ライフサイエンスコーパス: HAV

1 HAV and HBV serologic testing prior to referral and at t

2 HAV and HCV replicons were similarly sensitive to interf

3 HAV contains no pocket factor and can withstand remarkab

4 HAV immunoglobulin G (IgG) values of >/=10 mIU/mL were c

5 HAV infections represent a distinctly different paradigm

6 HAV infects in a stealth-like manner and replicates effi

7 HAV thus disrupts host signaling by a mechanism that par

8 HAV vaccination in HIV-infected patients with a higher C

9 HAV vaccination of all HCV-infected persons is costly an

10 HAV was detected in sewage samples: 16/27(59.2%) from Te

11 HAV was genetically stable in Huh7 cells for at least ni

12 HAV-induced liver injury was associated with interferon-

13 HAV-N impaired the learning-induced phosphorylation of a

14 HAV-related hospitalizations increased from 7.3% in 1999

15 HAV-specific CD8(+) T cells were either not detected in

16 Hepatitis A (HAV) and hepatitis B (HBV) vaccination in patients with

17 ed by several agents, including hepatitis A (HAV), B (HBV), and C (HCV) virus.

18 Viruses studied were hepatitis A (HAV), hepatitis B (HBV), varicella zoster virus (VZV), m

19 health programs to increase awareness about HAV vaccination in patients with chronic liver disease a

20 Acute HAV accounted for 3.1% of patients enrolled in the ALFSG

21 Acute HAV infection is typified by minimal type I IFN response

22 ns of 182 serum proteins obtained from acute HAV- (18), HBV- (18), and HCV-infected (28) individuals,

23 Immune mechanisms that terminate acute HAV infection, and prevent a relapse of virus replicatio

24 At the peak viremia, patients with acute HAV infection had no Treg-cell suppression function, pro

25 e 15 and IFIT1 responses peaked 1-2 wk after HAV challenge and then subsided despite continuing high

26 eropositive responses up to 6-10 years after HAV vaccination.

27 greater NKT cell cytolytic activity against HAV-infected liver cells, compared with the shorter TIM-

28 revalence of salivary IgG antibodies against HAV and subsequent incident infections (or immunoconvers

29 significantly greater neutralization against HAV in vitro.

30 group showed higher antibody titres against HAV 3 and 4 wk after vaccination [19% (P = 0.037) and 22

31 gleplex rRT-PCR assay designed to detect all HAV genotypes infecting humans.

32 years ago, while the common ancestor of all HAV-related viruses including phopivirus can be traced b

33 ed conditions were frequently reported among HAV-infected individuals who died.

34 cidence of superinfection with acute HBV and HAV was low, but it was significantly lower in patients

35 he QM rates were 57.0% and 45.5% for HBV and HAV, respectively.

36 ination rates of 21.9% and 20.7% for HBV and HAV, respectively.

37 infection, HAV-related hospitalization, and HAV-related mortality.

38 cleotide sequence relatedness between it and HAV.

39 Anti-HAV levels through 10 years of age correlated with initi

40 Anti-HAV levels were measured at 1 and 6 months and at 3, 5,

41 Anti-HAV persists in adults and children for more than 10 yea

42 Anti-HAV seroprevalence had decreased whereas anti-HEV seropr

43 n group 1 born to anti-HAV-negative and anti-HAV-positive mothers, respectively, and 4% of group 3 ch

44 hough unexplained mechanistically, both anti-HAV antibody and inactivated whole-virus vaccines preven

45 ults tested at 8-9 years had detectable anti-HAV.

46 Importantly, elevated anti-HAV Ig titers were broadly observed across plasma units

47 Recent trends show a decrease in anti-HAV antibodies in the general population, with concomita

48 105 children, immunization resulted in anti-HAV levels of 17-572 mIU/mL.

49 up, infants were randomized by maternal anti-HAV status.

50 group randomized according to maternal anti-HAV status.

51 nificantly by vaccine group or maternal anti-HAV status.

52 tibodies to hepatitis A virus (maternal anti-HAV) may lower the infant's immune response to the vacci

53 6 months (50%-75%), and among maternal anti-HAV-positive children in groups 2 and 3 (67%-87%), who i

54 ears regardless of presence of maternal anti-HAV.

55 hepatitis A subclinically (>8000 mIU/mL anti-HAV).

