ライフサイエンスコーパス: parasite

1 o evaluate its effect on the invasion by the parasite.

2 a disease caused by the Leishmania donovani parasite.

3 ction, and 31.0% had at least one intestinal parasite.

4 ection, benefitting neither the host nor the parasite.

5 2 define effective monocyte responses to the parasite.

6 falciparum, the most virulent human malaria parasite.

7 ressed by the three life cycle stages of the parasite.

8 ts, making this pathway indispensable to the parasite.

9 another important aetiological kinetoplastid parasite.

10 dual host being infected by a haemosporidian parasite.

11 licated in intraerythrocytic survival of the parasite.

12 a conserved LIFT pathway in these protozoan parasites.

13 osoma brucei gambiense and Trypanosoma cruzi parasites.

14 infected with viruses, bacteria, fungi, and parasites.

15 red blood cells with unicellular Plasmodium parasites.

16 al background driving the evolution of these parasites.

17 oteins in purine-starved Leishmania donovani parasites.

18 evalence and diversity of vector-transmitted parasites.

19 d patients and artemisinin-induced quiescent parasites.

20 vity against pathogenic bacteria, fungi, and parasites.

21 uglenozoa and all known species are obligate parasites.

22 and recently identified also in apicomplexan parasites.

23 ology and evolution of prokaryotes and their parasites.

24 ion and during coevolution with manipulative parasites.

25 trongly to the total burden of P. falciparum parasites.

26 ning multiple classes, a single class, or no parasites.

27 duction of NO, and subsequent destruction of parasites.

28 ay between phagocytes and invasive coccidian parasites.

29 nce alters the outcome of interactions among parasites.

30 that initiates apoptosis-like cell death of parasites, adding fascinating insight into host-pathogen

31 ights into the remarkable flexibility of the parasite, addressing the dependency on biosynthesis or s

32 parasite density could act as predictors of parasite age and synchrony.

33 As obligate parasites, all viruses exploit common cellular pathways,

34 uitoes, tsetse flies, sandflies) to transmit parasites and disease.

35 The interactions between Plasmodium parasites and human erythrocytes are prime targets of bl

36 e roles in intercellular communication among parasites and influence growth kinetics.

37 organelle extrudes in extracellular invasive parasites and is associated to the apical polar ring (AP

38 rt, or to an actual rise in the abundance of parasites and pathogens?

39 Leishmania transmission sand flies inoculate parasites and saliva into the skin of vertebrates.

40 gy laboratory by augmenting the detection of parasites and slide interpretation using a convolutional

41 , a parasitic infection caused by Plasmodium parasites and transmitted through the bite of infected f

42 tes were characterized for the first time in parasites and various fish matrices (muscle, liver, and

43 otential to detect viruses, bacteria, fungi, parasites, and archaea, including organisms that were pr

44 y origins of potential allergens, toxins and parasites, and how they might have influenced early-mamm

45 ange, increased vulnerability to disease and parasites, and pesticide use.

46 Patients presenting with older parasites, and with asynchronous infections, have been r

47 rally occurring human antibody response to a parasite antigen that initiates apoptosis-like cell deat

48 These results suggest that apicomplexan parasites appropriated polyspecific I domains in part fo

49 Our results reveal malaria parasites are at least partly responsible for scheduling

50 Parasites are by definition organisms that utilize resou

51 During blood-stage development, malaria parasites are challenged with the detoxification of enor

52 In many systems, host traits exploited by parasites are constrained by use in other functions, lea

53 Zoonotic and vector-borne parasites are important preventable risk factors for epi

54 s, caused by Leishmania species of protozoan parasites, are neglected tropical diseases with millions

55 In the incessant host-parasite arms race, viruses evolved multiple anti-defens

56 articular invasion-related genes in switched parasites, as well as a large number of genes encoding p

57 od cells (RBCs) on completion of the malaria parasite asexual cell cycle.

58 facilitative priority effects, which altered parasite assembly during natural epidemics.

