ライフサイエンスコーパス: P. falciparum

1 P. falciparum accounted for 110 (11%), 45 (6%), and 23 (

2 P. falciparum and P. knowlesi, the only two Plasmodium s

3 P. falciparum infections returned during the follow-up p

4 P. falciparum parasites express Pfs47 haplotypes compati

5 P. falciparum strains lacking PfHRP2, due to pfhrp2 gene

6 P. falciparum susceptibility to heme-binding antimalaria

7 P. falciparum-infected RBCs induced NK cell degranulatio

8 We analysed 1218 P. falciparum clinical isolates, and the results show th

9 chloroquine prophylaxis and bites from 12-15 P. falciparum-infected mosquitoes (CVac-chloroquine arm)

10 chloroquine prophylaxis and bites from 12-15 P. falciparum-infected mosquitoes (CVac-chloroquine arm)

11 isson model fitted to our data predicted 16% P. falciparum-positive individuals that are likely to tr

12 Gametocytes were identified in 58% (93/161) P. falciparum-positive individuals.

13 Genome clustering of 2263 P. falciparum isolates from 24 malaria-endemic settings

14 ravenous inoculation with approximately 2800 P. falciparum parasitized erythrocytes on day 13.

15 w (sero-low) previous exposure received 3200 P. falciparum sporozoites (PfSPZ) of PfSPZ Challenge by

16 ivity and specificity on clinical samples (5 P. falciparum and 10 P. vivax samples).

17 and future potential of the RCR complex as a P. falciparum vaccine target.

18 Here, we imposed a P. falciparum life cycle time on a genetic distance like

19 Here, we show that a P. falciparum patatin-like phospholipase (PfPATPL1) with

20 us-RDT identified few additional P. falciparum-positive patients as compared to co-RDT (2

21 Kinobeads profiling we identified additional P. falciparum protein kinases targeted by the thiazoles

22 idgut proteins that interact with and affect P. falciparum invasion.

23 f the gene encoding PfPATPL1 does not affect P. falciparum blood stage growth or gametocyte developme

24 After P. falciparum initially acquired free cholesterol or inn

25 erythrocyte membranes, both during and after P. falciparum invasion of human erythrocytes.

26 sure to atovaquone before, or shortly after, P. falciparum infection causes full parasite arrest in t

27 pounds were then tested for activity against P. falciparum asexual blood stage growth, selectivity an

28 In addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and pr

29 lizing antibody can cause protection against P. falciparum blood-stage infections, and highlight the

30 MA1-RON2L) induces better protection against P. falciparum malaria in Aotus monkeys.

31 e fail to provide optimal protection against P. falciparum, especially submicroscopic infections.

32 inhibition and exquisite selectivity against P. falciparum parasites (3D7 and Dd2 strains) in vitro.

33 atment-based intervention strategies against P. falciparum malaria.

34 S/AS01 - the leading malaria vaccine against P. falciparum (Pf) - has been associated with the humora

35 ved in each functional activity differ among P. falciparum strains.

36 sights into the pfhrp2 gene deletion amongst P. falciparum population from Sudan.

37 ic and erythrocytic stages of P. berghei and P. falciparum infection, suggesting inclusion of ivermec

38 d to inhibit the interaction between CSA and P. falciparum-infected erythrocytes expressing different

39 , we report the detection of pan malaria and P. falciparum species using a dye-based reaction catalyz

40 Plasmodium lactate dehydrogenase (pLDH), and P. falciparum histidine-rich protein 2 (PfHRP2) antigens

41 ant surface antigens of Plasmodium vivax and P. falciparum following controlled human malaria infecti

42 urface protein 1 (MSP-1(42)) of P. vivax and P. falciparum using an enzyme-linked immunosorbent assay

43 teers infected with blood-stage P. vivax and P. falciparum, and were higher in P. vivax infection.