56 The GMC of anti-HAV antibody at week 48 for three-dose HIV-infected MSM

57 e geometric mean concentration (GMC) of anti-HAV antibody was determined at weeks 48 and 72.

58 We obtained levels of anti-HAV at intervals through age 15-16 years among three gro

59 A broad range of anti-HAV Ig plasma titers was observed among these centers, w

60 icited an average 29.7-fold increase of anti-HAV levels.

61 ars of age correlated with initial peak anti-HAV levels (tested at 1 month after the second dose).

62 Seropositivity (anti-HAV >/=20 mIU/mL) 30 years after the second vaccine dose

63 s, all children retained seroprotective anti-HAV levels except for only 7% and 11% of children in gro

64 Nonetheless, the model indicated that anti-HAV seropositivity should persist for >/=30 years after

65 and 11% of children in group 1 born to anti-HAV-negative and anti-HAV-positive mothers, respectively

66 At 10 years, children born to anti-HAV-negative mothers in group 3 had the highest geometri

67 ely, and 4% of group 3 children born to anti-HAV-negative mothers.

68 al, 71-133 mIU/mL) and children born to anti-HAV-positive mothers in group 1 had the lowest GMC (29 m

69 nce of antibodies to hepatitis A virus (anti-HAV) and hepatitis E virus (anti-HEV) was 65.2% (95% CI,

70 sted for antibody to hepatitis A virus (anti-HAV) by ELISA.

71 maternal antibody to hepatitis A virus (anti-HAV) on the duration of seropositivity after hepatitis A

72 e presenting features of 29 adults with anti-HAV IgM positive ALF enrolled in the ALFSG_between 1998

73 hen contracted slowly over several months as HAV genomes were eliminated from liver.

74 We assessed HAV susceptibility and self-reported nonvaccination to H

75 A load (AOR, 1.90; 95% CI, 1.10-3.28) before HAV vaccination were predictive of seroconversion in HIV

76 CR1/TIM1 and the inverse association between HAV infection and prevention of atopy are not well under

77 Interaction between HAV and its receptor HAVCR1 inhibits Treg-cell function,

78 rter forms of the TIM-1 protein, which binds HAV less efficiently, thereby protecting against severe

79 he 157insMTTTVP insertion polymorphism bound HAV more efficiently.

80 Membrane hijacking by HAV blurs the classic distinction between 'enveloped' an

81 Whereas the hijacking of membranes by HAV facilitates escape from neutralizing antibodies and

82 We characterized HAV infections in three chimpanzees, quantifying viral R

83 hibits the function of Treg cells to control HAV infection.

84 Similarly, in primary neuronal cultures, HAV-N prevented NMDA-induced dendritic Erk-1/2 phosphory

85 aliva samples afforded the ability to detect HAV infections in beachgoers.

86 method based on DNA hybridization to detect HAV.

87 We determined HAV and HBV vaccination rates in a tertiary care referra

88 ting, early seroreversion following two-dose HAV vaccination occurred in 3.9% of HIV-positive patient

89 d HIV RNA levels are associated with durable HAV responses.

90 Quasi-enveloped HAV (eHAV) mediates stealthy cell-to-cell spread within

91 understand the biogenesis of quasi-enveloped HAV (eHAV) virions, we conducted a quantitative proteomi

92 mination Survey 2007-2016 data, we estimated HAV susceptibility prevalence (total HAV antibody negati

93 fect cells(9), mediates HAV infection by exo-HAV, which indicates that viral infection via this exoso

94 hepatitis A virus (HAV)-infected cells (exo-HAV) by clathrin-mediated endocytosis.

95 the exosomes, is mainly responsible for exo-HAV infectivity as assessed by methylene blue inactivati

96 membrane fusion and delivery of RNA from exo-HAV into the cytoplasm.

97 In contrast to exo-HAV, infectivity of HAV particles is pH-independent and

98 onded during a transient resurgence of fecal HAV shedding.

99 ealed an immunoprevalence rate of 16.17% for HAV with 1.43% of the cohort immunoconverting to HAV.

100 gthen public health surveillance efforts for HAV outbreak detection and response.

101 assay and the ISO 15216-1 rRT-PCR method for HAV detection.

102 ith control subjects who tested negative for HAV infection.

103 ibinin as a potential therapeutic option for HAV infections.