59 effects of early-arriving strains can drive parasite assembly, with implications for how strain dive

60 genous and endogenous sources of immunity to parasite attack may represent an underappreciated conseq

61 s a result of exposure to the alkaloids, the parasites became swollen and rounded in shape, with hype

62 malaria (IBSM) model of P. malariae to study parasite biology, diagnostic assays, and treatment.

63 different aspects of the disease, including parasite biology, disease ecology, human/animal infectio

64 ks of fatal outcomes, associated with higher parasite biomass and multiplication rates respectively.

65 analysis demonstrated that mothers with low parasite burden and in good body condition were more lik

66 the study, we evaluated CNS inflammation and parasite burden in the surviving mice.

67 of infection, but migration can also reduce parasite burdens within host populations via migratory e

68 ocytes in response to infection with malaria parasites, but the extent of this phenomenon remains unk

69 e clone by 40%, and increased biomass of the parasite by 50%.

70 We found that the intracellular bacterial parasite 'Ca.

71 ry mortality effects and indirect effects of parasites can be very important, we need to study temper

72 Though neglected, these parasites can cause major pathology and mortality to liv

73 escribes how these proventriculus-colonizing parasites can either migrate to the ectoperitrophic spac

74 This work reveals that wtf parasites can exploit protein aggregate management pathw

75 These dormant parasites can remain quiescent for months or years, then

76 erine proteases but are potent inhibitors of parasite cathepsins L and host lysosomal cathepsin L, S

77 Trypanosoma brucei is a protist parasite causing sleeping sickness and nagana in sub-Sah

78 nfections by forming ion channels within the parasite, causing lysis.

79 The parasite clearance half-life following artemether-lumefa

80 The rate of parasite clearance was greater in subjects administered

81 ory T cell response that persists well after parasite clearance.

82 pe, geography and host phylogeny on regional parasite community assembly.

83 Both closely and distantly related parasites comprise an infection, suggesting sequential t

84 une receptors, and inflammatory cytokines on parasite control and disease symptoms.

85 g experimental malaria unexpectedly hindered parasite control by impeding germinal center responses.

86 ins, but infections due to viruses, fungi or parasites could also lead to sepsis.

87 alaria transmission is regulated so that the parasite decreases its endothelial binding capacity, all

88 whole genome sequencing of samples with low parasite density (i.e. one sample with a parasitaemia of

89 gated if clinical features such as fever and parasite density could act as predictors of parasite age

90 Two parasite-derived miRNAs, cel-miR-71-5p and bma-lin-4, an

91 and surface plasmon resonance, we identified parasite-derived peptides that have the sequence-specifi

92 tial expression strategies to determine true parasite-derived sRNAs within host cells.

93 WASH interventions decreased the number of parasites detected (difference in number compared to non

94 cretion of a subset of proteins required for parasite development and invasion of erythrocytes.

95 expression that could be related to reduced parasite development in vivo.

96 aturation of proteins required for invasion, parasite development, and egress.

97 dii biology, including the genes controlling parasite development, the mechanisms of cell-intrinsic i

98 microti biology, host modulation and diverse parasite developmental stages using reverse genetics and

99 ing a more stringent CHMI, with heterologous parasites (different Pf strain), we assessed the impact

100 pidemiology and biology of P. vivax, how the parasite differs from P. falciparum, and the key feature

101 Infection rates and parasite diversity also tended to be higher in cooler re

102 Astyanax mexicanus to understand how loss of parasite diversity influences the evolutionary trajector

103 neither predicted infection probability nor parasite diversity.

104 the surviving mice, we found no evidence of parasite DNA, cysts, or inflammation in the CNS.

105 ility of preventing disease by targeting the parasite during the blood stage of infection.

106 The exponential growth of the parasites during the blood stage is responsible for almo

107 we need to study temperature effects on host-parasite dynamics in a community context to truly know t

108 and thus likely see the most changes to host-parasite dynamics.

109 sic pathways with external signals to direct parasite egress from host cells.

