 d contained anti-HEV capable of neutralizing HEV antigen.

162 We found that compared to nonenveloped HEV virions, eHEV attachment to the cell was much less e

163 Of note, HEV Ag remained detectable for >100 days after HEV RNA c

164 Of HEV's three ORFs, the function of ORF3 has remained elus

165 th of treatment but without the clearance of HEV.

166 n AOM episodes and simultaneous detection of HEV (adjusted odds ratio for the detection of virus in s

167 sensitive than real-time PCR at detection of HEV infection.

168 f HEV infection is based on the detection of HEV-specific antibodies, viral RNA, and/or antigen (Ag).

169 Diagnosis of HEV infection is based on the detection of HEV-specific

170 uantiferon" assay for the rapid diagnosis of HEV infection.

171 ater could contribute to the epidemiology of HEV infection in France.

172 ently, 91 cases without clinical evidence of HEV-related hepatitis were enrolled in 1 year of prospec

173 nstrate a previously undescribed function of HEV ORF3 as a viroporin, which may serve as an attractiv

174 with class I viroporins, and the function of HEV ORF3 can be maintained by replacing it with the well

175 ctors for SVR, and to evaluate the impact of HEV RNA mutations on virological response.

176 However, the kinetics of HEV Ag expression during infection remains poorly unders

177 d understanding of the complex mechanisms of HEV biology.IMPORTANCE Hepatitis E virus (HEV) is an eme

178 onclusion, this robust cell culture model of HEV infection provides a powerful tool for studying vira

179 GS analysis reveals differential patterns of HEV-specific antibody lineages and highlights the necess

180 Prevalence of HEV viremia was 3 of 2,606 and 0 of 313 in tested plasma

181 To determine the prevalence of HEV-associated GBS in a Belgian cohort, study the clinic

182 tes, but there are few data on prevalence of HEV/human immunodeficiency virus (HIV) coinfection in U.

183 is known that the nonstructural proteins of HEV ORF1 are expressed as a single transcript, there is

184 simultaneous detection and quantification of HEV RNA in human serum was developed based on an adaptat

185 says for the detection and quantification of HEV RNA.

186 ound in this study do not affect the rate of HEV clearance.This large-scale retrospective study that

187 the ISG15-mediated type I IFN sensitivity of HEV.

188 the ISG15-mediated type I IFN sensitivity of HEV.

189 ng frame 2/3 (ORF2/3) nucleotide sequence of HEV.

190 Nevertheless, the reported seroprevalence of HEV varies greatly depending on the geographical area an

191 syndrome (GBS), but the clinical spectrum of HEV-associated GBS is not yet documented, and diagnosing

192 lgian cohort, study the clinical spectrum of HEV-associated GBS, and discuss difficulties in diagnosi

193 Finally, RNA sequencing studies of HEV-infected primary human hepatocytes demonstrated a te

194 viously reported as a model for the study of HEV infection, but published data were focused on the qu

195 microscopy, we defined the ultrastructure of HEV cell culture-produced particles and particles from p

196 In this review, the structural plasticity of HEVs, the regulatory pathways underpinning this plastici

197 ribavirin did not have a negative impact on HEV clearance.

198 2 of 6 patients with positive reactivity on HEV IgM assays also revealed positive test results for c

199 sferase levels showed positive reactivity on HEV IgM assays.

200 the human hepatocyte donor, viral isolate or HEV infection duration.

201 Like many other viral pathogens, HEV has been classified into several distinct genotypes.

202 cultured cells and in samples from patients, HEV produced 3 forms of the ORF2 capsid protein: infecti

203 ven the increasing concerns about persistent HEV infection and its potential for transmission via the

204 The risk of persistent HEV infection in patients with antibody deficiency appea

205 We aimed to determine the risk of persistent HEV infection in patients with primary or secondary anti

206 5 recently treated patients with persistent HEV infection, and 5 healthy patients recovered from acu

207 body-deficient patient had detectable plasma HEV RNA.