104 targets and potential treatment options for HAV and set the ground for future studies to unravel det

105 Quality measure rates for HAV and HBV are suboptimal for patients with chronic HCV

106 human genetic variants conferring a risk for HAV infection among the three major racial/ethnic popula

107 cularly targeting adults at highest risk for HAV infection, to mitigate the current outbreaks.

108 ged 18 to 40 years who were seronegative for HAV were enrolled in the study.

109 A ssDNA probe specific for HAV (capture probe) was designed and tested on DNAs from

110 patients requiring liver transplantation for HAV in the UNOS database significantly decreased from 0.

111 Hepatologists recommended vaccination for HAV in 63% and for HBV in 59.7% of eligible patients.

112 However, HEV differs from HAV in that infectivity is lower, perinatal transmission

113 Multiple peptides were identified from HAV capsid proteins (53.7% coverage), but none from nons

114 to vaccinate (NNV) to prevent mortality from HAV superinfection.

115 s, which could distinguish HCV patients from HAV- and HBV-infected individuals or healthy controls.

116 IL-18BP deficiency thus underlies fulminant HAV hepatitis by unleashing IL-18.

117 The median age range of decedents who had HAV infection and a liver-related condition was 51.0 to

118 nhibitors revealed that, in contrast to HCV, HAV does not depend on cyclophilin A, but rather on aden

119 In contrast to HCV, HAV replicated independently from microRNA-122 and phosp

120 era immunoprecipitated and neutralized human HAV, suggesting conservation of critical antigenic deter

121 ion in small mammals mimicked those of human HAV in hepatotropism, fecal shedding, acute nature, and

122 ivorous mammals and a rodent origin of human HAV.

123 edicare and Medicaid Services has identified HAV and HBV vaccination as a priority area for quality m

124 pooled odds ratio (OR) for mortality risk in HAV superinfection of HCV-infected persons was 7.23 (95%

125 vaccination) against most viruses, including HAV, measles, mumps, and VZV (P < 0.05 for all).

126 ss trends in the incidence of HAV infection, HAV-related hospitalization, and HAV-related mortality.

127 IgA did not inhibit HAV infection of African green monkey cells, suggesting

128 travenous formulation, efficiently inhibited HAV genome replication in vitro, suggesting oral silibin

129 ive' precursor insect viruses; for instance, HAV retains the ability to move from cell-to-cell by tra

130 virus exploits to infect cells(9), mediates HAV infection by exo-HAV, which indicates that viral inf

131 ic peptide containing the His-Ala-Val motif (HAV-N) transiently disrupted hippocampal N-cadherin dime

132 Antibodies to a neoantigen, HAV, developed when vaccination was delayed after initia

133 variability was identified in alignments of HAV sequences near the 5' end of the 3D(pol)-coding sequ

134 Binding of HAV to HAVCR1 blocked phosphorylation of Akt, prevented

135 f eHAV egress involving endosomal budding of HAV capsids into multivesicular bodies.

136 We demonstrate that the capacity of HAV to evade MAVS-mediated type I interferon responses d

137 arly stages of infection-a characteristic of HAV pathogenesis.

138 ition, it can be useful for rapid control of HAV infections as it takes only a few minutes to provide

139 acilitates an early but limited detection of HAV infection by pDCs.

140 ew assays will permit the rapid detection of HAV RNA and discrimination among subgenotypes IA, IB, an

141 To define determinants of HAV growth, we introduced a blasticidin (Bsd) resistance

142 for the identification and discrimination of HAV subgenotypes IA, IB, and IIIA and a singleplex rRT-P

143 seroresponses after completing two doses of HAV vaccination during a recent outbreak of acute hepati

144 ve achieved seroresponses after two doses of HAV vaccination remain unclear.

145 IV-infected MSM received either two doses of HAV vaccine (1,440 enzyme-linked immunosorbent assay uni

146 ogic response rate to three and two doses of HAV vaccine was similar in HIV-infected MSM, which was l

147 nd HIV-uninfected MSM receiving two doses of HAV vaccine.

148 -infected adults who had received 2 doses of HAV vaccine.

149 We studied the effects of HAV interaction with HAVCR1 on human T cells using bindi

150 ew insights into the origin and evolution of HAV and a model system with which to explore the pathoge

151 In conclusion, the frequency of HAV patients enrolling in the ALFSG and being listed for

152 factors required for the efficient growth of HAV in cell culture.

153 During 1999-2011, the incidence of HAV infection declined from 6.0 cases/100 000 to 0.4 cas

154 ged >/=80 years had the highest incidence of HAV infection in 2011 (0.8 cases/100 000).

