ライフサイエンスコーパス: P. falciparum

1 P. falciparum apPOL, the first structural representative

2 P. falciparum erythrocytic stage growth in vitro is redu

3 P. falciparum exclusively infects human erythrocytes dur

4 P. falciparum malaria originated in Africa from a single

5 P. falciparum merozoites that lack PfMSP3.1 showed a mar

6 P. falciparum phenotypic plasticity is linked to the var

7 P. falciparum population genetic approaches offer promis

8 P. falciparum rapid diagnostic tests (RDTs) and molecula

9 P. falciparum virulence is related to adhesion and seque

10 d at least one P. vivax parasitaemia and 10% P. falciparum, by qPCR, both of which were predominantly

11 A total 1392 P. falciparum positive samples collected from eight ende

12 retrospectively sequenced the genomes of 194 P. falciparum isolates from five sites in Northwest Thai

13 Among the total 397 P. falciparum episodes, 310 were treated with oral regim

14 similar; 5601 P. vivax parasites/mL and 5158 P. falciparum parasites/mL.

15 ensitive (NF54) and -resistant (Dd2 and 7G8) P. falciparum strains with 5/6 having IC50 < 100 nM agai

16 From 2011-2015, 8653 P. falciparum cases leading to 98 deaths (11.3 per 1000

17 to 10 commonly used antimalarial drugs in 94 P. falciparum isolates from the China-Myanmar border are

18 Among potential new biomarkers, a P. falciparum homolog of insulin-degrading enzyme (PfIDE

19 8, are fast-acting compounds that can cure a P. falciparum infection in a humanized NOD/SCID mouse mo

20 lasma IgG in adults and children living in a P. falciparum malaria-endemic area in West Africa.

21 he discovery that mutations in portions of a P. falciparum gene encoding kelch (K13)-propeller domain

22 ge parasitaemia undetectable in vivo using a P. falciparum SCID mouse model.

23 In contrast to canonical actin, P. falciparum actin 1 (PfAct1) does not readily polymeri

24 lts also show that recruitment of FH affords P. falciparum merozoites protection from complement-medi

25 r results reveal differences between African P. falciparum strains in their capacity to evade TEP1-me

26 isplay nanomolar inhibitory activity against P. falciparum and P. vivax IspD and prevent the growth o

27 unctional growth inhibitory activity against P. falciparum in vitro.

28 possess potent antimalarial activity against P. falciparum parasites comparable to the known antimala

29 for in vitro antiplasmodial activity against P. falciparum strains.

30 e, an inhibitor with potent activity against P. falciparum, and low toxicity toward mammalian cells.

31 compared with that of latrunculin B against P. falciparum and a 16-fold improved selectivity ex vivo

32 of higher chloroquine concentrations against P. falciparum with resistance-conferring genotypes.

33 nd P. vivax in vitro, is efficacious against P. falciparum in in vivo rodent models, produces parasit

34 lts suggest that protective immunity against P. falciparum can be achieved via multiple mechanisms an

35 vivo efficacy models were 3.7 mg/kg against P. falciparum (95% confidence interval: 3.3-4.9 mg/kg) a

36 ted during the early immune response against P. falciparum infection, we investigated whether they co

37 e is a potential target for vaccines against P. falciparum.

38 Alarmingly, P. falciparum strains have acquired resistance to ART ac

39 -deleted parasites, representing 6.4% of all P. falciparum infections country-wide (95% confidence in

40 -binding cassette transporter known to alter P. falciparum susceptibility to multiple first-line anti

41 of pathogen antigens from both S. aureus and P. falciparum, and delivered by either DNA vaccination,

42 vivo IC50 64 nM), and murine P. berghei and P. falciparum infections (day 4 ED90 0.34 and 0.57 mg kg

43 ium falciparum and P. vivax: P. chabaudi and P. falciparum infect red blood cells (RBC) of all ages (

44 f the Erythrocyte binding antigen family and P. falciparum reticulocyte binding-like families.

