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 in stool but not sera from three 12

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

11 HEVs have very low emission rates compared to tier 2 veh

12 rtion was placed into a strain of genotype 1 HEV which infects only humans, it expanded the host rang

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

14 Accordingly, HEV-HIV coinfection leads to accelerated liver cirrhosis

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

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

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

18 Acute HEV infection was frequently associated with GBS in our

19 Acute HEV infection was independently associated with piglet s

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

21 and discuss difficulties in diagnosing acute HEV infection.

22 ction for >4 years whereas 2 women had acute HEV detectable at only a single study visit.

23 al transmission is a potential mode of acute HEV infection.

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

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

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

27 We utilized these cell culture-adapted HEV strains to assess how the HVR may be involved in vir

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

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

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

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

32 ificantly associated with protection against HEV infection in non-Hispanic blacks; additional studies

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

34 All HEV isolates were genotype 3a.

35 ating tolerant mice with anti-ER-TR7 altered HEV basement membrane structure and the distribution of

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

37 ipe CO2 emissions and fuel consumption of an HEV passenger car to a CV of the same make and model dur

38 ter dramatically decreases replication of an HEV subgenomic replicon.

39 ostly associated with either traveling to an HEV endemic area or contact with pigs, which represent a

40 cycle ownership costs of non-plug-in (CV and HEV) and plug-in light-duty vehicles.

41 uences belonged to genotypes A, D, or G, and HEV sequences belonged to genotype 3.

42 icivirus, while the sensitivity for HAdV and HEV was low.

43 NGS-based detection of HBV and HEV infections is more sensitive than using commercially

44 HBV and HEV may be cryptically associated with HUE.

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

46 i-HEV and, if positive, for IgM anti-HEV and HEV RNA.

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

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

49 Anti-HEV IgG(+) subjects were significantly older, less likel

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

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

52 for anti-HEV immunoglobulin (Ig) M and anti-HEV IgG levels.

53 her single-nucleotide polymorphisms and anti-HEV seropositivity in non-Hispanic blacks or between any

54 any single-nucleotide polymorphisms and anti-HEV seropositivity in non-Hispanic whites or Mexican Ame

55 ulation that showed association between anti-HEV seropositivity and functional epsilon3 and epsilon4

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

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 ologic assay, we compared the estimated anti-HEV immunoglobulin G (IgG) prevalence and risk factors f

61 ver Failure Study Group were tested for anti-HEV immunoglobulin (Ig) M and anti-HEV IgG levels.

62 f associations between antibody to HEV (anti-HEV) immunoglobulin G seropositivity indicating past or

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

64 n = 63) as controls were tested for IgG anti-HEV and, if positive, for IgM anti-HEV and HEV RNA.

65 IgG anti-HEV was detected in sera from 10% of pigs aged 6 to 8 we

66 IgG anti-HEV and, if positive, for IgM anti-HEV and HEV RNA.

67 lood donors; none were positive for IgM anti-HEV or HEV RNA.

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

69 The effectiveness of anti-HEV Ag-specific ELISA at detecting HEV genotype 3 infect

70 The low and similar seroprevalence of anti-HEV between the at-risk group and age-matched blood dono

71 ter was associated with a lower rate of anti-HEV IgG (P = 0.02).

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

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

74 blacks had the lowest seroprevalence of anti-HEV immunoglobulin G (15.3%, 95% confidence interval [CI

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

76 The prevalence of anti-HEV was 3.1% among personnel compared to 3.2% among bloo

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

78 The anti-HEV prevalence is declining in the United States.

79 wer overall 3-week survival compared to anti-HEV IgG(-) subjects (63% vs. 70%; P = 0.018).

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

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

82 Both HEV-positive cases were coinfected with HBV.

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

84 found the patient to be infected by camelid HEV.

85 sumed camel meat and milk, therefore camelid HEV, which is genotype 7, might infect human beings.

86 world, the most common genotype (gt) causing HEV infection is gt 3.

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

88 plant recipient with cirrhosis after chronic HEV infection.

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

90 pecificity to distinguish acute from chronic HEV infection.

91 sting of stored samples, 1 woman had chronic HEV infection for >4 years whereas 2 women had acute HEV

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

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

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

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

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

97 may facilitate the establishment of chronic HEV infection.

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

99 We also confirm that chronic HEV infection can persist despite a CD4(+) count >200 ce

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

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

102 e in ribavirin-treated patients with chronic HEV.