110 effective design and management of long-term parasite elimination, it is becoming clear that transmis

111 partner drug to discern whether blood-stage parasite exposure impacts protection against homologous

112 e (PfSPZ) challenge, but whether blood-stage parasite exposure is required for protection remains unc

113 -term evolutionary consequences of decreased parasite exposure on an immune system are not well under

114 he metacyclic pool is diverse, and that each parasite expresses only one of the unique metacyclic var

115 sue not only in pathology (allergic disease, parasite expulsion) but also during normal postnatal dev

116 Several host and parasite factors are involved in this heterogeneity.

117 ast, the direct impacts of host nutrition on parasite fitness and the mechanisms underpinning these e

118 sceptibility, without significantly altering parasite fitness in culture.

119 s, respectively, we test the implications of parasites for annual mortality in wild bird populations

120 P2 factors that dominate our current view of parasite gene regulation.

121 processing remains unaffected, PV5-deficient parasites generate less hemozoin.

122 cytosis of hemoglobin, which is required for parasite growth and artemisinin activation.

123 For this, we compared the survival and parasite growth and distribution in miR-155(-/-) and wil

124 -linear and sine-wave models to estimate the parasite growth rate of the 3D7 strain of Plasmodium fal

125 ynthesis inhibitors (azoles), independent of parasite growth rate.

126 Parasite growth rates were similar across different IBSM

127 l PIEZO1 were shown to ameliorate Plasmodium parasite growth, blood-brain barrier dysfunction, and mo

128 vival of wild-type and artemisinin-resistant parasites harboring the PfKelch13:C580Y mutation.

129 Research on Plasmodium parasites has driven breakthroughs in reducing malaria m

130 ostasis in the single mitochondrion of these parasites has remained largely unknown.

131 he disease and the population biology of the parasite have been limited by the molecular tools curren

132 Malaria-causing parasites have a life cycle with unique cell-division cy

133 scriptomic analyses of several Orobanchaceae parasites have revealed fascinating molecular insights i

134 Ticks, as blood-sucking parasites, have developed a complex strategy to evade an

135 The complexity of the parasite-host interactions hampers the identification an

136 arison of TbDYRK null mutants with wild-type parasites identified molecules that operate on both the

137 Antibodies that bind PIMMS43 interfere with parasite immune evasion when ingested with the infectiou

138 s (8.7% individual flowers) had at least one parasite in or on them, respectively.

139 CSP-expressing vaccines effectively targeted parasites in hepatocytes.

140 Growth rate of malaria parasites in the blood of infected subjects is an import

141 .039), indicating a significant reduction in parasites in the liver.

142 ite), Bla g 7 (cockroach), and Ani s 3 (fish parasite)-in terms of IgE binding, structural stability,

143 t forms compared with the blood stage of the parasite, including several proteins associated with dif

144 has emerged as a useful drug target in many parasites, including Fasciola hepatica TIM (FhTIM).

145 anding of the mechanisms by which Plasmodium parasites induce CM.

146 pt that other antigens can be sufficient for parasite-induced protective immunity.

147 1, has been found to constrain intracellular parasite infection by disrupting their vacuole membranes

148 We found that parasite infection had no impact on age-associated decli

149 ing 20E signaling pathways to reduce malaria parasite infection in the mosquito vector and provide ne

150 s of their physiology that may influence the parasite infection is essential to better understanding

151 tive caseinolytic protease, as important for parasite infection of host macrophages and a potential t

152 on of electron-dense band at the base of the parasite infection site.

153 rstanding of hemoparasite infections and how parasites influence their native hosts, through decreasi

154 Even though parasites initially adhere to RBCs with a random orienta

155 Third, for some responses like parasite intensity, as long as the lethal limit of the p

156 How this life cycle unfolds and how host and parasite interact remain largely to be discovered.

157 hyperdiverse snail proteins may mediate host-parasite interaction at the cell surface, offering promi

158 , including molecular targets in the malaria parasite, interaction data for ligands with antimalarial

159 rnal microenvironment, mediates crucial host-parasite interactions.