45 rences in the specificities of the human and P. falciparum proteasome.

46 rum histidine-rich protein II (PfHRP-II) and P. falciparum lactate dehydrogenase (PfLDH) antigens are

47 ls for malaria, P. berghei-infected mice and P. falciparum-infected NOD-scid IL-2Rgamma(null) mice.

48 mined human infectiousness to mosquitoes and P. falciparum carriage by an ultrasensitive RNA-based di

49 imilar to that observed in human, mouse, and P. falciparum profilin.peptide complexes.

50 usters of malaria incidence for P. vivax and P. falciparum corresponded to the pre- and first two yea

51 Both P. vivax and P. falciparum density distributions were unimodal and lo

52 mpared with women with no detected antenatal P. falciparum infection, women with positive RDT finding

53 Subpatent antenatal P. falciparum infections were not associated with advers

54 ion against one of the lead malaria antigens P. falciparum CSP.

55 d invasion ligand knockout lines, as well as P. falciparum Senegalese clinical isolates and a short-t

56 equence data from over 400 African and Asian P. falciparum isolates to show that dblmsp and dblmsp2 e

57 We assessed P. falciparum-specific T-cell responses among Ugandan ch

58 o did or did not harbor chronic asymptomatic P. falciparum infection during the dry season.

59 allenge the notion that chronic asymptomatic P. falciparum infection maintains malaria immunity and s

60 Chronic asymptomatic P. falciparum infection predicted decreased clinical mal

61 ldren who did or did not harbor asymptomatic P. falciparum infections.

62 . vivax infections, 13% were predicted to be P. falciparum infections, and 4% were predicted to be mi

63 e challenged with double chimeric P. berghei-P. falciparum parasites expressing both PfUIS3 and PfTRA

64 n low transmission areas co-endemic for both P. falciparum and P. vivax are unknown.

65 tal structure-activity relationships in both P. falciparum and S. cerevisiae.

66 osome motor complex (GAP50, GAPM1-3) of both P. falciparum and P. berghei.

67 infection, CD8+ T cell responses induced by P. falciparum or P. vivax vaccine candidates based on MS

68 Placental accumulation is mediated by P. falciparum protein VAR2CSA, a leading PAM-specific va

69 but the immune regulatory mechanisms used by P. falciparum remain largely unknown.

70 as coadministered with the vaccine candidate P. falciparum thrombospondin-related adhesion protein (P

71 igen 175 (EBA-175) is the best-characterized P. falciparum invasion ligand, reported to recognize gly

72 echanism proposed for maintenance of chronic P. falciparum infections(7-9).

73 o both P. berghei and clinically circulating P. falciparum from malaria endemic areas in Kenya, but n

74 erythrocytes from recently sampled clinical P. falciparum samples, we measured serological conservat

75 In addition, we found that concurrent P. falciparum parasitemia also increases the likelihood

76 Microscopically confirmed P. falciparum and P. vivax infections during follow-up w

77 id lysophosphatidylcholine (LysoPC) controls P. falciparum cell fate by repressing parasite sexual di

78 Pfhrp2-deleted P. falciparum is a common cause of RDT-/PCR+ malaria amo

79 Spread of pfhrp2-deleted P. falciparum mutants, resistant to detection by HRP2-ba

80 malaria rapid diagnostic tests (RDTs) detect P. falciparum histidine rich protein 2 (PfHRP2) and cros

81 e stage-specific molecular methods to detect P. falciparum, we show that gametocytes-and not their no

82 that the common drug resistance determinants P. falciparum chloroquine resistance transporter (PfCRT)

83 l Set (TCAMS) using the previously developed P. falciparum female gametocyte activation assay (Pf FGA

84 g sensitivity profile of normally-developing P. falciparum ring stages and DHA-pretreated dormant rin

85 recognize erythrocytes infected by different P. falciparum isolates and opsonize these cells by bindi

