ライフサイエンスコーパス: Plasmodium

1 Plasmodium falciparum causes a spectrum of malarial dise

2 Plasmodium falciparum causes malaria in humans with over

3 Plasmodium falciparum causes most life-threatening cases

4 Plasmodium falciparum infection was assessed by blood sm

5 Plasmodium falciparum malaria detected at delivery in pe

6 Plasmodium falciparum parasitemia was less frequent than

7 Plasmodium falciparum reticulocyte-binding protein homol

8 Plasmodium falciparum sporozite (PfSPZ) Vaccine is a met

9 Plasmodium falciparum-specific antibody kinetics during

10 Plasmodium has therefore evolved strategies to prepare f

11 Plasmodium invasion of anopheline mosquitoes is an oblig

12 Plasmodium knowlesi parasitemia correlated with age (Spe

13 Plasmodium liver hypnozoites, which cause disease relaps

14 Plasmodium parasitemia had no impact on EVD outcomes.

15 Plasmodium parasites, the causative agents of malaria, h

16 Plasmodium species cause malaria by proliferating in hum

17 Plasmodium species were identified using nested polymera

18 Plasmodium sporozoites, the mosquito-transmitted forms o

19 Plasmodium spp. target erythrocytes of different ages, b

20 Plasmodium vivax invasion into human reticulocytes is a

21 Plasmodium vivax sporozoites consist of tachysporozoites

22 evel revealed Plasmodium falciparum (92.0%), Plasmodium ovale (5.6%), and Plasmodium malariae (2.4%).

23 Also present were Plasmodium vivax (14.3%), Plasmodium falciparum (10.5%) and Plasmodium malariae (3

24 on of mosquito midgut screen candidate 2), a Plasmodium berghei protein with structural similarities

25 To address this challenge, a Plasmodium falciparum gamma-irradiated long-lived merozo

26 new permeability pathways (NPP) including a Plasmodium surface anion channel (PSAC).

27 candidates have slowed the development of a Plasmodium falciparum multiantigen vaccine.

28 al that the pathogenic response of mice to a Plasmodium berghei infection is dominated by a Vbeta8.1

29 Little is known about Plasmodium malariae, a relatively rare cause of malaria

30 phoid development in the spleen during acute Plasmodium infection.

31 stereomers 5a and 5c showed activity against Plasmodium falciparum malaria parasites (IC50 approximat

32 activity of the benzoxaborole AN3661 against Plasmodium falciparum laboratory-adapted strains (mean I

33 stem measures presence of antibodies against Plasmodium vivax, a causing agent for malaria.

34 important immune effector mechanism against Plasmodium falciparum-infected erythrocytes (IE); howeve

35 e and confers significant protection against Plasmodium falciparum infection in humans.

36 ncy is believed to confer protection against Plasmodium falciparum malaria, but the precise nature of

37 group-believed to confer resistance against Plasmodium vivax infection-was recently introduced to Pa

38 cited a potent melanization response against Plasmodium berghei ookinetes and exhibited significantly

39 by the complement-like protein TEP1 against Plasmodium malaria parasites and other microbial infecti

40 x (14.3%), Plasmodium falciparum (10.5%) and Plasmodium malariae (3.4%).

41 iparum (92.0%), Plasmodium ovale (5.6%), and Plasmodium malariae (2.4%).

42 n both our Plasmodium gallinaceum (>80%) and Plasmodium falciparum (>40%) models, an activity that wa

43 ance to infections with fungi, bacteria, and Plasmodium parasites.

44 ding parasitemia in Plasmodium chabaudi- and Plasmodium berghei-infected mice and the 48-hour in vitr

45 ited oocyst development of P. falciparum and Plasmodium berghei expressing PfCelTOS in Anopheles gamb

46 infecting species: Plasmodium falciparum and Plasmodium knowlesi.

47 malaria in humans, Plasmodium falciparum and Plasmodium vivax, rely on two distinct host cell surface

48 Apicomplexan parasites Toxoplasma gondii and Plasmodium spp. use latent stages to persist in the host

49 uanine phosphoribosyltransferase (HGPRT) and Plasmodium falciparum (Pf) hypoxanthine-guanine-xanthine

50 iparum histidine-rich protein-II (HRPII) and Plasmodium lactate dehydrogenase (pLDH).

51 AE1 in interactions between mosquito SGs and Plasmodium, and suggest the need for further research.

52 tive agent of African sleeping sickness; and Plasmodium spp., the causative agents of malaria.