103 lyses were performed to compare the clinical HEV strains.

104 ine CV with a CNG CV, or a CNG CV with a CNG HEV, can provide life cycle air emissions impact benefit

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

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

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

108 r fuel consumption defined the corresponding HEV "benefit" factor for each VSP class (1 kW/ton resolu

109 st infections occur in developing countries, HEV appears to be an emerging problem in several industr

110 account for measured road grade, the mean CV/HEV ratios of CO2 tailpipe emissions or fuel consumption

111 t predictive factor for SVR, and a decreased HEV concentration of 0.5 log copies/mL or greater had an

112 Defining HEV T-cell targets will be important for the investigati

113 s of anti-HEV Ag-specific ELISA at detecting HEV genotype 3 infections remains undefined.

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

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

116 cy of mono-macs and DCs was increased during HEV infection compared to HC (P < 0.001).

117 ential immunomodulatory role of ISG15 during HEV replication.

118 IFN-stimulated gene expression levels during HEV replication.

119 Furthermore, eliminating HEV tailpipe emissions via plug-in vehicles has an insig

120 %), Norwalk virus (6.6%), Human enterovirus (HEV) (9.2%), Human parechovirus (1.3%), Sapporo virus (1

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

122 Among US-born persons, the estimated HEV antibody prevalence declined significantly for all s

123 All the patients with protracted fecal HEV shedding during treatment suffered a relapse.

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

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

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

127 The major risk groups for HEV infection and its ensuing complications are elderly

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

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

130 , the cases became a temporary reservoir for HEV, which was detected in the island's untreated wastew

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 lack of an efficient cell culture system for HEV, the molecular mechanisms of HEV replication and pat

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

138 ication of the passenger vehicle fleet (from HEVs to PHEVs to BEVs) increases in response to climate

139 ntify the in-use benefit of one popular full HEV technology.

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 train resizing increases the FRVs for ICEVs, HEVs and PHEVs.

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

146 This data identifies HEVs as a clinically relevant vascular recruitment site

147 re significantly higher in immunocompromised HEV-infected pigs.

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

149 nstrate that the RPS17 sequence insertion in HEV bestows novel nuclear/nucleolar trafficking capabili

150 ence that insertion of the RPS17 sequence in HEV likely confers nuclear trafficking capabilities to t

151 bined model explained 95% of the variance in HEV benefit for city, 75% for arterial and 57% for highw

152 ence with L-selectin-mediated trafficking in HEVs could represent a novel strategy to block dissemina

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

154 Our investigation attributed this large HEV outbreak to the consumption of an undercooked pig li

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

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

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

158 Monitoring HEV fecal excretion could be used to determine the optim

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

160 Unlike nonenveloped HEV virions, eHEV entry requires Rab5 and Rab7, small GT

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

162 Twenty-three novel HEV CD4(+) and CD8(+) T-cell targets were mapped predomi

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

164 th of treatment but without the clearance of HEV.

165 The life cycle of HEV has been understudied due to a lack of sufficient ce

166 The life cycle of HEV is still poorly understood and the lack of efficient

167 We observed that the density of HEV blood vessels was increased in CLL LNs and that CD20

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

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

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

171 Moreover, eradication of HEV is hampered by long-term environmental persistence o

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

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

174 the mechanism of cross-species infection of HEV in the future.

175 s will be important for the investigation of HEV-associated autoimmune disease.

176 system for HEV, the molecular mechanisms of HEV replication and pathogenesis are poorly understood.

177 viral protein-protein interactions (PPIs) of HEV by systematic Yeast two-hybrid (Y2H) and LuMPIS scre

178 The prevalence of HEV antibody among those aged >/=6 years declined from 1

179 termine whether changes in the prevalence of HEV antibody have occurred over time.

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

184 says for the detection and quantification of HEV RNA.

185 f cross-species infection and replication of HEV.

186 h pigs, which represent a major reservoir of HEV.

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 smission and determine the seroprevalence of HEV among animal handlers at the institute.

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

192 ptimal duration of therapy in the setting of HEV infection.

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

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

195 Recently, a unique genotype 3 strain of HEV recovered from a chronically infected patient was ad

196 have been used successfully for treatment of HEV, but this treatment is contraindicated in certain pa

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

198 w, we will discuss the molecular virology of HEV, mode of transmission in industrialized countries, a

199 2 of 6 patients with positive reactivity on HEV IgM assays also revealed positive test results for c

200 sferase levels showed positive reactivity on HEV IgM assays.