208 OT recipients and shows that the predominant HEV RNA polymerase mutations found in this study do not

209 Pretreatment HEV polymerase mutations and de novo mutations under rib

210 As reported previously, HEV G3 group 2 (also known as "G3 abcdhij") is the predo

211 in a previously healthy man caused by a rat HEV with a considerably divergent genomic sequence compa

212 ent genomic sequence compared with other rat HEV strains.

213 It is possible that rat HEV is an underrecognized cause of hepatitis infection,

214 mportant immunomodulatory role and regulates HEV sensitivity to exogenous type I IFN.IMPORTANCE Hepat

215 trans-complementation of subgenomic reporter HEV replicons.

216 HEV RNA, HEV-specific T-cell responses, IgG anti-HEV antibody, an

217 Robust HEV-specific T-cell responses generated during acute dis

218 Our results suggest that subclinical HEV infection exists among LT patients in this high-prev

219 ontributing to protection against subsequent HEV reinfection are unknown.

220 We describe 2 cases of acute symptomatic HEV infection after hepatitis C therapy in patients carr

221 struct containing an HEV RNA insert (SynTura HEV) was developed, value assigned with the first World

222 Broadly reactive RT-qPCR primers targeting HEV ORF2/3 were successfully adapted for use in an assay

223 HEV Ag-specific ELISA is less sensitive than HEV RNA real-time PCR but represents a useful tool to di

224 Recently, we demonstrated that HEV produces three different forms of ORF2: (i) the ORF2

225 We hypothesized that HEV might persist at a subclinical level and might pose

226 not routinely obtained, we hypothesized that HEV-related ALF might be present and unrecognized in Nor

227 The results revealed that HEV induced high levels of ISG15 production both in vitr

228 Results showed that HEV infection of immunocompromised pigs reduced the seru

229 titis E virus (HEV) infection and shows that HEV RNA polymerase mutations do not play a role in HEV c

230 Overall, though, these data suggest that HEV infection is rare in the HIV(+) U.S. population.

231 The HEV genome encodes 3 proteins, including the ORF2 capsid

232 nosorbent assay (ELISA) directed against the HEV capsid became commercially available.

233 We show that most of the HEV genome is evolutionarily constrained.

234 rstanding of the molecular mechanisms of the HEV genome.

235 The presence of the HEV helicase in cis dramatically increases the binding o

236 ndings will advance our understanding of the HEV life cycle and improve diagnosis.

237 Detailed analyses of the HEV life cycle has been hampered by the lack of an effic

238 Based on the structural homology of the HEV protein with known structures, along with the presen

239 We performed phylogenetic analyses of the HEV sequence (partial and full-length) from 1 patient fr

240 tudy, we established a protocol based on the HEV genotype 3 p6 (Kernow C-1) and the human hepatoma ce

241 at the identified protein corresponds to the HEV protease, which could require activation or repressi

242 ecific CD4+ T cell entry into the CR through HEVs, suppressed T cell activation, and altered T cell d

243 y regulating type I IFN signaling and, thus, HEV sensitivity to type I IFN.

244 It is becoming clear that alterations to HEV network density and/or morphology can result in immu

245 Contrary to HEV RNA, ORF2 Ag levels were higher in mouse plasma than

246 Past exposure to HEV with detectable anti-HEV IgG was significantly more

247 alone cannot totally explain the exposure to HEV, and contaminated water could contribute to the epid

248 nfected animals after subsequent exposure to HEV.

249 sed to chronicity, because 8/10 drug-treated HEV-infected pigs continued fecal virus shedding beyond

250 whereas the majority (7/10) of mock-treated HEV-infected pigs cleared fecal viral shedding at 8 wk p

251 No ISG induction was observed in untreated HEV gt3 and gt1 infected humanized livers compared to co

252 n-treated humanized mice were analyzed using HEV antigen-specific enzyme-linked immunosorbent assay,

253 milar emissions to hybrid electric vehicles (HEVs) in about 25% of the counties in the US and lower t

254 es (EVs) including hybrid electric vehicles (HEVs), plug-in hybrid electric vehicles (PHEVs), and bat

255 and firm arrest on high endothelium venules (HEV), thereby attributing their inefficient trafficking

256 eater expansion of high endothelial venules (HEVs) and lymphatic vessels in comparison to the TPLNs.

