ライフサイエンスコーパス: infected animal

1 lly increased in the blood serum of M. bovis-infected animals).

2 lly increased in the blood serum of M. bovis-infected animals).

3 caspase-1-dependent immune responses in the infected animal.

4 ansfusion of whole blood from a persistently infected animal.

5 orkers that come into close contact with HEV-infected animals.

6 8(+) and CD163(+) macrophages in DRGs of SIV-infected animals.

7 nalog, to reduce viral DNA production in HBV-infected animals.

8 e upper respiratory tract of influenza virus-infected animals.

9 gulated 3-fold on LN NK cells in chronically infected animals.

10 in the full extent of the disease in virally infected animals.

11 host antibody response were observed in all infected animals.

12 lenge with H1N1 and prevented weight loss in infected animals.

13 duced pathological changes in the spleens of infected animals.

14 ponsiveness of macrophages isolated from SIV-infected animals.

15 n, and kidneys with concomitant morbidity in infected animals.

16 ranuloma formation in lungs from M.tb DK9897 infected animals.

17 and accumulating in the lesions of M. bovis-infected animals.

18 uals and those with occupational exposure to infected animals.

19 acrophage infiltration in the lungs of HIV-1-infected animals.

20 nited States in 2003 from the importation of infected animals.

21 ing 11 known and 13 new, were detected in 65 infected animals.

22 aminated with leptospire-containing urine of infected animals.

23 nsasii- and M. avium subsp. paratuberculosis-infected animals.

24 sic apoptotic signaling within the brains of infected animals.

25 icroglia in response to cerebral ischemia in infected animals.

26 ntravenous inoculation of the same strain in infected animals.

27 y reduce virus transmission from vaccinated, infected animals.

28 cells could be expanded upon vaccination of infected animals.

29 not detected, even among three persistently infected animals.

30 ell function and reduced viral loads in LCMV-infected animals.

31 lower set-point viremia and 100% survival of infected animals.

32 hyzoites and in mature bradyzoites from 30-d infected animals.

33 the impact of antibodies on pathogenesis in infected animals.

34 ation in the lungs and enhancing survival of infected animals.

35 ciated viremia and mitigates pathogenesis in infected animals.

36 d specific test for ante-mortem detection of infected animals.

37 first time that the pathway is activated in infected animals.

38 the organs, in comparison to M. tuberculosis-infected animals.

39 significantly increased in target tissues of infected animals.

40 ignificantly different between protected and infected animals.

41 v X5-transduced cells were selected in HIV-1-infected animals.

42 presumably contributes to viral clearance in infected animals.

43 long-term potentiation in the hippocampus of infected animals.

44 he polarized clinical outcomes noted for the infected animals.

45 ical changes similar to those observed in WT-infected animals.

46 d in lymphoid tissues and in the meninges of infected animals.

47 t failed to limit the colonization of MAP in infected animals.

48 -regulated viral replication in the liver of infected animals.

49 thionine (Met), shows decreased viability in infected animals.

50 nfection and no cost-effective treatment for infected animals.

51 increases the bacterial load in the blood of infected animals.

52 ilar to that observed in the brains of prion-infected animals.

53 ce imaging revealed transient disease in all infected animals.

54 d CCL5 was also significantly lower in AZ(2)-infected animals.

55 s clone 13- and reduced viral load in DOCILE-infected animals.

56 l nervous system in preclinical and clinical infected animals.

57 n and prevention of mortality in chronically infected animals.

58 reductions in cortical N-acetyl aspartate in infected animals.

59 asteurized dairy products or by contact with infected animals.

60 he lungs and draining lymph nodes of virally infected animals.

61 thway to the heightened susceptibility of co-infected animals.

62 his hypothesis remained untested in latently infected animals.

63 es, were distinctly induced in the SIVmac239-infected animals.

64 loped tumors more frequently than Z-KO virus-infected animals.

65 ed in the livers as well as in the plasma of infected animals.

66 DeltaqseC strain was similar to that in sham-infected animals.

67 e detected in feces and in gut segments from infected animals.

68 inguishable from that of marker rescue virus-infected animals.

69 s established long-term viral latency in all infected animals.

70 of bone resorption similar to those of sham-infected animals.

71 hoid tissues, and gastrointestinal tracts of infected animals.

72 e bacterial burden and prolonged survival of infected animals.

73 ignificantly down-regulated on NK cells from infected animals.

74 duces lymphomas in approximately half of the infected animals.

75 not previously been applied in mycobacteria-infected animals.

76 -fold in simian immunodeficiency virus (SIV)-infected animals.