155 th data to assess trends in the incidence of HAV infection, HAV-related hospitalization, and HAV-rela

156 The incidence of HAV is low, and the aim of this study was to determine t

157 In contrast to exo-HAV, infectivity of HAV particles is pH-independent and requires HAVCR1 or a

158 We investigated whether the interaction of HAV with its cellular receptor 1 (HAVCR1), a T-cell co-s

159 (s) in 3D(pol) that controls the kinetics of HAV growth.

160 describe a novel immune evasion mechanism of HAV.

161 whereas positive seroresponse at 6 months of HAV vaccination and higher CD4 lymphocyte counts at vacc

162 enhanced significantly the neutralization of HAV by HAVCR1/TIM1 Fc.

163 with concomitant increases in the numbers of HAV outbreaks.

164 interval [CI], 1.5-7.9) times higher odds of HAV infection, 2.5 (95% CI, 1.7-3.9) times higher odds o

165 t 3.3 (95% CI: 1.5-7.9) times higher odds of HAV infection, 2.5 (95% CI: 1.7-3.9) times higher odds o

166 is provide novel insight into the origins of HAV and highlight the utility of analyzing animal reserv

167 mens collected during unrelated outbreaks of HAV in California and Michigan compared to a nested RT-P

168 llow better insight into the pathogenesis of HAV and the development of attenuated vaccines.

169 em with which to explore the pathogenesis of HAV infection.

170 Predictors of HAV susceptibility were age group 30-49 years, non-Hispa

171 Prevalences of HAV susceptibility and nonvaccination to HepA, respectiv

172 The enigmatic properties of HAV may reflect its position as a link between 'modern'

173 In addition, the proportion of HAV cases enrolled in the ALFSG significantly decreased

174 ng comparative studies on RNA replication of HAV and HCV in a homogenous cellular background with com

175 lines with subgenomic reporter replicons of HAV as well as of different HCV genotypes, we found that

176 surveillance of an intrahepatic reservoir of HAV genomes that decays slowly.

177 d to be associated with an increased risk of HAV infection: TGFB1 rs1800469 (adjusted odds ratio [OR]

178 study was to determine the mortality risk of HAV superinfection and the consequences of routine vacci

179 To determine the mortality risk of HAV superinfection, a meta-analysis including studies re

180 the 5' end of the 3D(pol)-coding sequence of HAV, consistent with noncoding constraints imposed by an

181 ole for CD4(+) T cells in the termination of HAV infection and, possibly, surveillance of an intrahep

182 n usage bias is also consistent with that of HAV.

183 d lower CD4 lymphocyte counts at the time of HAV vaccination were associated with early seroreversion

184 ence, predictors, and age-adjusted trends of HAV susceptibility by sociodemographic characteristics.

185 me lumen, but not the endosomal uncoating of HAV particles contained in the exosomes, is mainly respo

186 obe and tested on complementary ssDNA and on HAV cDNA.

187 ed to receive vaccinations with either TT or HAV vaccines during the first 6 months of HAART.

188 med Huh7-A-I cells, did not contain virus or HAV antigens and were sensitive to blasticidin.

189 ith hepatitis symptoms documented persistent HAV circulation in the communities studied.

190 insect viruses and mammalian picornaviruses, HAV is enigmatic in its origins.

191 structure-based phylogenetic analysis places HAV between typical picornaviruses and the insect viruse

192 Although vaccine-preventable, HAV-related hospitalizations increased greatly, mostly a

193 didate genes and serologic evidence of prior HAV infection using a population-based, cross-sectional

194 al that, while membrane envelopment protects HAV against neutralizing antibody, it also facilitates a

195 low titer, although the group that received HAV vaccine after receiving TT vaccine performed somewha

196 Here we demonstrate that eIF4E regulates HAV IRES-mediated translation by two distinct mechanisms

197 ely three-fourths of US-born adults remained HAV susceptible.

198 We report HAV antibody concentrations 17 years after childhood imm

199 These data challenge the use of routine HAV vaccination in HCV-infected persons and its incorpor

200 sy-to- use and low cost method for screening HAV in contaminated food and water.

201 ficiently, thereby protecting against severe HAV-induced disease, but which may predispose toward inf

202 ell culture is a major roadblock to studying HAV pathogenesis and producing live vaccines that are no

203 3D(pol), ablated replication of a subgenomic HAV replicon in transfected human hepatoma cells.

