ライフサイエンスコーパス: parasite

1 sed on control targets, including vector and parasite.

2 with extensive hemoglobin degradation by the parasite.

3 orous vacuolar membrane (PVM) harbouring the parasite.

4 n EVs secreted by the infective forms of the parasite.

5 maxima, tipping the balance in favor of the parasite.

6 ey effectors of calcium signaling in malaria parasite.

7 speed and transient curvature changes of the parasite.

8 are expressed in the bloodstream form of the parasite.

9 e and IFN-alpha secretion in response to the parasite.

10 ncluding viruses, intracellular bacteria and parasite.

11 for the proliferation and virulence of this parasite.

12 o their activity against multidrug resistant parasites.

13 domains (ApiAP2s) was identified in malaria parasites.

14 ic labile heme levels in intact, blood-stage parasites.

15 epresent an important reservoir for zoonotic parasites.

16 ility and host cell invasion of apicomplexan parasites.

17 ange in insular assemblages of hemosporidian parasites.

18 ause they have failed when applied to animal parasites.

19 the hepatic stage of infection by Plasmodium parasites.

20 exa are single-celled obligate intracellular parasites.

21 tion against bacteriophage (phage) and other parasites.

22 ety of pathogens, from persistent viruses to parasites.

23 low proportion of parasites and asynchronous parasites.

24 he focus of research within the apicomplexan parasites.

25 drug with nanomolar activity against asexual parasites.

26 and invasive stages of both human and rodent parasites.

27 1 (CPH1), which is conserved in apicomplexan parasites.

28 and allows vesicles to be exchanged between parasites.

29 plays key roles in nematodes and many other parasites.

30 egested into host skin alongside Leishmania parasites.

31 's ability to distinguish parasites from non-parasites.

32 Our data demonstrates that Leishmania parasites activate the PERK/eIF2alpha/ATF-4 pathway in c

33 ism that has been linked to recrudescence of parasites after monotherapy with ART and, possibly contr

34 plays a key role in the early control of the parasite and disease severity.

35 lapping timescales and the interplay of host-parasite and host-ecosystem interactions.

36 r understanding of the basic biology of this parasite and how it interacts with its ruminant host.

37 ntrinsic role for autophagy in the T. gondii parasite and its close relatives.

38 which typically display a low proportion of parasites and asynchronous parasites.

39 electrical (impedance) properties of single parasites and demonstrate rapid discrimination based on

40 ite primary outcome was clearance of asexual parasites and fever by day 7, and absence of recrudescen

41 ild animal populations, hosts are at risk of parasites and malnutrition and resource costs of defence

42 This work demonstrates that parasites and non-parasites interact in networks in stat

43 an arrest liver stage development of malaria parasites and speculated that TMP-SMX prophylaxis during

44 multitude of interactions occurring between parasites and the gut microbiota, with a profound impact

45 tion to host organs, phagocytic clearance of parasites, and regulation of immunity.

46 D11b(+) migrating DCs and fewer DCs carrying parasite antigens to the lymph nodes.

47 ment simultaneously enhances exposure to key parasite antigens, accelerating the development of prote

48 Eggs produced by the mature female parasite are responsible for the pathogenesis and transm

49 ver stage of a malaria infection, Plasmodium parasites are targeted by the autophagy machinery of the

50 TEs, generally considered genomic parasites, are the most common components of woody plant

51 onal AP2-G knockdown line and NF54 wild-type parasites at multiple stages of development, we show tha

52 resistant strain of P. falciparum and arrest parasites at the ring phase of the asexual stage and als

53 aviour depends strongly on assumptions about parasite-based mortality rates.

54 independent of the host, and which regulates parasite biology throughout the day.

55 ex europaeus supported significantly greater parasite biomass (also per unit host biomass) than A. pa

56 , and healthy controls (n = 50), we measured parasite biomass, systemic inflammation (interleukin 6 [

57 se tissues, how the immune response controls parasite burden and contributes to tissue damage, and wh

58 pe I IFN treatment increased lesion size and parasite burden, quantitatively reproducing the LRV1-bea

59 osing schistosomiasis in patients with a low parasite burden.