77 AGMs was significantly more severe than NiVM-infected animals.

78 ompared to that with equivalent IgG from pre-infected animals.

79 d animals, compared with EBOV-C07- or EBOV-K-infected animals.

80 the innate and adaptive immune responses in infected animals.

81 med in HEV gt1, but not in Hepatitis B Virus infected animals.

82 roteins react only marginally with sera from infected animals.

83 ls were depleted from blood in the SIVmac239-infected animals.

84 ion are key to virus spread and virulence in infected animals.

85 g to CPSF6 emerged in three out of four A77V-infected animals.

86 to a second antigen is also hampered in BTV-infected animals.

87 ched specifically against sera from multiple infected animals.

88 erson and objects contaminated with virus or infected animals.

89 the innate and adaptive immune responses of infected animals.

90 vered from the olfactory bulbs and brains of infected animals.

91 d chronic setpoint viremia in 13 of 17 (76%) infected animals.

92 ding in LUJV infection than that in the LASV-infected animals.

93 o significantly enhanced disease in L. major-infected animals.

94 ty, was significantly reduced in chronically infected animals.

95 so significantly reduced on eosinophils from infected animals.

96 vities and consumption of venison from prion-infected animals.

97 Half of the vaccinated, infected animals (7/13) promptly controlled virus replic

98 CD8(+) T cell pool was decreased in latently infected animals, abrogating the boosting effect normall

99 However, the movement of infected animals across the region likely contributes to

100 reduction in lung M. tuberculosis burden of infected animals after prophylactic vaccination.

101 In acutely infected animals, Ag stimulation leads to upregulation o

102 EBOV replication and protected 100% of EBOV-infected animals against lethal disease, ameliorating cl

103 le expression of the fluorescent proteins in infected animals allows their detection by different typ

104 One SHIV(AD8)-infected animal also developed NAbs against clades A and

105 VN/1203-infected animals also exhibited an earlier and more pote

106 The P. inui-infected animals also had correspondingly lower CD4(+) c

107 Schistosome-infected animals also had significantly lower parasite b

108 DeltaGY-infected animals also showed no infection of macrophages

109 increased with longer contact times with an infected animal and is possible without direct contact b

110 he mean time of death was 6 days for VN/1203-infected animals and 9 days for mice infected with the 1

111 loads following a challenge in elderly MCMV-infected animals and also reduced the differentiation of

112 s are observed in herpes simplex virus (HSV)-infected animals and cells.

113 t RT-QuIC is useful for both identifying CWD-infected animals and facilitating epidemiological studie

114 ed the B-cell and plasma-cell populations in infected animals and found that B cells are present prim

115 tigens by antibodies present in the serum of infected animals and humans and by monoclonal antibodies

116 Activation of p38-MK2 in infected animals and humans suggests that this pathway i

117 gy for stimulation of T cells in chronically infected animals and humans to achieve the clearance of

118 ells in house dust mite-allergic or helminth-infected animals and in vitro Th2 cells, which are disti

119 Direct contact with infected animals and indirect contact with infectious pr

120 e, can be recovered from different organs of infected animals and patients, indicating that the spiro

121 lays a crucial role in the identification of infected animals and several tests have been developed.

122 and associated oxidative stress in H. pylori-infected animals and that these conditions, along with t

123 e absence of vesicles (gross lesions) in SVA-infected animals and the variability of RT-qPCR results

124 survival of Y. pestis in the bloodstreams of infected animals and thus might be regarded as a promisi

125 her than that observed in WT M. tuberculosis-infected animals and was associated with enhanced freque

126 also detectable in foreskin of SIV- and SHIV-infected animals and were at least comparable in magnitu

127 Previously infected animals and wP-vaccinated animals possess stron

128 d study animals, plasma from chronically SIV-infected animals, and a panel of SIV-specific monoclonal

129 ion in lungs, increases the survival time of infected animals, and decreases expression of key inflam

130 ection was delayed and attenuated in the HCV-infected animals, and the number of HBV-infected hepatoc

131 oxins present in the sera and body fluids of infected animals, and toxemia is significantly correlate

132 However, some infected animals are able to develop efficient virus-spe

133 udies with this model have demonstrated that infected animals are able to transmit the virus to naive

134 and immunologic signs, whereas the remaining infected animals are clinically asymptomatic.

135 it is unlikely that significantly more truly infected animals are removed.