160 The malaria parasite interfaces with its host erythrocyte (RBC) usin

161 d provide further insights on how Plasmodium parasites interfere with erythropoiesis and contribute t

162 Malaria parasites invade healthy red blood cells (RBCs) during t

163 CpEF1alpha plays a role in the parasite invasion by participating in the formation of e

164 ld synergize with other vaccines that target parasite invasion of hepatocytes or the invasion of and

165 cycle, is variable and reflects the relative parasite investment between transmission and maintaining

166 Underlying the resilience of this parasite is its remarkable ability to undergo genome mod

167 ntensity, as long as the lethal limit of the parasite is not crossed, on average, there may be a biol

168 The erythrocytic cycle of Pbyop1Delta parasites is severely attenuated and the incidence of ex

169 ly accompanies infection or mere exposure to parasites is traditionally considered a negative byprodu

170 Interestingly, some parasite isolates possessed mixed PfRh2b deletion and fu

171 mediated cytotoxicity has not been linked to parasite killing.

172 Parasites lacking GRA45 are more susceptible to IFNgamma

173 ture levels (NDWI), whereas the diversity of parasite lineages decreased with increasing NDVI.

174 Patients harbored up to seventeen unique parasite lineages.

175 Parasite load in slit aspirate was monitored using qPCR.

176 ding cerebral malaria (CM), driven by a high parasite load, leading to parasite sequestration in orga

177 signaling in mice increases lesion size and parasite load.

178 ulted in enhanced CD8-dependent reduction of parasite load.

179 ned clinical cure with a gradual decrease in parasite load; however, 25% relapsed within 18 months of

180 hereby providing a source of amino acids for parasite metabolism and preventing osmotic stress of thi

181 important for both mitochondrial and general parasite metabolism.

182 ain reaction (PCR) protocol that targets the parasite mitochondrial cytochrome b gene.

183 ion [1, 2], indicating there is selection on parasite morphology to match the host (Batesian and/or W

184 smission hotspots, migratory recovery due to parasite mortality, and migratory culling of infected in

185 life and zoonotic pathogens are the types of parasites most likely to be affected by changes to biodi

186 ular parasite research is collection of high parasite numbers separated from host contamination.

187 raphic selection mosaics across gradients of parasite occurrence maintain genetic diversity in sorghu

188 ardia duodenalis is a major gastrointestinal parasite of humans and animals across the globe.

189 Many non-ant parasites of ant colonies are known to mimic the morphol

190 sistently experience infection by a virulent parasite Ophryocystis elektroscirrha, and some medicinal

191 There was no difference in bacteria, parasites, or cumulative quantity of stunting-associated

192 oxoplasma gondii is an incredibly successful parasite owing in part to its ability to persist within

193 se assays are capable of detection below two parasites per microliter blood, a limit of detection sug

194 e and enabling several months of subclinical parasite persistence.

195 promising target genes for crop improvement, parasite/pest control, bioconservation and genetic diagn

196 mplex is integrally associated with both the parasite plasma membrane and an intermediate filament cy

197 POL1 forms a cytotoxic cation channel in the parasite plasma membrane.

198 Disruption of PIMMS43 in the rodent malaria parasite Plasmodium berghei triggers robust complement a

199 For instance, the malarial parasite Plasmodium falciparum and the Lyme disease spir

200 Malaria caused by the apicomplexan parasite Plasmodium falciparum has served as a strong ev

201 The intricate interactions the parasite Plasmodium falciparum has with its host allows

202 l crosses carried out with the human malaria parasite Plasmodium falciparum played a key role in dete

203 yisoprenoids are more diverse in the malaria parasite Plasmodium falciparum than previously postulate

204 In the human malaria parasite Plasmodium falciparum, a unicellular eukaryotic

205 applied this approach to the malaria-causing parasite Plasmodium falciparum, an organism that has res

206 In the malaria parasite Plasmodium falciparum, the switch from asexual

207 , is also needed by the lethal human malaria parasite Plasmodium falciparum.