86 as optimized using 12 geographically diverse P. falciparum reference strains and successfully applied

87 e forces in vitro, we genetically engineered P. falciparum to express geographically diverse PfCRT ha

88 Furthermore, the European P. falciparum mtDNA indicates a link with current Indian

89 his observational cohort study, we evaluated P. falciparum pathogenesis in vitro in RBCs from pregnan

90 transgenic P. berghei parasites that express P. falciparum sporozoite antigens, we have been able to

91 he folding state of heterologously expressed P. falciparum actin 1 (PfACTI) with the aim of assessing

92 screened proteomic data for highly expressed P. falciparum proteins and compared their features to th

93 id generation of transgenic DiCre-expressing P. falciparum lines in any genetic background.

94 mbining chimeric rodent parasites expressing P. falciparum antigens and a flow cytometric readout of

95 d the mitochondria of Plasmodium falciparum (P. falciparum) NF54-attB blood-stage parasites and evalu

96 nnate T cells that expand markedly following P. falciparum (Pf) infection in naive adults, but are lo

97 As for P. falciparum, CHMI studies with P. vivax will provide a

98 ed functional genetics toolkit available for P. falciparum, we establish the utility of this strategy

99 a, and Plasmodium species with a callout for P. falciparum (the DLM assay) that demonstrated sensitiv

100 nd that CD55 is an essential host factor for P. falciparum invasion.

101 n gametocyte prevalence decreased 3-fold for P. falciparum and 29% for P. vivax from 2010 to 2014.

102 s, but a higher proportion were positive for P. falciparum histidine rich protein 2 (192/246 [78.0%])

103 Current protocols for P. falciparum gametocyte culture usually require complex

104 omparative analysis of treatment regimen for P. falciparum malaria in adults in Stockholm during 2000

105 Antibodies specific for P. falciparum antigens were determined in uncomplicated

106 ty to seven anti-malarial drugs for 40 fresh P. falciparum field isolates via a flow cytometry method

107 elivery were tested for IgG to antigens from P. falciparum, P. vivax and other infectious diseases.

108 d capture-enrichment using gDNA derived from P. falciparum Plasmodium mitochondrial genome sequences

109 Furthermore, P. falciparum-infected erythrocytes isolated from patien

110 een Pfs47 genotype and resistance of a given P. falciparum isolate for TEP1 killing.

111 exhibited greater diversity than the global P. falciparum population, indicating a large and/or stab

112 Cultured clinical-grade P. falciparum parasites (NF54, 7G8, and 3D7B) and ex viv

113 smodium falciparum coinfection, although how P. falciparum exposure affects the dynamics of EBV infec

114 gene knockouts were not viable in the human P. falciparum pathogen, we used conditional knockdowns t

115 cular target within the parasites identified P. falciparum enolase (Pf enolase) as the strongest cand

116 In P. falciparum parasites that lack Pf92, we observed chan

117 In P. falciparum-infected patients, Vgamma9Vdelta2 T cells

118 e that the unexpected target of actinonin in P. falciparum and Toxoplasma gondii is FtsH1, a homolog

119 Together, the data show that changes in P. falciparum Ag-specific B cell subsets in HIV-infected

120 In conclusion, high AT content in P. falciparum is driven by a systematic mutational bias

121 185 potently and selectively inhibits Dxr in P. falciparum, and represents a promising lead compound

122 e have characterised replication dynamics in P. falciparum throughout schizogony, using DNA fibre lab

123 validated both in vitro by CRISPR editing in P. falciparum and in vivo by evolution of resistant Plas

124 O E1-activating and E2-conjugating enzyme in P. falciparum are distinct compared with human, suggesti

125 BRD3914 was evaluated in P. falciparum-infected mice, providing a cure after four

126 nd that RxLR motifs cannot mediate export in P. falciparum.