136 ghlighting immunopathology as a death cause, infected animals are rescued by the neutralization of IL

137 Splenic infected DCs recovered from chronic infected animals are similarly capable to polarize ex vi

138 alley fever, often initiated by contact with infected animals, are characterized by a febrile disease

139 t provide net benefits that were specific to infected animals, as cooler temperatures increased lifet

140 ation of NK cells obtained from lungs of AIV-infected animals, as judged by the lower frequency of CD

141 ected with M. gallisepticum Rlow and 20 mock-infected animals at days 1, 3, 5, and 7 postinoculation,

142 protein specific CD8 T cells in the lungs of infected animals at early time points after infection.

143 AVV and treated with NP siRNA-LNP, with MARV-infected animals beginning treatment four or five days a

144 lter immune cell recruitment to the lungs of infected animals but was associated with an elevation of

145 Instead, we find that cold-seeking benefits infected animals by increasing their late-age reproducti

146 sinia spp. undermine the immune responses of infected animals by translocating Yops directly into hos

147 Thus, natural prions obtained from infected animals can be compared with model systems such

148 of blood collected from asymptomatic scrapie infected animals can transmit the disease.

149 However, in SIV-infected animals, CD4+ T-cell functionality decreased af

150 , can trigger innate immunity in bacterially infected animal cells and is involved in developmental c

151 polyadenylate mRNAs within the cytoplasm of infected animal cells.

152 gnostic screening test for quickly detecting infected animals chute-side, pen-side, or even remotely

153 The appearance of fever in infected animals coincided with the detection of serum v

154 tly stronger induction of CD25+ B cells from infected animals compared to L3P.

155 nificantly upregulated in the SC of reovirus-infected animals compared to mock-infected controls.

156 In an analysis of all infected animals compared to uninfected animals (indepen

157 ficantly reduced Pneumocystis lung burden in infected animals compared with control serum.

158 remia level was elevated 10-fold in EBOV-C05-infected animals, compared with EBOV-C07- or EBOV-K-infe

159 ammatory cells were found in sections of all infected animals, compared with minimal changes in secti

160 cific CD4(+) and CD8(+) cells in the P. inui-infected animals, compared with uninfected animals.

161 e how early SIV diversification in vaginally infected animals compares with HIV-1 in humans.

162 body-based assays is important for detecting infected animals, confirming previous virus exposure, an

163 elated with markers of liver damage, and SIV-infected animals consistently had evidence of hepatitis

164 that these M. avium subsp. paratuberculosis-infected animals could have been infected as adults by c

165 t infection, but were not able to prove that infected animals could transmit the virus exclusively vi

166 In MARV-infected animals, day-4 treatment initiation resulted in

167 ame proportions (2/6) of the WT and SL virus-infected animals developed B-cell lymphomas by day 60 po

168 The mutant-infected animals developed balanced TH1- and TH2-based i

169 (SHIV(AD8-EO)) revealed that eight of eight infected animals developed cross-reactive neutralizing a

170 majority of analyzed organs, and sublethally infected animals developed virus-specific neutralizing a

171 Interestingly, the Th2 response in the co-infected animals did not impair the onset and developmen

172 EBOV-C07 died of EVD, whereas 2 of 3 EBOV-K-infected animals died.

173 Micro-CT studies of brains from infected animals displayed gross morphological changes s

174 tabolism as ELISPOT assays demonstrated that infected animals do not have suppressed Ab production.

175 fected habitats, reduces disease levels when infected animals do not migrate successfully, and may le

176 These infected animals do not, however, develop AIDS.

177 s, the virus was detected in nasal washes of infected animals during the first 7 days postinfection.

178 ervations of viral load and dissemination in infected animals, even following clearance of a subletha

179 ligand 2, and CXCL13 and pleocytosis in all infected animals, except dexamethasone-treated animals.

180 These findings show that infected animals exhibit fundamentally different reprodu

181 Surprisingly, HAV-infected animals exhibited very limited induction of typ

182 umococcal superinfection, we found that dual-infected animals experienced rapid weight loss and succu

183 lent strain type 3 SA+ (T3SA+) and monitored infected animals for survival.

184 e simian-human immunodeficiency virus (SHIV)-infected animal from which the env variants were cloned,

185 DeltaespZ mutant-infected animals gained weight steadily over the infecti

186 endotoxin contents between the inocula, CO99-infected animals had a median survival of 3 days with gr

187 Red cells from P. chabaudi/P. berghei-infected animals had increased surface IgG and C3 by flo

188 Consistent with this, infected animals had less neutrophil-specific chemokines

189 moderate DRG pathology, the CD8-depleted SIV-infected animals had moderate to severe DRG damage, with

190 P. chabaudi/P. berghei-infected animals had more intense splenic hematopoiesis,

191 Although all vaccinated and previously infected animals had robust serum antibody responses, we

192 neutralizing antibody response in mucosally infected animals has not been defined.