204 Despite the UTV success, HAV circulation in the Israeli population continues, app

205 es, we found that Huh7-Lunet cells supported HAV- and HCV-RNA replication with similar efficiency and

206 Surprisingly, HAV-infected animals exhibited very limited induction of

207 a comparison, nRT-PCR quantified the target HAV cDNA with a limit of detection of 6.4fg/microL.

208 We found that HAV-induced severe liver disease was associated with a 6

209 Collectively, these findings indicate that HAV is far stealthier than HCV early in the course of ac

210 Here we show that HAV released from cells is cloaked in host-derived membr

211 Furthermore, these results suggest that HAV infection has driven the natural selection of shorte

212 The HAV patients listed for transplantation by UNOS were als

213 HAVCR1 (157insMTTTVP), the gene encoding the HAV receptor.

214 imilar variables were related to meeting the HAV QM.

215 abbreviated 45-nt stem-loop) upstream of the HAV coding sequence in the replicon.

216 the blasticidin-resistant Huh7 cells of the HAV infection.

217 rcentages > or = 20% responded better to the HAV vaccine if they had undetectable HIV RNA.

218 Despite this, HAV RNA persisted in the liver for months, remaining pre

219 frequency) of seropositivity for antibody to HAV was 958 (24.9%), 802 (39.2%), and 1540 (71.5%), resp

220 CMI to HAV was virtually absent.

221 The similarity of E25 to HAV may obscure accurate diagnosis in some cases of hepa

222 an estimated 60% of children were exposed to HAV encounters during follow-up.

223 at it is most closely related genetically to HAV.

224 eiving vaccination or documented immunity to HAV and HBV in patients with chronic HCV.

225 with 1.43% of the cohort immunoconverting to HAV.

226 susceptibility factor shown to predispose to HAV-induced acute liver failure.

227 Serologic responses to HAV were infrequent and of low titer, although the group

228 Lower and delayed seroresponses to HAV vaccination, a higher weight, and HIV viremia and lo

229 morphologically and structurally similar to HAV.

230 pear to be associated with susceptibility to HAV infection among Mexican Americans.

231 iously uninfected persons are susceptible to HAV infection, yet the susceptibility in the US populati

232 timated HAV susceptibility prevalence (total HAV antibody negative) among persons aged >=2 years.

233 nd hepatocellular injury were studied in two HAV-infected chimpanzees.

234 hage depletion on herpes simplex virus type (HAV)-1 replication in the eye and on the establishment o

235 tive children received one dose of virosomal HAV vaccine in 2005, followed by yearly serological and

236 endemic settings, a single dose of virosomal HAV vaccine is sufficient to activate immune memory and

237 Herein, we show that hepatitis A virus (HAV) 3C protease (3Cpro) cleaves NEMO at the Q304 residu

238 des long-term immunity to hepatitis A virus (HAV) among the general population, but there are no such

239 Hepatitis A virus (HAV) and hepatitis C virus (HCV) are two positive-strand

240 f FVH upon infection with hepatitis A virus (HAV) at age 11 yr and who was homozygous for a private 4

241 nd sensitive detection of hepatitis A virus (HAV) in food and water are of particular interest in man

242 iver failure (ALF) due to hepatitis A virus (HAV) infection is an uncommon but potentially lethal ill

243 escribe a murine model of hepatitis A virus (HAV) infection that recapitulates critical features of t

244 Hepatitis A virus (HAV) infection typically resolves within 4-7 wk but symp

245 reduced the incidence of hepatitis A virus (HAV) infection, but new infections continue to occur.

246 has broad similarities to hepatitis A virus (HAV) infection, with most cases being subclinical.

247 Remarkably, the hepatitis A virus (HAV) IRES requires eIF4E for its translation, but no mec

248 Hepatitis A virus (HAV) is a common infection that is transmitted through t

249 Hepatitis A virus (HAV) is a hepatotropic picornavirus that causes acute li

250 Hepatitis A virus (HAV) is an ancient and ubiquitous human pathogen recover

251 Hepatitis A virus (HAV) is an hepatotropic human picornavirus that is assoc

252 ike other picornaviruses, hepatitis A virus (HAV) is cloaked in host membranes when released from cel