44 tion has been achieved for both P. vivax and P. falciparum, controlled human transmission to mosquito

45 Plasmodium vivax and P. falciparum, the parasites responsible for most human

46 stigated combining two liver-stage antigens, P. falciparum LSA1 (PfLSA1) and PfLSAP2, and investigate

47 implemented in human malaria species such as P. falciparum and P. knowlesi, in part because the exten

48 Asymptomatic P. falciparum and Plasmodium vivax infections were clear

49 Asymptomatic P. falciparum infections are associated with decreased i

50 onitor gametocyte production in asymptomatic P. falciparum carriers allowing early detection and trea

51 in a cross-sectional survey of asymptomatic P. falciparum infections across all ages in Bongo Distri

52 Because P. falciparum lacks a cholesterol synthesis pathway and

53 previously documented compatibility between P. falciparum parasites expressing different Pfs47 haplo

54 rising prediction that mutations which block P. falciparum infection are most likely to be found in p

55 emale and male gametocytes per 2.5 uL blood, P. falciparum-positive individuals detected exclusively

56 For both P. falciparum and Plasmodium vivax, there is a solid evi

57 of the M1 and M17 aminopeptidases from both P. falciparum ( Pf-M1 and Pf-M17) and P. vivax ( Pv-M1 a

58 ries, a higher risk for severe malaria, both P. falciparum and non-falciparum, was observed among new

59 ose who are susceptible-to malaria caused by P. falciparum.

60 d thereby provides insights into invasion by P. falciparum.

61 c phosphorylation of erythrocyte proteins by P. falciparum but not by Plasmodium knowlesi, which does

62 ock protein (Hsp)70-class protein chaperone, P. falciparum Hsp70-x (PfHsp70-x).

63 bitor scaffold was previously shown to clear P. falciparum infection in a rodent model in vivo and bl

64 Individuals living in households of clinical P. falciparum patients were more likely to have qPCR det

65 al participants usually harbour multi-clonal P. falciparum infections, deep amplicon sequencing (AmpS

66 and children with microscopically confirmed P. falciparum malaria.

67 or of this work, BH267.meta, killed cultured P. falciparum parasites with nanomolar efficacy and did

68 by continuous culturing of the W2mef and Dd2 P. falciparum strains in moving suspension as opposed to

69 duced DV destabilization in PI(3)P-deficient P. falciparum precedes cell death and is reversible afte

70 Artemisinin resistance (delayed P. falciparum clearance following artemisinin-based comb

71 iparum malaria or Pfhrp2- and Pfhrp3-deleted P. falciparum parasites.

72 ion can inexpensively screen for low-density P. falciparum, non-falciparum, and Pfhrp2/3-deleted para

73 rum malaria species and low parasite density P. falciparum infections.

74 Blood samples were collected to detect P. falciparum by microscopy and polymerase chain reactio

75 sts are not sufficiently sensitive to detect P. falciparum in asymptomatic individuals.

76 ients were more likely to have qPCR detected P. falciparum infections (22.0%, 9/41) compared to indiv

77 e to recognize native VAR2CSA from different P. falciparum genotypes and to inhibit the interaction b

78 ory of var gene expression in three distinct P. falciparum clones, 3D7, HB3, and IT4/FCR3 by promoter

79 ng of distinct nutritional signals can drive P. falciparum to alter the key blood-stage processes of

80 of endothelial activation increased in early P. falciparum and P. vivax infection and preceded change

81 Clemastine destabilized all eight P. falciparum TRiC subunits based on thermal proteome pr

82 We estimated P. falciparum parasite loads in three groups of children

83 dies inhibited binding of VAR2CSA expressing P. falciparum-infected erythrocytes to CSA in a standard

84 e (AGAP008138, FREP1, and HPX15) facilitated P. falciparum transmission to mosquitoes.

85 against P. vivax and Plasmodium falciparum (P. falciparum) NMTs.

86 85 single-cell genome sequences from fifteen P. falciparum malaria patients from Chikhwawa, Malawi-an

87 aria-naive adults upregulated PD-1 following P. falciparum stimulation in vitro Additionally, functio

88 cases and 0.089 (95% CI = 0.076, 0.103) for P. falciparum cases.

89 ) for P. vivax and 3.0 (95% CI: 1.7-5.4) for P. falciparum (both P < .001).

90 d for HRP2 by bead-based immunoassay and for P. falciparum 18S rDNA by photo-induced electron transfe

91 , we screened a yeast two-hybrid library for P. falciparum proteins that interact with P. falciparum

92 erized by a panel of microsatellite loci for P. falciparum (26) and P. vivax (11), respectively.

93 infected An. arabiensis tested negative for P. falciparum gametocytes and, on experimental infection

94 nancy is a particularly high-risk period for P. falciparum infection during pregnancy, especially for

95 , mathematical models have been proposed for P. falciparum SMFA (PfSMFA), but such study for DMFA is

96 This is particularly relevant for P. falciparum, the only known human-infective species of

97 Screening for P. falciparum infections, using both microscopy- and pol

98 ch to reactive case detection strategies for P. falciparum in Ethiopia.