208 e mechanisms that the most lethal of malaria parasites, Plasmodium falciparum, uses to sense nutrient

209 3) or uninfected (n = 45) by acanthocephalan parasites Pomphorhynchus sp. from differently contaminat

210 t de novo mutations in Plasmodium falciparum parasite populations in Southeast Asia and South America

211 ndergo genome modifications, thus, providing parasite populations with extensive genetic variability

212 e that parasite rhythms are generated by the parasite, possibly to anticipate its circadian environme

213 been good progress in understanding how the parasites prepare for transmission, detect their changed

214 al scales and influence immune function: (a) parasite pressure, (b) abiotic and biotic factors and (c

215 mmon metrics of malaria transmission such as parasite prevalence are under powered in elimination con

216 Parasite prevalence by rapid diagnostic test (RDT) decli

217 sing sex-specific blood and gastrointestinal parasite prevalence from 96 and 54 avian host species, r

218 isingly, STAT6 did not enhance intracellular parasite proliferation, but rather modulated the size an

219 Obligate avian brood parasites provide a particularly tractable system for un

220 (HPR), which can function as a ligand for a parasite receptor.

221 he bone marrow (BM) is a major reservoir for parasite replication and the development of transmission

222 A major challenge of intracellular parasite research is collection of high parasite numbers

223 is suffer from toxicity and the emergence of parasite resistance, and so a better solution would be t

224 ot recommended because of concerns regarding parasite resistance.

225 major natural vector of Leishmania infantum parasites, responsible for transmission of visceral leis

226 Thus, we propose that parasite rhythms are generated by the parasite, possibly

227 Overall, host richness predicted parasite richness, and as predicted, this effect was mod

228 can modify the relationship between host and parasite richness.

229 relationship between post-assembly host and parasite richness.

230 w that gene copy number variation affect the parasite's ability to evade anti-PvDBP humoral immunity.

231 RT transports peptides from the lumen of the parasite's digestive vacuole to the cytosol, thereby pro

232 abdomen flukes) enables kin selection of the parasite's host-manipulating trait, which facilitates tr

233 We also discuss the relevance of the malaria parasite's intravacuolar lifestyle for successful erythr

234 , driven by a high parasite load, leading to parasite sequestration in organs and consequent excessiv

235 ious reports in Plasmodium knowlesi, another parasite species shown to infect humans, demonstrated th

236 ple, Lychnis flos-cuculi) harboured multiple parasite species whilst others (for example, Lythrum sal

237 SLOPE can be used on multiple parasite species, under multiple media formulations, and

238 an essential cyclin-dependent kinase for the parasite-specific mode of pre-mRNA processing.

239 the parasitic infections, some of which are parasite-specific, opens up new therapeutic possibilitie

240 protein secreted by monocytes in response to parasite stimulation, as a rosette-stimulator for Plasmo

241 d support the existence of P. vivax-adherent parasite subpopulations in the microvasculature of the h

242 Several medically important protozoan parasites such as Plasmodium, Entamoeba, Toxoplasma, and

243 rbon metabolism are required for blood-stage parasite survival and organelle maintenance.

244 treatment of CL, supporting participation of parasite-sustained inflammation or deregulated innate im

245 Importantly, parasites switch from COQ-2a to COQ-2e as they transit i

246 loidiasis, schistosomiasis, other intestinal parasites, syphilis, gonorrhea, chlamydia, and human imm

247 The fate of organic micropollutants in host-parasite systems and the combined effect of parasitism a

248 d antibody responses to Plasmodium spp., the parasite that causes malaria, are critical for control o

249 s vaginalis is a common sexually transmitted parasite that colonizes the human urogenital tract causi

250 wn-headed cowbirds (Molothrus ater), a brood parasite that commonly lays eggs in blackbird nests.

251 Toxoplasma gondii (T. gondii) is a protozoan parasite that uses conserved mechanisms to infect rodent

252 l conversion rate, the proportion of asexual parasites that convert into gametocytes at each multipli

253 constant threat posed by the diverse genetic parasites that endanger them.