193 The importation of infected animals has, in the past, spread melioidosis to

194 Ear histology 24 h after challenge showed infected animals have reduced cellular infiltration in t

195 mation for regimen selection in treating SIV-infected animals in models of therapy and virus eradicat

196 LN CD103(+) CD11b(-) CD8(+) DC isolated from infected animals in the generation of an IEL response ag

197 ng all serotypes of FMDV from experimentally infected animals, including the porcinophilic FMDV strai

198 Infected animals initially mount a cell-mediated CD4 T c

199 eal pockets and in one of three persistently infected animals inoculated only in the cervix.

200 A recent importation of MPXV-infected animals into the United States raises the possi

201 n of IDO1/2 and of two downstream enzymes in infected animals is detrimental to the Eimeria growth.

202 a, but that transmission risk from saliva of infected animals is low.

203 espiratory status of mitochondria from prion-infected animals is unknown.

204 Whereas C227-11-infected animals lost weight or gained less weight over

205 LN NK cells from chronically infected animals lysed K562 cells more efficiently than

206 Consequently, management actions targeting infected animals might lead to unnecessary removal of yo

207 azinamide resistance both in vitro and in an infected animal model.

208 nt spores can be recovered from the lungs of infected animals months after the initial spore exposure

209 t microbiome were observed in the jejunum of infected animals on day 5.

210 Compared with SIV-infected animals only given ART, SIV-infected RMs given

211 s were infected with either blood from a BTV-infected animal or from the same virus isolated in cell

212 n conditions that favour direct contact with infected animals or animal products.

213 in the foregut of fleas that feed on plague-infected animals or humans.

214 d liver microvascular permeability vs. KIM6+-infected animals (p<.05).

215 Positron emission tomography in live infected animals, postmortem pimonidazole immunohistoche

216 In M. bovis-infected animals, PPDB specific IL-22 and IL-17A respons

217 C57BL/6 infected animals predominantly exhibited mild to moderat

218 ound to infiltrate the brains of chronically infected animals, reaching highest levels at the latest

219 isease or latent infection and that latently infected animals reactivated upon neutralization of TNF.

220 ions of lymph node and spleen in chronically infected animals regardless of epitope specificity.

221 hondrial electron transport proteins in 263K-infected animals relative to that in controls.

222 tudies, but suppressing viral replication in infected animals remains challenging.

223 T cells from vaccinated mice or prepatently infected animals responded primarily with Th1 lymphokine

224 experimentally feline immunodeficiency virus-infected animals resulted in improved motor and memory p

225 inal transplantation of mouse NPCs into JHMV-infected animals resulted in selective colonization of d

226 However, in vivo imaging of infected animals revealed persistently higher levels of

227 l tissues isolated from these M. catarrhalis-infected animals revealed the presence of significant in

228 infection) were compared with untreated SIV-infected animals sacrificed at similar times.

229 Infected animals show very limited acute morbidity and m

230 Although all infected animals showed evidence of advanced disease inc

231 Infected animals showed histological findings consistent

232 V-GA replicates in the livers and spleens of infected animals similarly to SUDV infections in nonhuma

233 t four or five days after infection and RAVV-infected animals starting treatment three or six days af

234 NiVB was uniformly lethal, only 50% of NiVM-infected animals succumbed to infection.

235 epidemiology, and it has been reported that infected animals suffer from an AIDS-like disease in the

236 Sublethally infected animals suffered increased morbidity, delayed r

237 lthough studies of humans and experimentally infected animals suggest that CHIKV infection persists i

238 Data from experimentally infected animals suggest that this target specificity co

239 ved on LN NK cells isolated from chronically infected animals than on those from naive macaques, is i

240 uid from normal animals or from Pneumocystis-infected animals that had been successfully treated for

241 infection by this mucosal route; in the two infected animals that had received 5 mg 2F5 IgG, infecti

242 CR4 coreceptor usage in approximately 50% of infected animals that progressed rapidly to disease.

243 bbasal corneal nerve fiber density among SIV-infected animals that rapidly progressed to AIDS compare

244 Infected animals that received EX-527, a selective SIRT1

245 Seventy-five percent of infected animals that received vehicle alone succumbed t

246 ammatory monocytes in the lung of 1918 virus-infected animals that was sustained throughout infection

247 ced by 67 and 82%, respectively, compared to infected animals that were either treated with vancomyci

248 tantially lowers the survival probability of infected animals, then populations that spend comparativ

249 of Cal PA-XFS was attenuated in the lungs of infected animals, this mutant induced a stronger humoral

250 lopment of neutralizing antibodies in SIVmac-infected animals, thus raising questions concerning the

251 itoes), and, importantly, close contact with infected animal tissues and fluids or aborted fetal mate

252 mice and in evoking cytokines/chemokines in infected animal tissues.