60 to Nippostrongylus brasiliensis, increasing parasite burden.

61 tandem with the recombinant protein reduced parasite burdens by 76% to >99% in comparison to a varie

62 in which a predator consumes a prey and its parasites, but not the number of interactions, improves

63 aria drug targets are expressed in quiescent parasites, but pathways involved in microbial dormancy,

64 (the STOP-CTX arm) were examined for malaria parasites by quantitative reverse transcription polymera

65 al care and advice for these patients as the parasite can be exterminated by eradication measures to

66 These data lead us to propose that any parasite can cause uncomplicated malarial disease and th

67 ction against homologous and heterologous Pf parasites can be achieved with PfSPZ Vaccine.

68 After drug removal, these parasites can resume growth.

69 only RDTs in the presence of PfHRP2-negative parasites caused an increase in prevalence, reduced RDT

70 with concurrently occurring major changes of parasite cell architecture.

71 or CTLA-4 in this precise window accelerated parasite clearance and generated species-transcending im

72 icipants withdrew from the AQ-13 group after parasite clearance and three were lost to follow-up.

73 pression, and phagocytic activity, enhancing parasite clearance by macrophages and neutrophils.

74 The median parasite clearance time was 24 hours in both the arms.

75 Parasite clone-specific growth was then analysed in co-c

76 Owing to a complex history of host-parasite coevolution, lentiviruses exhibit a high degree

77 rulence is often under selection during host-parasite coevolution.

78 quare Error of Cross Validation (RMSECV) for parasite concentration (0-5%) was 0.58%.

79 nhance (CCL2, CCL5) or hinder (CXCL10) early parasite control, (iv) may promote granuloma maturation

80 ared with nonimmunized mice that resulted in parasite control.

81 To better understand how such microbial parasites control animal behavior, we examine the cell-l

82 epidemiological studies found the protozoan parasite Cryptosporidium to be a leading cause of paedia

83 bels filamentous actin structures within the parasite cytosol and labels an extensive F-actin network

84 Helminth parasites defy immune exclusion through sophisticated ev

85 Parasite densities decreased 5-fold from 2006 to 2010; 7

86 the 6-cysteine domain protein P36 as a major parasite determinant of host cell receptor usage.

87 d mathematical modeling of intraerythrocytic parasite development revealed an unexpected and substant

88 1.6 microM) is stably maintained throughout parasite development within red blood cells, even during

89 genes encoding effector molecules that block parasite development within the vector, and then use the

90 sses where lincRNAs might be involved during parasite development.

91 y in Africa, but resistance mutations in the parasite dhps gene (combined with dhfr mutations) threat

92 lower frequency of cellular responses to the parasite (DTH).

93 mulate around Plasmodium berghei liver-stage parasites during development, and whether this is a host

94 monstrate that repeated exposures to malaria parasites during TMP-SMX administration induces stage-sp

95 uitination of the vacuole and restriction of parasite early replication without interfering with vacu

96 Many parasite effector proteins, including perforins, adhesin

97 nter was sufficient to significantly inhibit parasite egress and dispersion.

98 cted erythrocytes for compounds that inhibit parasite egress.

99 Here, we report that the parasite-encoded RhopH complex contributes to both invas

100 Parasite epidemics may be influenced by interactions amo

101 interactions and ultimately the magnitude of parasite epidemics.

102 ing parasite exposure is not correlated with parasite establishment in adult frogs.

103 rial diversity is negatively correlated with parasite establishment in adult frogs: adult frogs that

104 treatment results in phosphorylation of the parasite eukaryotic initiation factor-2alpha (eIF2alpha)

105 duct, the structure through which saliva and parasites exit the glands, form?