201 nors; none were positive for IgM anti-HEV or HEV RNA.

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

203 n allow for the ability of the Kernow C-1 P6 HEV to adapt in cell culture and allow for expanded host

204 The adaptation of the Kernow C-1 P6 HEV to propagate in HepG2C3A cells selected for a rare v

205 apabilities to the ORF1 protein of Kernow P6 HEV and that lysine residues within the RPS17 insertion,

206 ion of 14 participants with evidence of past HEV infection.

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

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

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

210 In 2011, the first prophylactic HEV vaccine, Hecolin, was approved in China, but it is n

211 ey PPIs correlate with the already published HEV 3D structure.

212 n G seropositivity indicating past or recent HEV infection and human genetic variants among three maj

213 sed whole-blood stimulation with recombinant HEV-capsid protein in the QuantiFERON kit.

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

215 The reported HEV benefits account for real-world road grade that is o

216 Sequencing revealed HEV genotype 3 with approximately 10% difference between

217 ut there is a paucity of real-world, on-road HEV emissions and performance data needed to assess ener

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

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

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

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

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

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

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

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

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

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

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

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

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

231 rrelate with the enhanced replication of the HEV Kernow C-1 P6 strain.

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

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

234 within the hypervariable region (HVR) of the HEV ORF1 protein.

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

236 ve and Treg cells within and surrounding the HEV.

237 of the hypervariable region (HVR) within the HEV genome, allowing for cell culture adaptation and exp

238 Before therapy, HEV RNA concentration was significantly greater in patie

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

240 strength of associations between antibody to HEV (anti-HEV) immunoglobulin G seropositivity indicatin

241 ctor controlling the binding of CLL cells to HEV walls in vivo.

242 is and increased mortality rates compared to HEV infection alone, which is, except during pregnancy,

243 with a different distribution as compared to HEV RNA.

244 e decline suggests a decrease in exposure to HEV over time, the risks associated with exposure remain

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

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

247 ation, and discovered that CLL cells bind to HEVs in vivo via a multistep adhesion cascade, which inv

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

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

250 al samples from commercial pigs with unknown HEV exposure were tested by all four assays.

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

252 Fuel use HEV benefit factors were 1.3 and 2 for the regulatory hi

253 vehicles (CV) and hybrid electric vehicles (HEV), and natural gas-derived electricity (NG-e) use in

254 Hybrid-electric vehicles (HEVs) have lower fuel consumption and carbon dioxide (CO

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

256 trucks (PTs), and hybrid electric vehicles (HEVs), variability in tailpipe emission rates was evalua

257 cation relative to high endothelial venules (HEV).

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

259 r interaction with high endothelial venules (HEVs), specialized blood vessels for lymphocyte extravas

260 Hepatitis E viral (HEV) infection imposes a heavy health burden worldwide a

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

262 tively high prevalence of hepatitis E virus (HEV) antibody.

263 what was observed in the hepatitis E virus (HEV) capsid structure.

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

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

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

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

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

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

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

275 t recipients with chronic hepatitis E virus (HEV) infections were given ribavirin therapy for 3 month

276 ittle knowledge about how hepatitis E virus (HEV) inhibits induction of host IFNs, though the viral g

277 Hepatitis E virus (HEV) is an emerging virus causing epidemic acute hepatit

278 Hepatitis E virus (HEV) is an important but extremely understudied human pa

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

280 Hepatitis E virus (HEV) is considered a zoonotic infection in developed nat

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

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

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

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

285 Hepatitis E virus (HEV) is yearly responsible for approximately 20 million

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

287 The hepatitis E virus (HEV) RNA concentrations were determined before treatment

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

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

290 d the pooled library, and hepatitis E virus (HEV) was detected in 2 individuals with HUE (16.7%) and

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

292 hepatitis-C virus (HCV), hepatitis-E virus (HEV), dengue virus (DENV), and West Nile (WNV) virus inf

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

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

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

296 Whereas HEV mainly causes acute self-limiting infections, chroni

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

298 nd workers that come into close contact with HEV-infected animals.

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

300 les from pigs experimentally inoculated with HEV genotype 3 and 186 fecal samples from commercial pig

301 nd that CD20(+) CLL cells accumulated within HEV pockets, suggesting intense trafficking.