253 titers and was also able to transmit from an infected animal to sentinel animals by contact.

254 eased IL-22 and IL-17A responses in M. bovis-infected animals to the level of protein production.

255 In SIV-infected animals, total CaMKII expression in the hippoca

256 ts illustrate heterologous immunity of virus-infected animals toward allergens.

257 ents, administration of bNAbs to chronically infected animals transiently suppresses virus replicatio

258 Furthermore, infected animals treated with 10 mug/kg 15d-PGJ(2)-NC ha

259 The infected animals treated with AG after the development o

260 RSV-infected animals treated with anti-IL-17 had reduced inf

261 Infected animals treated with the 15d-PGJ(2)-NC presente

262 In contrast, all WT and SL virus-infected animals treated with the OKT3 anti-CD3 antibody

263 Notably, CD56(+) NK cells in SIV-infected animals up-regulated perforin, granzyme B, and

264 regulator of carbohydrate metabolism in the infected animal, via JAK/STAT and insulin signaling in t

265 iant within each inoculum and in plasma from infected animals was determined by using a novel real-ti

266 is of K562 cells by LN NK cells from acutely infected animals was greater than lysis by preinfection

267 The Th2 response in infected animals was shown to be induced by schistosome

268 read into the subarachnoid space in rCDV(SH)-infected animals was triggered by infection of vascular

269 In the infected animals, we detected increased endothelial leve

270 ts of the cellular immune response in STLV-1-infected animals, we used intracellular cytokine stainin

271 nsfer, mice receiving cells from chronically infected animals were able to contain infection more rap

272 Retinal cells from Toxoplasma-infected animals were able to suppress T-cell activation

273 hyposthesis, lymphocytes from vaccinated or infected animals were compared for their ability to prod

274 fluid and central nervous system tissues of infected animals were culture positive for B. burgdorfer

275 The colder temperatures preferred by infected animals were detrimental to the pathogen becaus

276 The higher viral loads in the P. inui-infected animals were durable and were observed at all s

277 in the duration of contact of naive gps with infected animals were evaluated for their impact on tran

278 78.8% (26/33) of the BAL fluid samples from infected animals were in agreement.

279 By comparison, previously infected animals were not colonized upon secondary infec

280 d that red cells from P. chabaudi/P. berghei-infected animals were removed at an accelerated rate in

281 bservations are related to aging, as the SIV-infected animals were significantly older than the uninf

282 The infected animals were then given water with ampicillin (

283 n exist as a mixture of strains in naturally infected animals, where they are able to interfere with

284 y from MRV infection and led to lethality in infected animals, whereas B cell-deficient mice showed C

285 of intrahepatic Treg numbers in chronically infected animals, whereas no differences were found in p

286 fected dogs, resulting in the vaccination of infected animals, which may lead to disease in vaccinate

287 ave chronodispersion in nerve roots of a few infected animals; which were absent in dexamethasone-tre

288 impact of treating a hepatitis C virus (HCV)-infected animal with synthetic hairpin-shaped RNAs that

289 Furthermore, treatment of WHV-infected animals with an adenovirus encoding IL-12 faile

290 how that a prophylactic inoculation of prion-infected animals with an anti-prion delays the onset of

291 A subset of the SHIV(AD8)-infected animals with higher viral loads and greater Env

292 3-5 weeks in some long-term chronically SHIV-infected animals with low CD4(+) T-cell levels.

293 Treatment of infected animals with MC-stabilizing drugs or a leukotri

294 sus cytomegalovirus by repeatedly immunizing infected animals with nonfunctional versions of the rhes

295 All six infected animals with persistent circulating viremia pre

296 results in a smaller number of lymphomas in infected animals, with an even more delayed time to tumo

297 alitis (SIVE) compared to uninfected and SIV-infected animals without encephalitis, a trend that was

298 Latency was established in all infected animals without evidence of viral reactivation,

299 J(2)-NC presented lower bone resorption than infected animals without treatment (p < 0.05).

300 Importantly, in mosquito-infected animals ZIKV tissue distribution was limited to