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 ere identified in the plasma of at least one infected animal.

5 ed by using histopathology images from these infected animals.

6 in IECs and increased the survival rates of infected animals.

7 his hypothesis remained untested in latently infected animals.

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

9 duces lymphomas in approximately half of the infected animals.

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

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

12 ainment relies on the control and culling of infected animals.

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

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

15 the innate and adaptive immune responses in infected animals.

16 ts a neutralizing antibody response in virus-infected animals.

17 roteins react only marginally with sera from infected animals.

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

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

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

21 ched specifically against sera from multiple infected animals.

22 erson and objects contaminated with virus or infected animals.

23 the innate and adaptive immune responses of infected animals.

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

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

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

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

28 ty, was significantly reduced in chronically infected animals.

29 so significantly reduced on eosinophils from infected animals.

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

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

32 umonia was observed in vaccinated SARS-CoV-2-infected animals.

33 8(+) and CD163(+) macrophages in DRGs of SIV-infected animals.

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

35 uses did not replicate to high titers in all infected animals.

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

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

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

39 host antibody response were observed in all infected animals.

40 duced pathological changes in the spleens of infected animals.

41 ter viral challenge in vaccinated SARS-CoV-2-infected animals.

42 ponsiveness of macrophages isolated from SIV-infected animals.

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

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

45 uals and those with occupational exposure to infected animals.

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

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

48 aminated with leptospire-containing urine of infected animals.

49 ificantly higher deaths in anthrose-negative infected animals.

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

51 sic apoptotic signaling within the brains of infected animals.

52 icroglia in response to cerebral ischemia in infected animals.

53 ntravenous inoculation of the same strain in infected animals.

54 y reduce virus transmission from vaccinated, infected animals.

55 cells could be expanded upon vaccination of infected animals.

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

57 HIV-45G-infected animals, but not in HIV-WT-infected animals.

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

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

60 the impact of antibodies on pathogenesis in infected animals.

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

62 ciated viremia and mitigates pathogenesis in infected animals.

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

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

65 significantly increased in target tissues of infected animals.

66 ignificantly different between protected and infected animals.

67 presumably contributes to viral clearance in infected animals.

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

69 he polarized clinical outcomes noted for the infected animals.

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

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

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

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

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

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

76 assays that are biased towards more heavily infected animals.

77 loss and gingival IL-17 expression over sham-infected animals.

78 l shedding and mortality in the icPEDV-EnUmt-infected animals.

79 ity and increased morbidity and mortality of infected animals.

80 after long cohabitation periods with scrapie-infected animals.

81 has previously been observed in chronically infected animals.

82 benefit or decrease of disease signs in EBOV-infected animals.

83 in the lip, trigeminal ganglia, and brain of infected animals.

84 revent infection and decrease viral loads in infected animals.

85 ible biomarkers may be useful in identifying infected animals.

86 V-infected cells as well as to treat already infected animals.

87 e, demonstrating that this process occurs in infected animals.

88 ed cattle compared to those from nonlethally infected animals.

89 the higher synaptosome depolarization in SIV-infected animals.

90 ia and splenic retention of damaged cells in infected animals.

91 not previously been applied in mycobacteria-infected animals.

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

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

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

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

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

97 not detected, even among three persistently infected animals.

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

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

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

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

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

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

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

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

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

107 Importantly, Fer-1-treated infected animals also exhibited marked reductions in bac

108 Schistosome-infected animals also had significantly lower parasite b

109 DeltaGY-infected animals also showed no infection of macrophages

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

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

112 similar to that in sera from wild-type virus-infected animals and dependent in part on PC-specific an

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 these predicted RNA products in samples from infected animals and humans have produced positive resul

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

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

119 d levels of norepinephrine (NE) in brains of infected animals and in infected human and rat neural ce

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

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

122 ssue and respiratory samples from known MTBC-infected animals and MTBC DNA was detected in 92% of sam

123 ive, with unclear pathogenicity in naturally infected animals and only one experimental study demonst

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

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

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

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

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

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

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

131 Previously infected animals and wP-vaccinated animals possess stron

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

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

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

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

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

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

138 w that the airborne particulates produced by infected animals are mainly non-respiratory in origin.

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

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

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

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

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

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

145 re observed between lethally and nonlethally infected animals at 12 dpi.

146 me in sterile animals was similar to that in infected animals at day 1; however, by day 5 postinfecti

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

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

149 e UK is carried out by test and slaughter of infected animals, based primarily on the tuberculin skin

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

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

152 elated with higher plasma viremia in HIV-45G-infected animals, but not in HIV-WT-infected animals.