257 High endothelial venules (HEVs) are specialised postcapillary venules that specifi

258 e demonstrate that high endothelial venules (HEVs) of the greater omentum constitute a main entry pat

259 ge (CR) and around high endothelial venules (HEVs).

260 Most cases of hepatitis E viral (HEV) infection in developed countries are autochthonous.

261 atients who fail to clear hepatitis E virus (HEV) following reduction of immunosuppressive therapy an

262 Hepatitis E Virus (HEV) genome encodes three proteins including the ORF2 ca

263 Hepatitis E virus (HEV) genotype 3 infections are frequent in Europe and No

264 zoonotic transmission of hepatitis E virus (HEV) genotype 3, which causes chronic infections in immu

265 Hepatitis E virus (HEV) has emerged as a cause of chronic hepatitis among i

266 ate the dispersion of the hepatitis E virus (HEV) in the environment.

267 ient for treating chronic hepatitis E virus (HEV) infection and shows that HEV RNA polymerase mutatio

268 nd immunopathology during hepatitis E virus (HEV) infection determines important clinical outcomes.

269 Acute hepatitis E virus (HEV) infection is a leading cause of acute liver failure

270 BACKGROUND & AIMS: Hepatitis E virus (HEV) infection is a major cause of acute hepatitis world

271 Chronic hepatitis E virus (HEV) infection is a significant clinical problem in immu

272 Persistent hepatitis E virus (HEV) infection is described in a number of immunosuppres

273 Hepatitis E virus (HEV) infection is increasingly being reported in immunoc

274 Secondary spread of hepatitis E virus (HEV) infection occurs often in endemic settings in devel

275 ous type I IFN.IMPORTANCE Hepatitis E virus (HEV) infection typically causes self-limiting acute vira

276 nded for treating chronic hepatitis E virus (HEV) infection.

277 tment options for chronic Hepatitis E Virus (HEV) infections are limited and immunological determinan

278 Hepatitis E virus (HEV) is a 7.2-kb positive-sense, single-stranded RNA vir

279 Hepatitis E virus (HEV) is a major public health concern in developing coun

280 of HEV biology.IMPORTANCE Hepatitis E virus (HEV) is an emerging virus found predominately in develop

281 Exposure to hepatitis E virus (HEV) is common in the United States, but there are few d

282 otypes 3 and 4.IMPORTANCE Hepatitis E virus (HEV) is increasingly recognized as a pathogen that affec

283 Although hepatitis E virus (HEV) is regarded as a self-limiting infection and anti-H

284 Hepatitis E virus (HEV) is the causative agent of hepatitis E in humans and

285 Hepatitis E virus (HEV) is the leading cause of enterically transmitted vir

286 Avian hepatitis E virus (HEV) is the main causative agent of big liver and spleen

287 Hepatitis E virus (HEV) is the most common cause of acute viral hepatitis g

288 t enterically transmitted hepatitis E virus (HEV) progeny particles are secreted basolaterally as qua

289 Hepatitis E virus (HEV) recently has been shown to be an antecedent infecti

290 hat the macro domain from hepatitis E virus (HEV) serves as an ADP-ribose-protein hydrolase for mono-

291 The hepatitis E virus (HEV) sheds into feces as nonenveloped virions but circul

292 Hepatitis E virus (HEV), a single-stranded positive-sense RNA virus, genera

293 Hepatitis E virus (HEV), rotavirus (RV), and astrovirus (AstV) are importan

294 the licensed vaccine for hepatitis E virus (HEV).

295 atedly detectable anti-HEV IgM, but all were HEV-RNA negative and had other putative diagnoses.

296 When HEV testing is considered, it is important to test for o

297 of secondary standards calibrated to the WHO HEV international standard can improve the standardizati

298 sofosbuvir for 6 months was associated with HEV RNA becoming undetectable in plasma.

299 Immunocompromised pigs infected with HEV progressed to chronicity, because 8/10 drug-treated

300 anti-HEV IgG and for antibody reacting with HEV antigen.

301 Zoonotic HEV cases have been increasingly described in Europe, Ja