253 The current Hepatitis A virus (HAV) molecular epidemiology in Israel was studied 13-14y

254 Coinfection with hepatitis A virus (HAV) or hepatitis B virus (HBV) in patients with chronic

255 Hepatitis A virus (HAV) remains enigmatic, despite 1.4 million cases worldw

256 ular diagnostic tools for hepatitis A virus (HAV) RNA detection, subgenotype identification, and sequ

257 Hepatitis A virus (HAV) superinfection in persons with hepatitis C virus (H

258 However, hepatitis A virus (HAV) temporarily inhibits Treg-cell functions.

259 ssness and infection with hepatitis A virus (HAV) using a test-negative study design comparing patien

260 sponse) and durability of hepatitis A virus (HAV) vaccination are reduced among human immunodeficienc

261 and Prevention recommends hepatitis A virus (HAV) vaccination for all children at age 1 year and for

262 Universal 2-dose hepatitis A virus (HAV) vaccination of toddlers effectively controls hepati

263 ng two and three doses of hepatitis A virus (HAV) vaccine and HIV-uninfected MSM receiving two doses

264 Among these, hepatitis A virus (HAV), a common cause of acute hepatitis in humans, is un

265 Here, we show that hepatitis A virus (HAV), a hepatotropic picornavirus, ablates type 1 IFN re

266 RNA viruses that includes hepatitis A virus (HAV), an ancient human pathogen that remains a common ca

267 Hepatitis A virus (HAV), an atypical member of the Picornaviridae, grows po

268 s were vaccinated against hepatitis A virus (HAV), and the increase of antibody titres was monitored

269 loped' viruses, including hepatitis A virus (HAV), are released non-lytically from infected cells as

270 ed for antibody titers to hepatitis A virus (HAV), measles virus (MeV), and cytomegalovirus (CMV).

271 During infection with the hepatitis A virus (HAV), most patients develop mild or asymptomatic disease

272 Human wild-type (wt) hepatitis A virus (HAV), the causative agent of acute hepatitis, barely gro

273 ture with cre function in hepatitis A virus (HAV), the type species of this genus, by phylogenetic an

274 dies were consistent with hepatitis A virus (HAV), with prozone phenomenon.

275 recommendations in 2006, hepatitis A virus (HAV)-associated outbreaks have increased in the United S

276 delivery from exosomes of hepatitis A virus (HAV)-infected cells (exo-HAV) by clathrin-mediated endoc

277 and resultant immunity to hepatitis A virus (HAV).

278 e picornaviruses, notably hepatitis A virus (HAV; genus Hepatovirus) and some members of the Enterovi

279 ith and without hepatitis A, B, and C virus (HAV, HBV, and HCV) and relative risks for the most frequ

280 l antigen and neoantigen (hepatitis A virus [HAV] vaccine) after 3 vaccinations.

281 unity to vaccine-preventable infections were HAV (31.8%), HBV (63.8%), measles (1.4%), mumps (6.6%),

282 When HAV and HBV groups were compared directly, 34 differenti

283 The mechanism by which HAV is cleared in the absence of Treg-cell function coul

284 While HAV-related mortality declined, the mean age at death am

285 n 2010, there were 18 473 (0.7%) deaths with HAV, HBV, and HCV listed among causes of death, dispropo

286 , the mean age at death among decedents with HAV infection increased from 48.0 years in 1999 to 76.2

287 verse consequences if they are infected with HAV.

288 PEH were at higher risk for infection with HAV and higher risk for severe hepatitis A disease outco

289 PEH were at higher risk of infection with HAV and of severe hepatitis A disease outcomes compared

290 ut causing opposing infection outcomes, with HAV always being cleared and HCV establishing persistenc

291 were analyzed in sera from 14 patients with HAV infection using bead arrays.

292 ith a poor prognosis among ALF patients with HAV infection.

293 ty by examining 30 Argentinean patients with HAV-induced acute liver failure in a case-control, cross

294 e more permissive than parental cells for wt HAV infection, including a natural isolate from a human

295 ws the genetically stable growth of human wt HAV.

296 ll lines with in vitro RNA transcripts of wt HAV containing the blasticidin resistance gene.

297 This genetic instability of wt HAV in cell culture is a major roadblock to studying HAV

298 ble of supporting the efficient growth of wt HAV, we transfected different cell lines with in vitro R

299 The cell lines susceptible to wt HAV growth may also be used to detect and isolate infect

300 Among US-born adults aged >=20 years, HAV susceptibility prevalence was 74.1% (95% confidence