53 Quantitative analysis of Wolbachia and Plasmodium sporozoite infection in field-collected mosqu

54 tially enhanced GC B cell responses and anti-Plasmodium Ab production.

55 T-bet suppress GC B cell responses and anti-Plasmodium humoral immunity.

56 y we report that IL-10 is essential for anti-Plasmodium humoral immunity.

57 genetically engineered for secretion of anti-Plasmodium effector proteins, and the recombinant strain

58 dified to alter expression of their own anti-Plasmodium immune genes in a mixed-cage population with

59 s system did not require the presence of any Plasmodium-specific factor such as post-translational ph

60 ate endocytic compartments accumulate around Plasmodium berghei liver-stage parasites during developm

61 sure of Africans to fatal pathogens, such as Plasmodium falciparum, Lassa Virus and Trypanosoma bruce

62 Parasites of the Apicomplexa phylum, such as Plasmodium spp. and Toxoplasma gondii, undergo complex l

63 nst complex intracellular pathogens, such as Plasmodium spp., where protection is likely mediated by

64 protists, including human pathogens, such as Plasmodium, Toxoplasma, Cryptosporidium and Babesia spec

65 We assessed Plasmodium falciparum drug resistance markers in parasit

66 Pregnancy-associated Plasmodium falciparum infection impacts the health of mo

67 Chronic asymptomatic Plasmodium falciparum infections are common in endemic a

68 ly by immunization with radiation-attenuated Plasmodium falciparum (Pf) sporozoites (PfSPZ) inoculate

69 n to viral fusion, indicating a way to block Plasmodium transmission and highlighting the impact of v

70 ly indicate platelets do not kill bloodstage Plasmodium at physiologically relevant effector-to-targe

71 Malaria is caused by mosquito-borne Plasmodium spp. parasites that must infect and survive w

72 osquito's innate immune system controls both Plasmodium and bacterial infections.

73 ethal form of malaria in humans is caused by Plasmodium falciparum.

74 We found that the activation of DCs by Plasmodium falciparum, the main causative agent of human

75 Invasion of erythrocytes by Plasmodium falciparum merozoites is necessary for malari

76 malaria is a deadly outcome of infection by Plasmodium falciparum, occurring when parasite-infected

77 ion during the hepatic stage of infection by Plasmodium parasites.

78 site interaction during red cell invasion by Plasmodium is important for developing newer antimalaria

79 ry adaptation in malaria parasites, clinical Plasmodium falciparum isolates were sampled from patient

80 ial source of DNA for PCR testing to confirm Plasmodium infections or for epidemiological studies of

81 Activity of pepstatin against cultured Plasmodium falciparum is highly variable depending on th

82 when an infected Anopheles mosquito deposits Plasmodium sporozoites in the skin during a bite.

83 f-of-concept, this sensor was used to detect Plasmodium falciparum histidine-rich protein 2 (PfHRP2),

84 or Arg-dependent polyamine production during Plasmodium's hepatic development and pave the way to the

85 to fully suppress effector responses during Plasmodium-induced CD4(+) T cell exhaustion.

86 to control key cell-cycle transitions during Plasmodium gametogenesis.

87 d with uninfected controls, women with early Plasmodium falciparum exposure had retarded intrauterine

88 how that wild-living bonobos are endemically Plasmodium infected in the eastern-most part of their ra

89 ne is the only licensed drug for eradicating Plasmodium vivax hypnozoites and, therefore, preventing

90 Our work explores Plasmodium DNA replication in unprecedented detail and o

91 at identifies host kinases, which facilitate Plasmodium yoelii liver stage infection.

92 se and subsequent parasite control following Plasmodium infection.

93 d expression of effector cytokines following Plasmodium yoelii infection and are therefore more resis

94 D8(+) T cell response in the liver following Plasmodium berghei sporozoite challenge.

95 For Plasmodium falciparum, the most widespread and virulent

96 For Plasmodium falciparum, the species responsible for the m

97 mission blocking vaccine (TBV) candidate for Plasmodium falciparum.

98 ated by mosquito bite: a major challenge for Plasmodium falciparum.

99 emia measurement and stage determination for Plasmodium falciparum-infected red blood cells (Pf-iRBCs

100 herapies are the first line of treatment for Plasmodium falciparum infections worldwide, but artemisi

101 could be considered for rescue treatment for Plasmodium falciparum malaria.