106 n contrast, adult bacterial diversity during parasite exposure is not correlated with parasite establ

107 Throughout its life cycle, the T. cruzi parasite faces several alternating events of cell divisi

108 eishmania guyanensis (LgyLRV1(-) ) strain of parasites followed by type I IFN treatment increased les

109 using a measure of "imbalance." We find that parasites form highly imbalanced groups, and that concom

110 times more mosquitoes than children who were parasite free, harbored asexual stages, or had gametocyt

111 ves the group model's ability to distinguish parasites from non-parasites.

112 ogical networks; that is, can we distinguish parasites from other species using network structure alo

113 taemia for the most prevalent haemosporidian parasites from the genus Plasmodium.

114 DACs play crucial roles in the modulation of parasite gene expression and many of them are pro-surviv

115 the most distantly related species pairs of parasite genera.

116 ting the evolutionary histories of hosts and parasites, genes and species, and other interdependent p

117 A major fraction of the bulk parasite genome is packaged as transcriptionally permiss

118 y comprising approximately 150-200 genes per parasite genome that are expressed on the surface of inf

119 he absence of reliable methods to manipulate parasite genomes and/or proteomes, identification of the

120 A longitudinal analysis of malaria parasite genomes has revealed new markers that can be us

121 of host range variation on the evolution of parasite genomes remains unknown.

122 In mixtures of reference parasite genomes, we quantitatively detected unique hapl

123 Parasite genotyping and drug concentrations were investi

124 and performed glycoproteomics on endogenous parasite glycoproteins using sequential endoglycosidase

125 smodium falciparum PKG, inhibits blood stage parasite growth in vitro and in mice and blocks transmis

126 acellular development following invasion and parasite growth.

127 These results demonstrate that parasites have an intrinsic circadian clock that is inde

128 Metazoan parasites have to survive in many different niches in or

129 ses of different developmental stages of the parasite; however, changes may reflect differences assoc

130 ith LdCen(-/-) Upon challenge with wild-type parasites, IL-17 and its differentiating cytokines were

131 Accumulation of erythrocytic parasites in bone marrow and the spleen has been reporte

132 le immunity targeting pre-erythrocytic stage parasites in mice.

133 hl et al. argue that the patchy landscape of parasites in the skin is necessary to explain infectious

134 e accumulation of mutations in the resistant parasites, in addition to variations in DNA copy-number.

135 toddlers or adults) with AC genotype carried parasites, including gametocytes, more often than their

136 wild-type L. donovani infection, LdCen(-/-) parasites induce significantly higher expression of Th17

137 ic fermentative metabolism or indirectly via parasite induction of gut inflammation.

138 abnormal amphibians are associated with both parasite infection and chemical contaminants, but that t

139 P. berghei we are able to robustly quantify parasite infection of hepatocyte cell lines by flow cyto

140 pose an improved indicator that incorporates parasite infection status (as assessed by a rapid diagno

141 Chronic, low-intensity parasite infections can reduce host fitness through nega

142 rmation, the exploration of the effects that parasite infections exert on populations of commensal gu

143 non-overlapping site to additively increase parasite inhibition.

144 ggest that fecal concentrations greater than parasite inhibitory concentrations correlate best with e

145 his work demonstrates that parasites and non-parasites interact in networks in statistically distinct

146 captures the observed biology of the vector-parasite interaction.

147 gression and outcome of disease-causing host-parasite interactions will be more clearly understood th

148 asma membrane, suggesting a role at the host-parasite interface.

149 These parasites invade erythrocytes, a complex process involvi

150 A BSG knockout was completely refractory to parasite invasion in a strain-transcendent manner, confi

151 Sexual differentiation of the malaria parasite is a pre-requisite for transmission from humans

152 efense strategy or active recruitment by the parasites is unknown.

153 of intracellular pathogens, such as malaria parasites, is intimately connected to that of their host

154 the expected number of sand flies acquiring parasites, it increases the infection load for sand flie

155 ited by IL-4R-signaling in vitro, uncoupling parasite killing from expulsion mechanisms.

156 eraquine-resistant and piperaquine-sensitive parasite lines.

157 in growth inhibition assays with transgenic parasite lines.