99 y of P. vivax, how the parasite differs from P. falciparum, and the key features that render it more

100 basis of CPS-induced immune protection from P. falciparum infection.

101 Overall, 14,146 (92.2%) patients had P. falciparum monoinfection and 1,195 (7.8%) mixed infec

102 oquine induces protection against homologous P. falciparum sporozoite (PfSPZ) challenge, but whether

103 and HIV, and co-infections between hookworm, P. falciparum and E. histolytica/dispar, were assessed u

104 How P. falciparum bridges two transmission seasons months ap

105 l help advance mechanistic research into how P. falciparum parasites acquire resistance to current fi

106 athway for the origin and evolution of human P. falciparum malaria and may inform molecular surveilla

107 Finally, since its transfer to humans, P. falciparum, and also the RH5 ligand, have evolved a s

108 tage P. falciparum parasites(2), we identify P. falciparum glutamic-acid-rich protein (PfGARP) as a p

109 ed parasite Toxoplasma gondii and implicated P. falciparum FtsH1 as a likely target in malaria parasi

110 ctors affecting disease severity in imported P. falciparum and non-falciparum malaria.

111 In P. falciparum, the heterochromatic virulence gene cluste

112 In P. falciparum, the most virulent species, the equilibrat

113 Prolongation of AA catabolism in P. falciparum-infected females also compromises the deve

114 y roles of PfHsp70-x and human chaperones in P. falciparum biology and how specific inhibitors may as

115 e, the metabolic dependency of chorismate in P. falciparum remains unclear.

116 ential metabolic dependency on chorismate in P. falciparum.

117 re tested either alone or in combinations in P. falciparum growth inhibition assay to determine Bliss

118 Target deconvolution in P. falciparum has shown that cladosporin inhibits lysyl-

119 according to WHO 2015 criteria was found in P. falciparum (9.4%), P. vivax (7.7%), P. ovale (5.3%),

120 Deleting the homologous gene in P. falciparum, PfDegP, similarly lowers heme levels and

121 CRP levels were moderately higher in P. falciparum infections with confirmed antigenemia vers

122 antimalarial drug by targeting the kinase in P. falciparum that phosphorylates Ser-33 of PfCRT.

123 e identification of resistance mechanisms in P. falciparum, the mode of action of IZPs remains unknow

124 ar, metabolomic, and chemogenomic methods in P. falciparum.

125 hylcytosine-like (5hmC-like) modification in P. falciparum asexual blood stages using a suite of bioc

126 stance is primarily mediated by mutations in P. falciparum Kelch13 protein (K13), a protein involved

127 Severe malaria was observed in P. falciparum and non-falciparum episodes.

128 ominant cytosine DNA modification pathway in P. falciparum and opens up exciting avenues for gene reg

129 Targeting these repair pathways in P. falciparum may be used to block adaptation to antimal

130 suggest the presence of two Ca(2+) pools in P. falciparum with differential sensitivity to the sarco

131 increases gametocyte quantity and quality in P. falciparum culture.

132 sufficient to confer actinonin resistance in P. falciparum.

133 release Ca(2+) from intracellular stores in P. falciparum parasites; (ii) Thg is able to induce Ca(2

134 are efficiently and accurately translated in P. falciparum cells.

135 evels of the major TRiC substrate tubulin in P. falciparum parasites.

136 te sequestration in postcapillary venules in P. falciparum malaria.

137 he Magude project fell short of interrupting P. falciparum transmission with the coverages achieved.

138 This study provides new insights into P. falciparum infection dynamics that should be consider

139 nd to infected RBCs and killed intracellular P. falciparum via the transfer of the granzymes, which w

140 eved to be benign bystanders, potently kills P. falciparum at low exogenous concentrations.

141 utations capable of blocking the more lethal P. falciparum have not succeeded in malarious zones.

142 opy to observe cholesterol transport in live P. falciparum parasites and structurally investigate ery

143 profile and metabolic roles of the 56-member P. falciparum serine hydrolase superfamily in the asexua

144 ange, successfully detecting sub-microscopic P. falciparum infections at less than 0.75 infected eryt

145 influencing submicroscopic (and microscopic) P. falciparum infections during the 3 trimesters of preg

146 ovale (5.3%), P. malariae (3.3%), and mixed P. falciparum episodes (21.1%).

147 The use of genetically modified P. falciparum revealed that PfEMP1 was a major target of

148 rt to the role of Pfs47 in the adaptation of P. falciparum to different vectors.