127 inactive pericentromeric heterochromatin in P. falciparum, a region devoid of the characteristic H3K

128 Heterogeneity in P. falciparum exposure and immunity can be independently

129 Drug-induced changes in metabolite levels in P. falciparum-infected erythrocytes were monitored over

130 nomics and experimental analysis of mRBPs in P. falciparum.

131 haracterize mRNA-binding proteins (mRBPs) in P. falciparum.

132 ed for sensitive detection of parasitemia in P. falciparum cultures.

133 under various environmental perturbations in P. falciparum can yield quantitative insights into funda

134 e first genome-wide nascent RNA profiling in P. falciparum.

135 otal of only thirteen prenylated proteins in P. falciparum, with suggestive evidence for an additiona

136 ting large scale translational repression in P. falciparum female gametocytes for the first time.

137 g a clear pathway to genome-scale screens in P. falciparum QIseq was also used to monitor the growth

138 The earliest transcriptomics studies in P. falciparum suggested a cascade of transcriptional act

139 and recently developed genetic technology in P. falciparum to show that the protein is essential for

140 a hierarchy of erythrocyte receptor usage in P. falciparum.

141 ent-infecting P. berghei and human-infecting P. falciparum parasites, we show that MTRAP is dispensab

142 idate fungal extract significantly inhibited P. falciparum infection in the midgut without cytotoxici

143 pathogen recognition molecule in inhibiting P. falciparum transmission in malaria endemic areas.

144 160 pM in a PfPKG kinase assay and inhibits P. falciparum blood stage proliferation in vitro with an

145 of the P. falciparum ENT1 (PfENT1) that kill P. falciparum parasites in culture.

146 a endemic areas in Kenya, but not laboratory P. falciparum strain NF54.

147 Estimated gestational age at last P. falciparum infection, but not P. vivax infection, was

148 EALs that support liver stage human malaria (P. falciparum) infection in vitro, and also after implan

149 rucially, also blocks transmission of mature P. falciparum gametocytes to Anopheles stephensi mosquit

150 properties of the multi drug resistant (MDR) P. falciparum Thai C2A parasite strain in the non-human

151 In the high-transmission setting, most P. falciparum-specific CD4(+) T-cells in children produc

152 Multiple P. falciparum lines selected in vitro for resistance to

153 e identify a parasite protein, which we name P. falciparum Merozoite Organizing Protein (PfMOP), as e

154 ociated with antibody levels in the neonate (P. falciparum merozoite, spearman rho median [range] 0.4

155 pses, children acquired equal numbers of new P. falciparum (Pf) and Pv blood-stage infections/year (P

156 injection with cryopreserved, isogenic NF54 P. falciparum sporozoites (PfSPZ) generated from 1 premo

157 s decreased 5-fold from 2006 to 2010; 72% of P. falciparum and 87% of P. vivax infections were submic

158 Anti-FBG serum also reduced >81% of P. falciparum infection to A. gambiae Finally, we showed

159 Therefore, binding of P. falciparum parasites to the erythrocyte directly acti

160 these topics highlight the unique biology of P. falciparum, and contribute to our understanding of me

161 sor expressed in subcellular compartments of P. falciparum provides the basis for studying complex pa

162 o explore antibody binding in the context of P. falciparum CSP, we used negative-stain electron micro

163 ted individuals or from in vitro cultures of P. falciparum, making them prone to high variation.

164 ay) that demonstrated sensitive detection of P. falciparum from plasma samples during initial evaluat

165 ntigens are widely deployed for detection of P. falciparum infection; however, these tests often miss

166 TOS strongly inhibited oocyst development of P. falciparum and Plasmodium berghei expressing PfCelTOS

167 toxicity or inhibition of the development of P. falciparum gametocytes or ookinetes.

168 that occur during sporogonic development of P. falciparum in the mosquito host.

169 rania subgenus, long before the emergence of P. falciparum.

170 e, we review the origin and globalization of P. falciparum and integrate this history with analysis o

171 and P. vivax IspD and prevent the growth of P. falciparum in culture, with EC50 values below 400 nM.