158 ed that a Wnt5a-Rac/Rho-mediated decrease in parasite load is associated with an increase in F- actin

159 not on ART or presenting with a high tissue parasite load.

160 Infants with clinical signs had higher parasite loads and were significantly more likely to be

161 s a tendency for foreign fish to have higher parasite loads than residents, after controlling for MHC

162 ) that co-purified with PfMyoA isolated from parasite lysates.

163 ndings suggest an unanticipated function for parasite lysosomal degradation in chronic infection, and

164 The parasite makes initial contact with the erythrocyte foll

165 lso include some of nature's most successful parasites, many of which have plagued humans throughout

166 sible because of the limited availability of parasite material.

167 led an unexpected and substantial slowing of parasite maturation in acutely infected mice, extending

168 Thus, impairment of parasite maturation represents a host-mediated, immune s

169 ion induces a compensatory response, linking parasite metabolism to the activation of sexual-stage-sp

170 eaction (PCR), to parasitemia limits of 0.02 parasite/microL and 0.78 parasite/microL in PfLDH- and P

171 emia limits of 0.02 parasite/microL and 0.78 parasite/microL in PfLDH- and PfIDEh-based assays, respe

172 or PfIDEh showed detection limits of 100-200 parasites/microL and 200-400 parasites/microL, respectiv

173 mits of 100-200 parasites/microL and 200-400 parasites/microL, respectively.

174 Malaria parasites modify their human host cell, the mature eryth

175 alled the glideosome, which is essential for parasite motility and includes the MyoA light chain myos

176 ired for structural integrity of the conoid, parasite motility, and host cell invasion.

177 Obligate intracellular parasites must efficiently invade host cells in order to

178 in and lipid damage inside intraerythrocytic parasites, necessitating macromolecule degradation.

179 iated with giardiasis remain unclear, as the parasite neither produces a known toxin nor induces a ro

180 Nonetheless, because persistent parasite numbers remain roughly constant over time, thei

181 Overall, these findings reveal a key parasite nutrient-sensing mechanism that is critical for

182 r of unnecessary stool cultures (STCUL), ova/parasite (O&P) examinations, and Giardia/Cryptosporidium

183 Parasites of medical importance have long been classifie

184 s of flies, nearly all of which are obligate parasites of nestling birds.

185 Fungi are important parasites of primary producers and nutrient cyclers in a

186 Malaria is caused by parasites of the genus Plasmodium.

187 et al. report CRISPR/Cas9 genome editing in parasites of the genus Strongyloides, generating both kn

188 of the biology and pathology associated with parasites of the phylum Apicomplexa.

189 ractions between the species-specific fungal parasite Ophiocordyceps unilateralis sensu lato and its

190 d functioning of tissues as well as for host-parasite or symbiotic interactions.

191 such as climate, severe winters, predators, parasites, or the combined effect of multiple factors.

192 gs established TbAAT10-1 and TbAAT2-4 as the parasite ornithine transporters, one of which can be mod

193 ing GFP expressing sporozoites of the rodent parasite P. berghei we are able to robustly quantify par

194 arasitic nematode Ascaris suum and the horse parasite Parascaris univalens.

195 or eligibility (>/=2000 asexual P falciparum parasites per muL of blood).

196 variance-mean relationship of the numbers of parasites per square meter is very well described by TL

197 s that elevate body temperature may decrease parasite performance or increase immune function, thereb

198 tes, and merozoites, MyoA was located at the parasite periphery.

199 levels and increased transcript abundance of parasite PfEMP1 DC8 and group A EPCR-binding domains.

200 Across hosts, parasite phenology altered host susceptibility to second

201 host individuals, interactions can depend on parasite phenology.

202 nsequences of these mitochondrion changes on parasite physiology.

203 The rodent parasite Plasmodium berghei has served as a model for hu

204 The malaria parasite Plasmodium falciparum and related apicomplexan

205 solution of red cell invasion by the malaria parasite Plasmodium falciparum has been possible.