102 atus were tested at each antenatal visit for Plasmodium falciparum, using an RDT and polymerase chain

103 that the Plasmodium yoelii orthologs of four Plasmodium falciparum proteins identified by an antibody

104 bition assays with proteasomes isolated from Plasmodium falciparum.

105 of L-45 with the homologous Brd PfGCN5 from Plasmodium falciparum rationalizes the high selectivity

106 gulated in vaccinees who were protected from Plasmodium falciparum infection.

107 group has relatively better protection from Plasmodium falciparum malaria, as reflected by fewer sym

108 XEL) found in malaria effector proteins from Plasmodium falciparum These findings imply a role for th

109 lent haemosporidian parasites from the genus Plasmodium.

110 Malaria is caused by parasites of the genus Plasmodium.

111 Hepatic Plasmodium development occurs inside a specialized membr

112 Yet, it is unclear how Plasmodium avoids the deleterious effects of selective a

113 two main species causing malaria in humans, Plasmodium falciparum and Plasmodium vivax, rely on two

114 and potent mediator of autophagy evasion in Plasmodium.

115 Gene expression in Plasmodium falciparum is tightly regulated to ensure suc

116 y, is shown to serve a different function in Plasmodium falciparum, protecting ookinetes from the mos

117 nt years, there has been renewed interest in Plasmodium vivax, with CHMI models developed by groups i

118 release of eight flagellated microgametes in Plasmodium berghei.

119 ation of new permeability pathways (NPPs) in Plasmodium-infected erythrocytes.

120 latelets during the ascending parasitemia in Plasmodium chabaudi- and Plasmodium berghei-infected mic

121 s at loci associated with drug resistance in Plasmodium falciparum isolated from subjects receiving D

122 of DNA replication throughout schizogony in Plasmodium falciparum.

123 Here, a systematic knockout screen in Plasmodium berghei identified ten ApiAP2 genes that were

124 show that origins are very closely spaced in Plasmodium compared to most model systems, and that repl

125 We show that hepcidin upregulation in Plasmodium berghei murine malaria infection was accompan

126 All human-infecting Plasmodium species can establish long-lasting chronic in

127 ring the liver stage of a malaria infection, Plasmodium parasites are targeted by the autophagy machi

128 The best ligands inhibited Plasmodium falciparum (Pf) and Arabidopsis thaliana (At)

129 For instance, Plasmodium falciparum reticulocyte-binding protein homol

130 ria parasite species, providing insight into Plasmodium evolution and raising the question of how man

131 We introduce Plasmodium falciparum gametocyte exported protein-5 (PfG

132 ts (including important human pathogens like Plasmodium)-suggests that many eukaryotic organisms shar

133 laria parasites of Southeast Asian macaques, Plasmodium knowlesi and P cynomolgi, can infect humans e

134 sible for the most virulent form of malaria, Plasmodium falciparum, invade erythrocytes.

135 rasite species and, in contrast to mammalian Plasmodium parasites, neither host specificity nor stron

136 s parasites are closely related to mammalian Plasmodium species, the causative agents of malaria.

137 tively, our data support that FREP1-mediated Plasmodium transmission to mosquitoes is a conserved pat

138 Analysis of multiple Plasmodium falciparum genomes showed that ICAM-1-binding

139 REP1 will limit the transmission of multiple Plasmodium species to multiple Anopheles species.

140 vere falciparum malaria following nosocomial Plasmodium falciparum transmission in nonendemic Germany

141 nosoma brucei rhodesiense and falcipain-2 of Plasmodium falciparum.

142 Hypnozoites express only 34% of Plasmodium physiological pathways, while 91% are express

143 protein (CSP), the major surface antigen of Plasmodium falciparum (Pf) sporozoites, can protect from

144 th regions, R0 and R2), and AMA1 antigens of Plasmodium falciparum.

145 Although the burden of Plasmodium falciparum malaria is gradually declining in

146 and the spleen has been reported in cases of Plasmodium vivax malaria.

147 ral malaria (CM) is a severe complication of Plasmodium falciparum infection.

148 l malaria (HCM) is a serious complication of Plasmodium falciparum infection.

149 n adequate source of DNA for confirmation of Plasmodium species infections and can be used for retros

150 rison to results of PCR for the detection of Plasmodium falciparum malaria.

151 om stained blood smears for the detection of Plasmodium species using real-time PCR.

152 e recombinant strains inhibit development of Plasmodium falciparum in mosquitoes.

153 CDPK1 is critical for asexual development of Plasmodium falciparum, but its precise function and subs

154 an important role in asexual development of Plasmodium falciparum.