172 Growth of P. falciparum treated with RCB-185 was rescued by isopre

173 aptation, affecting most laboratory lines of P. falciparum.

174 rming that beta-catenin is a key mediator of P. falciparum adverse effects on endothelial integrity.

175 n agent-based stochastic simulation model of P. falciparum transmission was used to investigate the s

176 rogeneous effects on the clinical outcome of P. falciparum infection.

177 e-off between different clinical outcomes of P. falciparum infection could have been a major cause of

178 us efforts to model the changing patterns of P. falciparum transmission intensity in Africa have been

179 um berghei ANKA and in vitro phagocytosis of P. falciparum-infected RBCs by macrophages from SHP-1-de

180 usion protein also increased phagocytosis of P. falciparum-infected RBCs.

181 gnaling resulted in enhanced phagocytosis of P. falciparum-infected RBCs.

182 nts that likely predisposed the precursor of P. falciparum to colonize humans.

183 The prenylome of P. falciparum is dominated by Rab GTPases, in addition t

184 s for mortality found in the rising rates of P. falciparum malaria importation to China can serve to

185 Reports of P. falciparum lacking this protein are increasing, creat

186 Here, we examined resistance of P. falciparum isolates of African origin (NF54, NF165 an

187 evidence that KDU691 also kills DP-rings of P. falciparum ART-resistant strains expressing mutant K1

188 ate cGAS as an important cytosolic sensor of P. falciparum genomic DNA and reveal the role of the cGA

189 to the choline/ethanolamine-binding site of P. falciparum choline kinase, reflecting different types

190 te of clearance of the erythrocytic stage of P. falciparum in the SCID mouse model with an ED90 of 11

191 -451840 against asexual and sexual stages of P. falciparum and the activity on P. vivax have the pote

192 tone PTMs in 8 distinct life cycle stages of P. falciparum parasites.

193 vity against a multidrug resistant strain of P. falciparum and arrest parasites at the ring phase of

194 ibitory activity against multiple strains of P. falciparum and P. vivax in vitro, is efficacious agai

195 emisinin-resistant and -sensitive strains of P. falciparum by combining liquid chromatography-mass sp

196 tivity against multiple resistant strains of P. falciparum in vitro and show no cytotoxicity to mamma

197 vitro activity against different strains of P. falciparum, the toxicity, and the metabolic stability

198 atistical model that infers the structure of P. falciparum mixtures-including the number of strains p

199 potentially explaining the susceptibility of P. falciparum to DHA during early blood-stage developmen

200 gh transmission areas have shown transfer of P. falciparum-specific IgG, but the extent and factors i

201 ew perspective broadens our understanding of P. falciparum population structure and the dispersal of

202 te membrane protein 1 (PfEMP1), expressed on P. falciparum-infected erythrocytes, is a major family o

203 These data reveal the unusually open P. falciparum beta2 active site and provide valuable inf

204 asites deficient for MSP3, MSP6, MSPDBL1, or P. falciparum MSP1-19 (PfMSP1-19) was similar to that of

205 n. stephensi and the human malaria parasite, P. falciparum to conduct a comprehensive evaluation of t

206 tion with the human and the rodent parasites P. falciparum and Plasmodium berghei, respectively.

207 f the Plasmodium falciparum var gene/PfEMP1 (P. falciparum erythrocyte membrane protein 1) family tha

208 acuole membrane-spanning transporter PfMDR1 (P. falciparum multidrug resistance gene-1) as a determin

209 s, we find that a parasite esterase, PfPARE (P. falciparum Prodrug Activation and Resistance Esterase

210 3) during their first seasonal PCR-positive P. falciparum infection with those from malaria-naive Du

211 The most prevalent P. falciparum RDTs detect histidine-rich protein 2 (PfHR

212 weight suggests the importance of preventing P. falciparum infection early in pregnancy.

213 , was horizontally transferred into a recent P. falciparum ancestor.