149 Metabolomic analysis of P. falciparum parasites in vitro showed no evidence that

150 an introgressed sequence in the ancestor of P. falciparum containing rh5, which likely allowed the a

151 ferred its genome segment to the ancestor of P. falciparum, while the other lineages exhibit host-spe

152 PfEMP1 is the major surface antigen of P. falciparum-infected erythrocytes, mediates endothelia

153 The burden of P. falciparum malaria was reduced to a greater extent th

154 ions related strongly to the total burden of P. falciparum parasites.

155 ich has one of the largest global burdens of P. falciparum malaria.

156 Dilution cloning of P. falciparum transfectants showed that individual clone

157 typing revealed a marked temporal cluster of P. falciparum infections, almost exclusively comprised o

158 ons of the circumsporozoite protein (CSP) of P. falciparum.

159 transport system operates in the cytosol of P. falciparum-infected erythrocytes as a cholesterol imp

160 ive and robust POC test for the detection of P. falciparum infection.

161 Here we show that the development of P. falciparum can be rapidly and completely blocked when

162 and fresh insight into why the efficiency of P. falciparum invasion might vary across the heterogenou

163 t, 12 episodes of P. vivax and 6 episodes of P. falciparum were observed in 11 splenectomised patient

164 a key step in the emergence and evolution of P. falciparum.

165 tection may be related to impaired export of P. falciparum virulence proteins.

166 and can support the intracellular growth of P. falciparum similar to wild-type cells.

167 A hallmark of P. falciparum malaria is extensive remodeling of host er

168 reatment-seeking behaviour, the incidence of P. falciparum malaria fell from 511 to 249 per 1,000 per

169 was variant dependent: binding inhibition of P. falciparum strain NF54 (P < 0.001) but not of the str

170 ddition of soluble CR1, a known inhibitor of P. falciparum invasion.

171 Here we show that low levels of P. falciparum parasites persist in the blood of asymptom

172 y using a newly generated transgenic line of P. falciparum (PfGCaMP3) that expresses constitutively t

173 Thus, antibody-dependent lysis of P. falciparum-infected RBCs by NK cells may be a mechani

174 Blood-stage merozoites of P. falciparum invade erythrocytes, and this requires int

175 Using a mathematical model of P. falciparum malaria transmission and RTS,S vaccine imp

176 ndividual based, spatially explicit model of P. falciparum malaria transmission that includes all the

177 nally associated with an increased number of P. falciparum infections (adjusted incidence rate ratio

178 fter 17 weeks of gestation, on the number of P. falciparum infections, focusing on submicroscopic inf

179 tic regions of interest such as orthologs of P. falciparum drug resistance-associated loci (Pfdhfr, P

180 RDTs allows detection and quantification of P. falciparum parasites from asymptomatic patients with

181 y play a key role in determining the rate of P. falciparum parasite proliferation and malaria virulen

182 by simultaneously tackling the reservoir of P. falciparum and P. vivax infections.

183 mens and understanding growing resistance of P. falciparum to ART.

184 well suited for high-throughput screening of P. falciparum isolates to identify these gene deletions.

185 here is no significant skin sequestration of P. falciparum gametocytes.

186 into the prevalence and potential spread of P. falciparum isolates that escape surveillance by RDTs.

187 rfamily in the asexual erythrocytic stage of P. falciparum.

188 lopment of both asexual and sexual stages of P. falciparum in a defined medium in the absence of an e

189 occurs during the live erythrocyte stages of P. falciparum.

190 parasite densities covering eight strains of P. falciparum from different geographical areas.

191 exual 3D7 (chloroquine-sensitive) strains of P. falciparum parasites.

192 e measured invasion of laboratory strains of P. falciparum relying on distinct invasion pathways into

193 7) and chloroquine-resistant (W2) strains of P. falciparum.

194 Most studies of P. falciparum genetic diversity have focused on single-n

195 Moreover, oral treatment of P. falciparum episodes with parasitemia >=2% without sev

196 of P. vivax parasitaemia after treatment of P. falciparum malaria that varied significantly between

197 of vivax parasitaemia following treatment of P. falciparum was 31.1% (95% CI 28.9-33.4) after AL, 14.

198 tent scaffold with mid-nanomolar activity on P. falciparum blood stage and gamete development.

199 of these post-translational modifications on P. falciparum biology and, in particular, the drug resis

200 r to rPfMSP2-elicited antibody at opsonizing P. falciparum merozoites for phagocytosis.