153 s were found in the spleens of CO92 Deltapgm-infected animals by 24 h postinfection and in the livers

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

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

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

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

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

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

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

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

162 creased in allergen-sensitized, M pneumoniae-infected animals compared with control animals, but OVA-

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

164 pulation size (cell death) in the DRG of SIV-infected animals compared with uninfected animals.

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

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

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

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

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

170 In chronically infected animals, CPT31 monotherapy rapidly reduced vira

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

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

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

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

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

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

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

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

179 Neurologic defects occasionally detected in infected animals (e.g., defective whisker touch and blin

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

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

182 These findings show that infected animals exhibit fundamentally different reprodu

183 a NK cells in mucosal tissues of chronically infected animals exhibited impaired cytokine production

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

185 r directly or as a result of the movement of infected animals from southeast England before the first

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

187 etics of the viral load decline (DeltaVL) in infected animals given a wild-type (WT) anti-HIV-1 immun

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

189 All ASFV-G-DeltaI177L-infected animals had low viremia titers, showed no virus

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

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

192 Blastocystis-infected animals had non-inflammatory CHS with increased

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

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

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

196 The rapid death of infected animals, however, appears to preclude the clona

197 ed that compared to sera from experimentally infected animals, immunizations enhanced humoral immunit

198 transmission of the virus from persistently infected animals.IMPORTANCE Persistent viral infections

199 dly and contagious herpesvirus that can kill infected animals in less than 4 weeks.

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

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

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

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

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

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

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

207 in the tonsil of experimentally or naturally infected animals long after resolution of the clinical d

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

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

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

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

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

213 In chronically SIV-infected animals, NKp44(+) ILCs negatively correlated wi

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

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

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

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

218 In contrast, sera from PC-negative virus-infected animals poorly neutralized virus on non-fibrobl

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

220 Strikingly, monocytes from lethally infected animals produced significant amounts of IL-10 m

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

222 ficantly lower in uninfected animals and SIV-infected animals receiving ART.

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

224 primary viral growth rate was similar in all infected animals regardless of the inoculum size.

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

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

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

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

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

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

231 RNA has been detected in lymphoid tissues of infected animals several weeks following resolution of t

232 Infected animals show very limited acute morbidity and m

233 SIV-infected animals showed decreased diversity of gut micro

234 Although all infected animals showed evidence of advanced disease inc

235 While CRF02_AG-infected animals showed higher viremia, subtype-B-infect

236 ted animals showed higher viremia, subtype-B-infected animals showed significantly more weight loss,

237 ients with severe disease and experimentally infected animals showed that robust viral replication an

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

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

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

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

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

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

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

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

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

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

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

249 ously derived a viral swarm (in the blood of infected animals) that can cause AIDS in this new host.

250 Upon the bite of an infected animal, the development of clinical disease can

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

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

253 RNAs from infected animal tissues or from laboratory strains have

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

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

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

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

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

259 RPV LA did delay WT HIV-1 dissemination in infected animals until genital and plasma RPV concentrat

260 G) and the brain stem from the same latently infected animal using direct assays of equivalent sensit

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

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

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

264 In the infected animals, we detected increased endothelial leve

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

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

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

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

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

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

271 78.8% (26/33) of the BAL fluid samples from infected animals were in agreement.

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

273 Synaptosomes from SIV-infected animals were physiologically tested using a syn

274 tized, M pneumoniae-infected or S pneumoniae-infected animals were reduced compared with those in uni

275 The infected animals were then given water with ampicillin (

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

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

278 11 virus replicated only in the lungs of the infected animals, whereas the NA-T342A and NA-F144C/T342

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

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

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

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

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

284 pe, we investigated how and why treatment of infected animals with anti-TcdA dramatically increased d

285 infusing simian immunodeficiency virus (SIV)-infected animals with CD8 T cells engineered to express

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

287 3-5 weeks in some long-term chronically SHIV-infected animals with low CD4(+) T-cell levels.

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

289 Therapeutic treatment of infected animals with MK-4482/EIDD-2801 twice a day sign

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

291 All six infected animals with persistent circulating viremia pre

292 n uninfected strain and found that mating of infected animals with uninfected animals resulted in inf

293 In chronically infected animals with viremia initially controlled by co

294 lity and arousal were altered in chronically infected animals, with a high correlation between DBH ex

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

296 SVA establishes persistent infection in SVA-infected animals, with the tonsil serving as one of the

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 d specific test for ante-mortem detection of infected animals would be of great value.

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