214 Mice immunized with recombinant P. falciparum CelTOS in combination with the glucopyrano

215 the nontoxic orlandin significantly reduced P. falciparum infection intensity in mosquitoes.

216 details all the steps required for reliable P. falciparum gametocyte production and highlights commo

217 lood stages of drug-sensitive and -resistant P. falciparum strains, inhibits development of P. berghe

218 drug effectiveness" in artemisinin resistant P. falciparum malaria infections.

219 ation therapy in a pre-artemisinin resistant P. falciparum Thai isolate in this animal model.

220 s for the expansion of artemisinin-resistant P. falciparum.

221 ence and transmission of multidrug-resistant P. falciparum malaria.

222 ite the existence of "chloroquine-resistant" P. falciparum.

223 of PfHRP2-only RDTs is sufficient to select P. falciparum parasites lacking this protein, thus posin

224 oroquine-resistant and chloroquine-sensitive P. falciparum and determined whether QC and AO affect th

225 [SD]: +/- 0.0 nM) against the drug-sensitive P. falciparum NF54 strain.

226 were performed by sequential cloning of six P. falciparum isolates growing in human erythrocytes in

227 We report the use of a blood-stage P. falciparum CHMI model to assess blood-stage vaccine c

228 of gametocytes and asynchronous blood-stage P. falciparum parasites by microarray technology.

229 nal hydrophobic modifications in blood-stage P. falciparum.

230 ne [QC] and methylene blue [MB]) or to study P. falciparum (acridine orange [AO]).

231 PEs by immune sera was observed, suggesting P. falciparum erythrocyte membrane protein 1 expression.

232 al development efforts selectively targeting P. falciparum choline kinase.

233 and P. gaboni are 10-fold more diverse than P. falciparum, indicating a very recent origin of the hu

234 ammalian and fungal prenylomes, we find that P. falciparum possesses a restricted set of prenylated p

235 is contrasts with the simple hypothesis that P. falciparum isolates with a serologically conserved gr

236 Here we show that P. falciparum uses immune inhibitory receptors to achiev

237 Our results suggest that P. falciparum has acquired multiple RIFINs to evade the

238 This suggests that P. falciparum infection is associated with increased EBV

239 The P. falciparum genome encodes 10 aspartic proteases calle

240 The P. falciparum resistance-conferring genotype (pfcrt 76T)

241 uilibrate close to the level seen across the P. falciparum reference genome (80.6% AT).

242 functional IgG antibody response against the P. falciparum parasite.

243 novel mutation within the gene encoding the P. falciparum chloroquine resistance transporter, PfCRT.

244 ent malaria chimeric parasite expressing the P. falciparum CelTOS (PfCelTOS), we evaluated the protec

245 which has identified a primary role for the P. falciparum K13 protein.

246 dosing in rodents leading to efficacy in the P. falciparum SCID mouse malaria model.

247 We determine the structure of the P. falciparum 20S proteasome bound to the inhibitor usin

248 ibit the ethanolamine kinase activity of the P. falciparum choline kinase, leading to a severe decrea

249 oughput screen to identify inhibitors of the P. falciparum ENT1 (PfENT1) that kill P. falciparum para

250 y characterize the regulatory regions of the P. falciparum gene PF3D7_1234700, encoding a CPW-WPC pro

251 sis, and in vitro biochemical studies of the P. falciparum SUMO E1 and E2 enzymes, resulting in the i

252 lass of enzyme contributes to regulating the P. falciparum acetylome.

253 d versatility of the system by targeting the P. falciparum merozoite surface protein 1 gene (msp1), w

254 barrier to malaria transmission and that the P. falciparum Pfs47 gene allows the parasite to evade mo

255 In this study, we report that the P. falciparum translation enhancing factor (PTEF) reliev

256 Our results suggest that the P. falciparum- infected human erythrocyte contains numer

257 w single nucleotide polymorphisms within the P. falciparum genome were identified and only marginal d

258 ng site as well as the binding mode of BV to P. falciparum enolase.