201 lowing inoculation with P. vivax (n = 16) or P. falciparum (n = 15), with the angiopoietin-2 level al

202 after CHMI with either P. vivax (n = 18) or P. falciparum (n = 18), were tested for the presence of

203 month following CHMI with either P. vivax or P. falciparum, >60% of subjects seroconverted to homolog

204 Our P. falciparum and P. vivax assays exhibited 100% sensiti

205 The primary outcome, P. falciparum prevalence by month 3 (M3), fell by 92% (f

206 ction on 7,393 samples, detecting an overall P. falciparum prevalence of 31.1% (SE = 1.1).

207 esistance by ~50% compared with the parental P. falciparum strain Dd2, whereas the phosphomimetic ami

208 cuole membrane-bound ABC transporter PfMDR1 (P. falciparum multidrug resistance 1 transporter).

209 h application with a large, multi-population P. falciparum dataset.

210 Prior P. falciparum infection was an important risk factor for

211 or recurrence (first or recurrent) was prior P. falciparum infection.

212 alarial activity against the human protozoan P. falciparum.

213 enetically modified isolates and recombinant P. falciparum erythrocyte membrane protein 1 (PfEMP1) do

214 Full Diversity Collection using recombinant P. falciparum PKG.

215 Silencing P47Rec expression reduced P. falciparum infection, indicating that the interaction

216 Genetically related P. falciparum, but not P. vivax infections showed strong

217 ssed selection by study regimens of relevant P. falciparum genetic polymorphisms associated with drug

218 P. berghei parasites expressing the relevant P. falciparum antigens and challenging mice at the peak

219 P. ovale infections and 2 (0.4%) represented P. falciparum parasites lacking Pfhrp2 and/or Pfhrp3.

220 ta T cells to kill late-stage blood-residing P. falciparum.

221 We generated actinonin resistant P. falciparum by in vitro selection and identified a spe

222 al therapy in areas of artemisinin-resistant P. falciparum in Viet Nam.

223 of low transmission or artemisinin-resistant P. falciparum, several single-site studies have been con

224 er-411 of PfCRT of the chloroquine-resistant P. falciparum strain Dd2 and show that kinase inhibitors

225 Prevalence of drug-resistant P. falciparum highlights the need to understand the biol

226 Selection of resistant P. falciparum in vitro was not achievable.

227 B02 inhibited a drug-sensitive P. falciparum strain (3D7) and multidrug-resistant paras

228 n Ghanaian and Gabonese children with severe P. falciparum malaria treated with parenteral artesunate

229 Factors associated with severe P. falciparum malaria were age <5 years and >40 years, o

230 Twenty-six P. falciparum microsatellites were genotyped in 66% of c

231 ke other human-infecting Plasmodium species, P. falciparum exports a family of 18 FIKK serine/threoni

232 une participants challenged with blood stage P. falciparum.

233 id killing of asexual liver- and blood-stage P. falciparum and blockade of gametocyte development, th

234 ethod to analyse the proteome of blood-stage P. falciparum parasites(2), we identify P. falciparum gl

235 In this study, we examined how mature-stage P. falciparum infected erythrocytes (IE) interact with t

236 al parasite-host cell ratios, schizont-stage P. falciparum-IE induced low levels of cell death.

237 re barrier disruptive than trophozoite-stage P. falciparum-IE and prolonged thrombin-induced barrier

238 Whereas trophozoite-stage P. falciparum-IE have limited effect on the viability of

239 y gametocyte-committed ring (gc-ring) stage, P. falciparum parasites in 260 uncomplicated malaria pat

240 tion of a systems genetics approach to study P. falciparum biology.

241 Of 221 participants with subclinical P. falciparum infections who participated in MDA and cou

242 of young age and those with a submicroscopic P. falciparum infection prior to pregnancy were at signi

243 The incidence rate of submicroscopic P. falciparum infections during pregnancy was 12.7 per 1

244 Here we show that all tested P. falciparum isolates contain an inactivating mutation

245 h risk of malaria, greater for P. vivax than P. falciparum.