155 te increasing evidence of the development of Plasmodium vivax chloroquine (CQ) resistance, there have

156 We therefore studied spatial distribution of Plasmodium falciparum infections to compare simulated ef

157 The spatio-temporal distribution of Plasmodium parasitaemia, dominated by P. vivax, was show

158 The radial distribution of Plasmodium vivax malaria burden has evoked enormous conc

159 rs underwent CHMI with a low or high dose of Plasmodium falciparum sporozoites.

160 munity, which may influence the emergence of Plasmodium falciparum artemisinin-resistant phenotypes a

161 The emergence of Plasmodium falciparum resistant to frontline therapeutic

162 The proteasome is the main engine of Plasmodium protein degradation.

163 ence specific for the sicavar gene family of Plasmodium knowlesi.

164 ence and micro-geographical heterogeneity of Plasmodium vivax parasitaemia in communities of the Peru

165 evaluated as noteworthy growth inhibitors of Plasmodium falciparum (3D7 and W2) in culture.

166 dicates that the prevalence and intensity of Plasmodium falciparum sporozoite infection is significan

167 evolutionary history and interrelatedness of Plasmodium species that infect humans has been hampered

168 Biosynthetic labeling of Plasmodium mRNAs is incredibly versatile, can be used to

169 flammation, was upregulated in the livers of Plasmodium berghei-infected mice; hepatic activin B was

170 -Orp1 in the cytosol and the mitochondria of Plasmodium falciparum (P. falciparum) NF54-attB blood-st

171 ombined an established mathematical model of Plasmodium falciparum transmission dynamics with epidemi

172 may be necessitated by the dynamic nature of Plasmodium actin filaments in the parasite.

173 tage Plasmodium falciparum The percentage of Plasmodium-infected (iRBCs) with bound platelets during

174 The performance of Plasmodium falciparum-specific histidine-rich protein 2-

175 sed a long-term decline in the prevalence of Plasmodium falciparum from 40% prevalence in the period

176 causal (ie, pre-erythrocytic) prophylaxis of Plasmodium falciparum malaria with prolonged activity wo

177 microbiota, expected to include relatives of Plasmodium.

178 s are common to most, if not all, species of Plasmodium(10), this process may be a common way of regu

179 nvestigating whether successful sporogony of Plasmodium falciparum parasites through to human-infecti

180 which targets the pre-erythrocytic stage of Plasmodium falciparum infection.

181 ged period of the intraerythrocytic stage of Plasmodium infection, as well as for transmission, revea

182 uired for development of all zoite stages of Plasmodium and it is part of a novel protein complex wit

183 ial activity against asexual blood stages of Plasmodium falciparum, excellent parasite selectivity, a

184 ali infection does not limit early stages of Plasmodium infection in the mosquito, but it has a stron

185 -) mice infected with a non-lethal strain of Plasmodium yoelii Compared with Cd36(-/-) mice, WT mice

186 drug or vaccine development.Many strains of Plasmodium differ in virulence, but factors that control

187 variant antigen expressed on the surface of Plasmodium falciparum-infected erythrocytes.

188 thenic acid (PA) is critical for survival of Plasmodium falciparum within human erythrocytes.

189 Treatment of Plasmodium falciparum 3D7 parasites with peptide corresp

190 Rapid diagnostic tests based on Plasmodium falciparum histidine-rich protein II (PfHRP-I

191 ical trials have almost entirely focussed on Plasmodium falciparum, providing a highly informative me

192 trols, and between P knowlesi and human-only Plasmodium spp malaria cases.

193 semisynchronous, Plasmodium berghei ANKA- or Plasmodium yoelii 17XNL-parasitized red blood cells (pRB

194 risk for P knowlesi infection but not other Plasmodium spp infection.

195 eptionally high AT content compared to other Plasmodium species and eukaryotes in general - nearly 80

196 laria mono-infection and 91 cases with other Plasmodium spp infection.

197 xhibited very promising activity in both our Plasmodium gallinaceum (>80%) and Plasmodium falciparum

198 laria is caused by the Apicomplexan parasite Plasmodium falciparum, and results in significant global

199 ogue from the human malaria-causing parasite Plasmodium falciparum.

200 mprising HIV-1, the malaria-causing parasite Plasmodium vivax, the fungus Aspergillus niger, and the

201 f two strains of the rodent malaria parasite Plasmodium chabaudi that differ in virulence.