254 ts, schistosomes, are intravascular flatworm parasites that feed on blood and lay eggs, resulting in

255 ypanosoma brucei and Trypanosoma congolense, parasites that share a common pathway in the early stage

256 Cryptosporidium is a genus of apicomplexan parasites, the causative agents of cryptosporidiosis in

257 In contrast, metabolite levels were lower in parasite tissues compared to fish matrices.

258 For this parasite to establish an infection in flies, it must fir

259 These modulatory effects assist parasites to establish and survive, while dampening immu

260 l-described strategy of Plasmodium and other parasites to evade host immunity.

261 re, PfHsp70-1 downregulation hypersensitizes parasites to heat shock and PI3K inhibitors.

262 The ability of malaria parasites to survive ART monotherapy may relate to an in

263 -stage transfection limited the tendency for parasites to take up multiple vectors.

264 dendritic cells infected with the protozoan parasite Toxoplasma gondii (Tg).

265 Here, deletion of the dpy19 gene in the parasite Toxoplasma gondii abolished C-mannosyltransfera

266 The protozoan parasite Toxoplasma gondii lives inside a vacuole in the

267 ent availability, the obligate intracellular parasite Toxoplasma gondii reprograms its metabolism.

268 ontrols invasion and egress by the protozoan parasite Toxoplasma gondii.

269 nfection challenge with the common coccidian parasites Toxoplasma gondii and Neospora caninum activat

270 Dictyostelium discoideum, and the protozoan parasite, Toxoplasma gondii, both lacking HIF.

271 l of malaria infection that allowed host and parasite traits to be linear functions (reaction norms)

272 Parasites transition between five distinctive body plans

273 es, the sexual stage responsible for malaria parasite transmission from humans to mosquitoes, are key

274 efforts it is important to better understand parasite transmission to mosquitoes and develop models f

275 y, these results suggest that, by modulating parasite transmission, community assembly can modify the

276 community assembly, which in turn, can alter parasite transmission.

277 s) within mosquitos is essential for malaria parasite transmission.

278 ne their potential for also reducing malaria parasite transmission.

279 considerable gain-of-fitness associated with parasite transmission.

280 sease, caused by the intracellular protozoan parasite Trypanosoma cruzi, is a public health problem a

281 o species of fire ants against the protozoan parasite Trypanosoma cruzi, the aetiologic agent of Chag

282 The sleeping sickness parasite, Trypanosoma brucei, uses quorum sensing (QS) t

283 nges found in two well-studied kinetoplastid parasites, Trypanosoma brucei and Leishmania, focusing o

284 h 5% within sample frequency in DBS with 100 parasites/uL).

285 st infections (55.6%) had parasitemias <= 10 parasites/uL.

286 it is possible to obtain transfected viable parasites under in vivo growing conditions.

287 Toxoplasma gondii, a protozoan parasite, undergoes a complex and poorly understood deve

288 Apicomplexan parasites use a specialized cilium structure called the

289 variation is linked to novel strategies the parasites use to replicate their unconventional genomes.

290 008 to 2018 were screened for haemosporidian parasites using a nested polymerase chain reaction (PCR)

291 genotyped polymerase chain reaction-detected parasites using deep sequencing of SP-resistance alleles

292 ormulations, and lacks measurable impacts on parasite viability.

293 s for each kinase, including phosphosites on parasite virulence factors and host erythrocyte proteins

294 ility that PCR detects DNA of haemosporidian parasite was higher for female birds, suggesting that th

295 Pfk13 C580Y parasites were observed in 1.6% (14/854) of samples coll

296 e C-mannosyltransferase-deficient Deltadpy19 parasites were strongly attenuated in virulence and indu

297 h good in vitro activity against the malaria parasite, which translated into in vivo efficacy in the

298 on or eliminate dormant P. vivax liver-stage parasites will be essential for malaria elimination.

299 ystems may facilitate the transfer of such a parasite with free-living stages between farmed and wild

300 Patient samples suggest that parasites with increased pvdbp copy number are able to i