246 ce drug susceptibility by demonstrating that P. falciparum can maintain expanded arrays of drug resis

247 In contrast to the common perception that P. falciparum diversity declines with decreasing transmi

248 We propose that P. falciparum virulence in areas of seasonal malaria tra

249 Here, we show that P. falciparum is an exception to this rule.

250 We provide data showing that P. falciparum malaria transmission is heterogeneous in t

251 These results suggest that P. falciparum has adopted a non-competitive evolutionary

252 ish between these hypotheses, we examine the P. falciparum cycle in an in vitro culture system and sh

253 Here we genotyped the P. falciparum K13 (Pfkelch13) propeller domain, mutation

254 uine, or piperaquine harbor mutations in the P. falciparum chloroquine resistance transporter (PfCRT)

255 with distinct sets of point mutations in the P. falciparum CQ-resistance transporter PfCRT, a 49-kDa

256 ian cells, we report 5hmC-like levels in the P. falciparum genome of 0.2-0.4%, which are significantl

257 hich translated into in vivo efficacy in the P. falciparum NOD-scid IL-2Rgamma(null) (NSG) mouse mode

258 end, we identified mRNA modifications in the P. falciparum transcriptome and performed a comprehensiv

259 Over the following 9 months, the P. falciparum prevalence increased to 3.3% (96/2,881) in

260 w-cost, high throughput interrogation of the P. falciparum genome, and can be tailored to simultaneou

261 summarizes the human-relevant stages of the P. falciparum life cycle and describes how licensed anti

262 targeting the pre-erythrocytic stages of the P. falciparum life cycle are the most advanced to date,

263 Members of the P. falciparum reticulocyte binding-like protein homolog

264 However, surface expression of the P. falciparum virulence protein PfEMP-1 was significantl

265 sequencing were identified, representing the P. falciparum heterozygome.

266 conditional mutants, we demonstrate that the P. falciparum Clp protease (PfClpP) has robust enzymatic

267 Thus, the P. falciparum reservoir in all ages can contribute to th

268 binant mosquito proteins interacted with the P. falciparum-infected cell lysates.

269 found that B02 is more potent against these P. falciparum strains than against mammalian cell lines.

270 as tested for immunoglobulin G antibodies to P. falciparum circumsporozoite protein (PfCSP) using enz

271 ent populations of unconventional T cells to P. falciparum infection.

272 P. vivax parasite stages but, in contrast to P. falciparum, does not affect trophozoites.

273 In contrast to P. falciparum, we observed that the higher transfection

274 We assessed the impact of exposure to P. falciparum on parasite kinetics, clinical symptoms, a

275 uine is safe and induces sterile immunity to P. falciparum in some recipients, but a single 45 mg dos

276 uine is safe and induces sterile immunity to P. falciparum in some recipients, but a single 45 mg dos

277 n of antibody-dependent NK cell responses to P. falciparum antigens is therefore warranted in the des

278 cantly changed mosquitoes' susceptibility to P. falciparum.

279 i) explain the rarity of strain-transcending P. falciparum infection blocking adaptations in humans;

280 bodies (mAbs) and perform a passive transfer-P. falciparum challenge study in Aotus nancymaae monkeys

281 Our goal was to generate transgenic P. falciparum lines that could complete the lifecycle an

282 egration site, we generated three transgenic P. falciparum lines in which tdtomato or gfp were stably

283 essential cellular functions to unannotated P. falciparum genes.

284 Unlike P. falciparum, which can invade all aged erythrocytes, P

285 Unfortunately, P. vivax, unlike P. falciparum, cannot be cultivated continuously in vitr

286 Additional in vitro P. falciparum culture studies were performed to determin

287 A total of 113 out of 300 patients were P. falciparum positive by microscopy.

288 The mechanism by which P. falciparum merozoites invade human erythrocytes is co

289 haracterize circulating acids in adults with P. falciparum malaria (n = 107) and healthy controls (n

290 partially protects against a challenge with P. falciparum.

291 wed varying sensitivities to compounds, with P. falciparum infected An. gambiae differing from P. ber

292 of patients presenting to the hospital with P. falciparum malaria (0.53% [100/18,965] versus 0.32% [

293 inical data from 17 volunteers infected with P. falciparum (3D7 strain) and reliably predicts observe

294 bind to erythrocytes that are infected with P. falciparum for diagnostic purposes, to disrupt host-p

295 to the surface of erythrocytes infected with P. falciparum.

296 ection and 1,195 (7.8%) mixed infection with P. falciparum and P. vivax.

297 SEP were at greatest risk of infection with P. falciparum, hookworm and E. histolytica/dispar, as we

298 etocytes and, on experimental infection with P. falciparum, sporozoites aren't detected in Microspori

299 g in participants following inoculation with P. falciparum For both species, the most pronounced incr

300 or P. falciparum proteins that interact with P. falciparum PKG (PfPKG) and tested peptide libraries t