259 d be recalled in human volunteers exposed to P. falciparum parasites in a controlled human malaria in

260 ro, Uganda, an area of very high exposure to P. falciparum We jointly quantified individual heterogen

261 inefficient, even after repeated exposure to P. falciparum, but the immune regulatory mechanisms used

262 The study suggests that early exposure to P. falciparum, which is not targeted for prevention by c

263 hese findings in the Xenopus model extend to P. falciparum in vivo, our data suggest that PfCRT might

264 onsistent to more susceptible An. gambiae to P. falciparum infection in the field.

265 Addition of external BV and haem to P. falciparum-infected red blood cell (RBC) cultures del

266 Immunity to P. falciparum declined prior to 2004, preceding the emer

267 This unexpected response of human mDCs to P. falciparum exhibited a transcriptional program distin

268 IgG levels were measured to P. falciparum and P. vivax antigens in 201 postpartum an

269 t of merozoite surface protein 1 (MSP119) to P. falciparum MSP8 (PfMSP8) facilitated antigen producti

270 Laverania species most distantly related to P. falciparum, as well as a new class of Duffy-binding-l

271 Antibody response to P. falciparum was determined in 4,112 individuals by ELI

272 Today, P. falciparum malaria is transmitted worldwide by more t

273 dium vivax where mefloquine is used to treat P. falciparum infection, drug pressure mediated by incre

274 study that reveals a mode of action for two P. falciparum choline kinase inhibitors both in vitro an

275 In the present study two P. falciparum isolates were cultivated using the two mos

276 CR)- and the prevalence of antibodies to two P. falciparum antigens (MSP-1, AMA-1).

277 o knockdown cells using a panel of wild-type P. falciparum laboratory strains and invasion ligand kno

278 und that the parasites causing uncomplicated P. falciparum disease in children were highly diverse an

279 ble to AL for the treatment of uncomplicated P. falciparum malaria in pediatric patients.

280 of MAS3 in 1005 patients with uncomplicated P. falciparum malaria in relation to molecular markers o

281 phase promoting factor of the unconventional P. falciparum cell cycle.

282 a classical LPS response, pointing to unique P. falciparum-induced activation pathways that may expla

283 s not associated with recent exposure unlike P. falciparum IgG, suggesting a difference in acquisitio

284 with mutations in two previously unreported P. falciparum drug resistance genes, an acetyl-CoA trans

285 ), (2) RDT-negative children whose untreated P. falciparum infections were detected retrospectively b

286 of hemoglobin (Hb) have been performed using P. falciparum maintained in mature erythrocytes, in vitr

287 d a genome-wide association study of ex vivo P. falciparum susceptibility to piperaquine.

288 I tests can give false-negative results when P. falciparum strains do not express this antigen.

289 for severe malaria in adults diagnosed with P. falciparum.

290 tory cytokine secretion, mDCs incubated with P. falciparum-infected erythrocytes activated antigen-sp

291 M form) colony experimentally infected with P. falciparum (NF54 strain) gametocyte cultures slightly

292 CR were >70% among individuals infected with P. falciparum and >85% among those infected with P. viva

293 were identified: (1) children infected with P. falciparum as detected by rapid diagnostic testing (R

294 10-14 years, respectively, and infected with P. falciparum genotypes conferring chloroquine resistanc

295 Infection with P. falciparum, hemoglobin concentration, use of intermit

296 s of the protozoan parasite Plasmodium, with P. falciparum being the deadliest.

297 blood mononuclear cells were stimulated with P. falciparum antigen, and interferon gamma (IFN-gamma),

298 n the phosphatidylethanolamine levels within P. falciparum, which explains the resulting growth pheno

299 First, C1INH bound to glycan moieties within P. falciparum glycosylphosphatidylinositol (PfGPI) molec

300 li, asymptomatic individuals with or without P. falciparum infection at the end of the 6-month dry se