206 nce of artemisinin resistance in the malaria parasite Plasmodium falciparum poses a major threat to t

207 The hepatic stage of the malaria parasite Plasmodium is accompanied by an autophagy-media

208 The human malaria parasite, Plasmodium falciparum, depends on a coordinate

209 y encoding this sensor in the human malarial parasite, Plasmodium falciparum, we have quantified cyto

210 We consider whether or not parasites play structurally unique roles in ecological n

211 mune system-dependent mechanism for limiting parasite population growth during the early stages of an

212 tters for the antigenic var diversity of the parasite population remaining after intervention.

213 tiation between wild-type and pfhrp2-deleted parasite populations (GST = .046, p </= .00001).

214 nvestigate the selective pressure exerted on parasite populations by use of RDTs for diagnosis of sym

215 n the transformation of this important human parasite, possibly through metabolic remodeling.

216 however the biomarkers of attenuation in the parasite preparations have not received adequate attenti

217 looding surfaces, yet the temporal trends of parasite prevalence and host shell length, cannot be exp

218 s observed between hotspots defined based on parasite prevalence by polymerase chain reaction (PCR)-

219 After randomization, parasite prevalence increased over time in the STOP-CTX

220 dary outcomes included incidence of malaria, parasite prevalence, and adverse birth outcomes.

221 moderate spatial scales differed in P. vivax parasite prevalence, and multilevel Poisson regression m

222 02 (Ungoye), and were strongly correlated to parasite prevalence.

223 This study identifies a host-parasite protein interaction during the hepatic stage of

224 lopment of mefloquine derivatives to inhibit parasite protein synthesis.

225 the often polymorphic nature of immunogenic parasite proteins make the robust identification of the

226 These erythrocytes display parasite proteins of the PfEMP1 family that bind various

227 eir strong conservation among highly reduced parasites, provides compelling evidence for the ancient

228 is a diverse, speciose group of microscopic parasites, recently placed within the phylum Cnidaria.

229 after recovery, small numbers of Leishmania parasites remain indefinitely in the host.

230 their utility against naturally circulating parasites remains unknown.

231 ated malarial disease and that these diverse parasite repertoires are composed of both upsA and non-u

232 ng mechanism that is critical for modulating parasite replication and virulence.

233 for inflammasome activation, restriction of parasite replication in macrophages, and mouse resistanc

234 Furthermore, parasites resistant to HHQs displayed increased suscepti

235 Whereas ecological studies of parasite response to environmental shifts are necessaril

236 Merozoites of the protozoan parasite responsible for the most virulent form of malar

237 ng HC morphology, which is important for the parasite's ability to take up molecules from its environ

238 Both display high relative expression in the parasite's intravascular life forms.

239 onotus castaneus) at a crucial moment in the parasite's lifecycle: when the manipulated host fixes it

240 d dysbiosis may be mediated directly via the parasite's unique anaerobic fermentative metabolism or i

241 ated trophozoites, which was not observed in parasites selected or engineered for AN3661 resistance.

242 of these genes exist in a large database of parasite sequences from uncultured clinical samples.

243 D36 plays several roles, including mediating parasite sequestration to host organs, phagocytic cleara

244 ntrols P. falciparum cell fate by repressing parasite sexual differentiation.

245 growth relative to high-infection fish, and parasite size was intermediate in F1 hybrid hosts.

246 Three parasite species are uniquely associated with AT during

247 irus 1 (LRV1) replicating stably within some parasite species has been associated with the developmen

248 Self-reactive antibodies and parasite-specific IgG in female Soay sheep.

249 Suppression of parasite-specific peripheral blood mononuclear cell (PBM

250 mmunomodulation, which was not restricted to parasite-specific responses.

251 Here we describe a parasite-specific transcription factor PfAP2-I, belongin

252 he epigenetic memory is likely erased before parasites start infection of a new human host.

253 models were created from multiple mouse and parasite strain combinations, so that the epilepsy obser

254 tal malaria, but alters its progression in a parasite strain-specific manner.