202 lls infected with the human malaria parasite Plasmodium falciparum (iRBCs) adhere to the vascular end

203 The malaria parasite Plasmodium falciparum and related apicomplexan pathogens

204 continuous exposure to the malaria parasite Plasmodium falciparum cause an accumulation of specific

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

206 Proteases of the malaria parasite Plasmodium falciparum have long been investigated as dru

207 temisinin resistance in the malaria parasite Plasmodium falciparum poses a major threat to the contro

208 Many genes of the malaria parasite Plasmodium falciparum show clonally variant expression r

209 For the malaria parasite Plasmodium falciparum, invasion of host red blood cells

210 ce transporter of the human malaria parasite Plasmodium falciparum, PfCRT, is an important determinan

211 The hepatic stage of the malaria parasite Plasmodium is accompanied by an autophagy-mediated host

212 of human malaria due to the monkey parasite Plasmodium knowlesi threatens elimination efforts in sou

213 of an infection with the protozoan parasite Plasmodium falciparum, which requires immediate treatmen

214 ed with the reticulocyte-restricted parasite Plasmodium berghei NK65 1556Cl1.

215 The rodent parasite Plasmodium berghei has served as a model for human malar

216 The human malaria parasite, Plasmodium falciparum, depends on a coordinated regulati

217 However, the human malaria parasite, Plasmodium falciparum, is incapable of pyrimidine salvag

218 s are vectors of the human malaria parasite, Plasmodium falciparum.

219 of the most virulent human malaria parasite, Plasmodium falciparum.

220 t widely distributed human malaria parasite, Plasmodium vivax, will be a major step towards malaria e

221 this sensor in the human malarial parasite, Plasmodium falciparum, we have quantified cytosolic labi

222 es the two related human parasitic pathogens Plasmodium falciparum and Toxoplasma gondii.

223 which could be moderated by using PfHRP2/Pf-Plasmodium lactate dehydrogenase combination RDTs.

224 e, we report the characterization of PIMMS2 (Plasmodium invasion of mosquito midgut screen candidate

225 Malaria, caused by the protozoan Plasmodium, is a devastating mosquito-borne disease with

226 Single low-dose primaquine (PQ) reduces Plasmodium falciparum infectivity before it impacts game

227 However, unlike related Plasmodium species, the pathogenesis of Babesia infectio

228 w era in effectively treating drug-resistant Plasmodium falciparum malaria.

229 s used for malaria treatment until resistant Plasmodium falciparum was identified.

230 CR-HRM results to the species level revealed Plasmodium falciparum (92.0%), Plasmodium ovale (5.6%),

231 fate of a single cohort of semisynchronous, Plasmodium berghei ANKA- or Plasmodium yoelii 17XNL-para

232 eases and obesity, is associated with severe Plasmodium falciparum malaria.

233 panzees, as well as a potential new species, Plasmodium lomamiensis sp. Rare co-infections with non-L

234 in only two of five human-infecting species: Plasmodium falciparum and Plasmodium knowlesi.

235 ro development or replication of blood-stage Plasmodium falciparum The percentage of Plasmodium-infec

236 ing the early stages of an acute blood-stage Plasmodium infection.

237 enuation of both liver-stage and blood-stage Plasmodium parasites has been investigated.

238 g erythrocytes and causing malaria symptoms, Plasmodium parasites undergo an obligatory phase of inva

239 Bicyclic azetidines targeting Plasmodium falciparum phenylalanyl-tRNA synthetase compr

240 an imidazopyridine that selectively targets Plasmodium falciparum PKG, inhibits blood stage parasite

241 ntigen lateral flow malaria RDT that targets Plasmodium falciparum histidine-rich protein-II (HRPII)

242 In this observational study, we tested Plasmodium falciparum isolates from Myanmar, northeaster

243 We conclude that Plasmodium growth in vitro is associated with elevated e

244 Here we show that Plasmodium berghei parasites infecting hepatic cells rel

245 Here we show that Plasmodium blood-stage parasites actively respond to hos

246 Here we show that Plasmodium DNA induces autoreactive responses against er

247 In this article, we show that Plasmodium falciparum merozoites, the invasive form of b

248 Controversially, it is also thought that Plasmodium vivax has driven the recent selection of G6PD

249 The Plasmodium falciparum Pfs25 protein (Pfs25) is a leading

250 The Plasmodium genus has evolved over time and across hosts,

251 eIF2alpha phosphorylation is mediated by the Plasmodium eIF2alpha kinase, PK4.

252 vere complications of human infection by the Plasmodium falciparum parasite.

