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 antibody testing was performed in 640 subjects (53.6

4 HAV contains no pocket factor and can withstand remarkab

5 HAV grew in MMH-D3 cells transfected with virion RNA but

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

7 HAV infections represent a distinctly different paradigm

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

9 HAV is often transmitted within networks of persons with

10 HAV thus disrupts host signaling by a mechanism that par

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

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

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

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

15 HAV-induced liver injury was associated with interferon-

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

17 HAV-related hospitalizations increased from 7.3% in 1999

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

19 Of 508 HAV-RNA-positive case patients, 449 (88.4%) were intervi

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

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

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

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

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

25 of the unvaccinated patients developed acute HAV infection during follow-up, and 1 of them died of ac

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

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

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

29 sequence analysis of the MMH-D3 cell-adapted HAV revealed that N1237D and D2132G substitutions were p

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

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

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

33 Vaccination of children against HAV should prevent future epidemics.

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

35 blished recommendations to vaccinate against HAV in patients with chronic HCV infection, we found tha

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

37 Although HAV vaccination is recommended for all patients with chr

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

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

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

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

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

43 cleotide sequence relatedness between it and HAV.

44 Having antibodies to both H. pylori and HAV did not add to this negative effect (adjusted OR, 0.

45 Anti-HAV antibody titers were measured at baseline and at 32,

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

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

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

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

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

51 When examined by 5-year birth cohorts, anti-HAV prevalence increased in children born between 1979 a

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

53 adjusted prevalence of antibody to HAV (anti-HAV) was 51% in 1983 and 49% in 1993 (P=.506).

54 at baseline was associated with higher anti-HAV antibody titers after the second vaccine dose.

55 105 children, immunization resulted in anti-HAV levels of 17-572 mIU/mL.

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

57 group randomized according to maternal anti-HAV status.

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

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

60 6 months (50%-75%), and among maternal anti-HAV-positive children in groups 2 and 3 (67%-87%), who i

61 ears regardless of presence of maternal anti-HAV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 nce for attempts to develop live, attenuated HAV vaccines that can be administered orally.

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

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

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

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

84 he 157insMTTTVP insertion polymorphism bound HAV more efficiently.

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

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

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

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

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

90 method based on DNA hybridization to detect HAV.

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

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

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

94 onded during a transient resurgence of fecal HAV shedding.

95 particles, indicating a cell entry block for HAV.

96 ibinin as a potential therapeutic option for HAV infections.

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

98 confidence interval [CI], 0.08-0.82]; OR for HAV, 0.45 [95% CI, 0.23-0.87]).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 ivorous mammals and a rodent origin of human HAV.

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

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

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

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

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

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

121 D1muc-Fc neutralized 10 times more HAV than did D1-Fc.

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

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

124 obin G1 (IgG1), D1-Fc, bound and neutralized HAV inefficiently.

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

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

127 D1 is required for binding of HAV, and a soluble construct containing D1 fused to the

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

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

130 n the 2 survey periods, 43 clinical cases of HAV infection were reported in these villages; all occur

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

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

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

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

135 In both species, 1 oral dose of HAV was equivalent to 10(4.5) intravenous doses.

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

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

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

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

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

141 e virion and may play a role in the entry of HAV into the mouse liver cells.

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

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

144 his study were to determine the frequency of HAV testing and vaccination among patients with chronic

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

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

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

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

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

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

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

152 describe a novel immune evasion mechanism of HAV.

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

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

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

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

157 The prevalence of HAV infection increased with age in both surveys.

158 s that are typically used for propagation of HAV.

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

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

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

162 n mouse cells, we studied the replication of HAV in immortalized and nontransformed MMH-D3 mouse live

163 onitoring the translation and replication of HAV RNA and show that critical mutations that enhance th

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

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

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

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

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

169 owth conditions resulted in the selection of HAV variants that grew efficiently in MMH-D3 cells cultu

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

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

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

173 Treatment of HAV with 100 nM D1muc-Fc resulted in low-level accumulat

174 n sucrose gradients showed that treatment of HAV with 20 to 200 nM D1muc-Fc disrupted the majority of

175 havcr-1 are required to trigger uncoating of HAV, we constructed D1muc-Fc containing D1 and two-third

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

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

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

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

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

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

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

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

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

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

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

187 We report HAV antibody concentrations 17 years after childhood imm

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

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

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

191 The age-specific HAV seroprevalences indicated a low incidence of infecti

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

193 anisms involved, we constructed a subgenomic HAV replicon by replacing most of the P1 capsid-coding s

194 3D(pol), ablated replication of a subgenomic HAV replicon in transfected human hepatoma cells.

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

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

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

198 17 (49.5%) of those tested were susceptible (HAV antibody negative).

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

200 ts with chronic HCV infection, we found that HAV testing and vaccination rates were low in clinical p

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

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

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

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

205 The HAV patients listed for transplantation by UNOS were als

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

207 rin) and cyclic pentapeptides (including the HAV motif) were used to perturb N-cadherin function.

208 imilar variables were related to meeting the HAV QM.

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

210 cleotide segment of the VP1-P2 region of the HAV genome was amplified and sequenced from serum of cas

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

212 94 of the 1,193 patients (7.9%) received the HAV vaccine, including 26.8% of the 317 susceptible pati

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

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

215 erall age-adjusted prevalence of antibody to HAV (anti-HAV) was 51% in 1983 and 49% in 1993 (P=.506).

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

217 CMI to HAV was virtually absent.

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

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

220 at it is most closely related genetically to HAV.

221 the 323 patients who were already immune to HAV, and 1.1% of the 553 subjects who were never tested.

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

223 body marking a past infection or immunity to HAV using an antibody-capture enzyme-linked immunosorben

224 to induce conformational changes leading to HAV uncoating.

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

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

227 morphologically and structurally similar to HAV.

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

229 of growth factors acquired susceptibility to HAV infection.

230 ed by children aged <15 years susceptible to HAV.

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

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

233 nfects African green monkey kidney cells via HAV cellular receptor 1 (havcr-1).

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

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

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

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

238 ka between 2 epidemics of hepatitis A virus (HAV) and after the second epidemic (1988-1990).

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

240 Hepatitis A virus (HAV) has been adapted to grow efficiently in primate and

241 Replication of hepatitis A virus (HAV) in cultured cells is inefficient and difficult to s

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

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

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

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

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

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

248 Hepatitis A virus (HAV) infects African green monkey kidney cells via HAV c

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

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

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

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

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

254 Hepatitis A virus (HAV) is naturally transmitted by the fecal-oral route bu

255 he genetic relatedness of hepatitis A virus (HAV) isolates was determined to identify possible infect

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

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

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

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

260 Hepatitis A virus (HAV) superinfection is associated with a high risk of li

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

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

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

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

265 unogenicity of 2 doses of hepatitis A virus (HAV) vaccine followed by a booster dose in HIV-infected

266 patitis E virus (HEV) and hepatitis A virus (HAV) was compared.

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

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

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

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

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 ects were also tested for hepatitis A virus (HAV).

276 These results pertain to hepatitis A virus (HAV).

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 Although HEV was less stable than was HAV, some HEV would most likely survive the internal tem

282 Of 151 subjects who were HAV seronegative at baseline, 97% seroconverted after 2

283 were higher than those in subjects who were HAV seronegative at baseline, but the responses showed s

284 In the 45 subjects who were HAV seropositive at baseline, responses to 2 and 3 vacci

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

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

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

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

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

290 verse consequences if they are infected with HAV.

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

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

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

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

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

296 ws the genetically stable growth of human wt HAV.

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

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

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

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