255 ences of eleven long-term laboratory-adapted parasite strains were examined, revealing four independe

256 (i) the infection phase, (ii) the infecting parasite strains, and (iii) organ damage type and intens

257 gh levels of expression, conservation in all parasite strains, and good correlation of antigen levels

258 Apicomplexan parasites such as Toxoplasma gondii rely on a unique for

259 issue and that this pathway is important for parasite survival and progression of the infection.

260 identification of the molecules critical for parasite survival within these niches has largely depend

261 mmarizes new and revised clinically relevant parasite taxonomy from January 2012 through December 201

262 the group model, and we test whether or not parasites tend to cluster in their own groups, using a m

263 racellular eukaryotic apicomplexan protozoan parasite that can cause fetal damage and abortion in bot

264 Trypanosoma brucei is a protozoan parasite that evades its host's adaptive immune response

265 Entamoeba histolytica is an intestinal parasite that infects 50-100 million people and causes u

266 countries have now reported the emergence of parasites that have decreased susceptibility to artemisi

267 Microsporidians are obligate intracellular parasites that have minimized their genome content and s

268 is caused by mosquito-borne Plasmodium spp. parasites that must infect and survive within mosquito s

269 Plasmodium parasites, the causative agents of malaria, have evolved

270 ies to impact liver infection by the malaria parasite through the modulation of Arg uptake and polyam

271 uccessful sporogony of Plasmodium falciparum parasites through to human-infectious transmission stage

272 he load of antimony-sensitive and -resistant parasites, thus confirming that Wnt5a signaling antagoni

273 This strategy may enable the parasite to balance the benefits of the enhanced host ca

274 Upon infection, the intracellular parasite Toxoplasma gondii co-opts critical functions of

275 By analysing more than 18,000 single parasite transcriptomes from a conditional AP2-G knockdo

276 ogramming of the transcriptome to facilitate parasite transition towards latency.

277 natural Pf exposure that potently inhibited parasite transmission and development in vivo.

278 nary simulations demonstrated that a risk of parasite transmission leads to the evolution of scavenge

279 manipulate their vertebrate hosts to enhance parasite transmission.

280 Here we show that parasites trap host autophagic factors in the tubovesicu

281 he most prominent defence of the unicellular parasite Trypanosoma brucei against the host immune syst

282 Chagas disease is caused by the protozoan parasite Trypanosoma cruzi and affects 5-8 million peopl

283 enes during infection with the intracellular parasite Trypanosoma cruzi, as evidenced by transcriptom

284 Parasites typically have broader thermal limits than hos

285 nd many of them are pro-survival for several parasites under various conditions, they are now emergin

286 n vivo infection assays, we demonstrate that parasites undergoing coat replacement are only vulnerabl

287 cluding genetically modified live-attenuated parasite vaccines.

288 damage results from the interaction between parasite virulence and genetically determined levels of

289 Investigations of parasite virulence have associated the expression of dis

290 ivity, and expression of LSA3 in blood-stage parasites was confirmed by western blotting.

291 ated by chronic infection upon reexposure to parasite, we compared their responses to known features

292 n L. donovani To test ARG function in intact parasites, we generated Deltaarg null mutants in L. dono

293 cell biology in early-diverging Apicomplexan parasites, which do not divide by canonical binary fissi

294 es (LEs) and lysosomes is reduced in uis4(-) parasites, which lack a parasitophorous vacuole membrane

295 es are poorly adapted for in vivo studies of parasites, which require prior in vitro culturing and pu

296 We genetically cross two lethal parasites with distinct disease phenotypes, and identify

297 Treatment of Plasmodium falciparum 3D7 parasites with peptide corresponding to the hemoglobin b

298 7, and absence of recrudescent infection by parasites with the same molecular markers from days 8 to

299 re otherwise detrimental for survival of the parasite within the infected macrophages.

300 s an extensive F-actin network that connects parasites within the parasitophorous vacuole and allows

301 disease-causing cells (e.g. cancer cells or parasites) without causing collateral damage to healthy