253 Invasion of the red blood cell (RBC) by the Plasmodium parasite defines the start of malaria disease

254 d B cell phenotypes and Abs specific for the Plasmodium falciparum vaccine candidate apical membrane

255 Here, we identify the Plasmodium protein LIMP (the name refers to a gliding ph

256 emonstrated in part curative activity in the Plasmodium berghei mouse model when administered peroral

257 on represents a population bottleneck in the Plasmodium life cycle and a key intervention target of o

258 n/hemozoin formation, essential steps in the Plasmodium life cycle, are targets of existing antimalar

259 A cryo-electron microscopy structure of the Plasmodium falciparum 80S ribosome with the (+)-mefloqui

260 Deletions of the Plasmodium falciparum hrp2 (pfhrp2) gene cause false-neg

261 Deletions of the Plasmodium falciparum hrp2 and hrp3 genes can affect the

262 re provide insight into the evolution of the Plasmodium genus as a whole.

263 d on an imidazopyridine series targeting the Plasmodium falciparum cyclic GMP-dependent protein kinas

264 Here, we show that the Plasmodium yoelii orthologs of four Plasmodium falciparu

265 Here, we show that the Plasmodium-specific kinase PfCRK4 is a key cell-cycle re

266 Among them, the Plasmodium falciparum Cysteine-Rich Protective Antigen (

267 We examined MyoA expression throughout the Plasmodium berghei life cycle in both mammalian and inse

268 required for CD8(+) T cell responses to the Plasmodium berghei GAP5040-48 epitope in mice expressing

269 For reasons that remain unknown, the Plasmodium falciparum genome has an exceptionally high A

270 to accurately place these species within the Plasmodium phylogeny.

271 transmission on maintenance of antibodies to Plasmodium falciparum merozoite antigens and infected er

272 However, the proportion of cases due to Plasmodium vivax is increasing, accounting for up to 90-

273 n humans lacking robust adaptive immunity to Plasmodium falciparum Nevertheless, the host may partly

274 dverse pregnancy and birth outcomes owing to Plasmodium falciparum accumulation in the placenta.

275 ibited significantly increased resistance to Plasmodium infections as well as to systemic and oral ba

276 ls produce the cytokine IL-17 in response to Plasmodium infection.

277 rentiates into mature B cells in response to Plasmodium yoelii infection in mice.

278 In the present study antibody responses to Plasmodium falciparum AMA-1, MSP-119 and CSP were measur

279 ct mice from infection with PfCSP transgenic Plasmodium berghei sporozoites.

280 tudies that establish the requirement of two Plasmodium spp. proteases of the plasmepsin family in pa

281 otect children from severe and uncomplicated Plasmodium falciparum malaria.

282 dely-recommended treatment for uncomplicated Plasmodium falciparum malaria worldwide.

283 ay of the current treatment of uncomplicated Plasmodium falciparum malaria, but ACT resistance is spr

284 most efficacious treatment of uncomplicated Plasmodium falciparum malaria.

285 ical (MBG) approach to detect hotspots using Plasmodium falciparum parasite prevalence and serologica

286 A live-attenuated malaria vaccine, Plasmodium falciparum sporozoite vaccine (PfSPZ Vaccine)

287 Also present were Plasmodium vivax (14.3%), Plasmodium falciparum (10.5%)

288 s are not well understood, including whether Plasmodium changes its translationally repressive comple

289 Adults with Plasmodium falciparum malaria were randomized to receive

290 previously identified to be associated with Plasmodium falciparum infection in natural Anopheles gam

291 ntrolled human malaria infection (CHMI) with Plasmodium falciparum (Pf) parasites homologous to the v

292 GSNOR knockout (KO) mice infected with Plasmodium berghei ANKA had significantly delayed mortal

293 verity and parasitemia in mice infected with Plasmodium chabaudi AS.

294 C57BL/6 mice infected with Plasmodium yoelii nigeriensis N67C display high levels o

295 ed at peak parasitemia during infection with Plasmodium chabaudi Concentrations of the closely relate

296 d by Controlled Human Malaria Infection with Plasmodium falciparum.

297 d NK cell responses following infection with Plasmodium has been challenging because the early stages

298 e Finally, we showed that FBG interacts with Plasmodium gametocytes and ookinetes, revealing the mole

299 859 patients aged 6 months to 12 years with Plasmodium falciparum malaria.

300 number in the plasmepsin II/III genes within Plasmodium falciparum has been associated with decreased