ライフサイエンスコーパス: falciparum

1 human-to-mosquito transmission of Plasmodium falciparum.

2 urs during the live erythrocyte stages of P. falciparum.

3 derpinnings of drug resistance in Plasmodium falciparum.

4 ansmit the human malaria parasite Plasmodium falciparum.

5 rtially protects against a challenge with P. falciparum.

6 e signaling during infection with Plasmodium falciparum.

7 who are susceptible-to malaria caused by P. falciparum.

8 rial activity against the human protozoan P. falciparum.

9 orm of human malaria is caused by Plasmodium falciparum.

10 gainst the human malaria parasite Plasmodium falciparum.

11 the surface of erythrocytes infected with P. falciparum.

12 ed thick blood smear that was positive for P falciparum.

13 ficient to confer actinonin resistance in P. falciparum.

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

15 the lethal human malaria parasite Plasmodium falciparum.

16 tly changed mosquitoes' susceptibility to P. falciparum.

17 of the circumsporozoite protein (CSP) of P. falciparum.

18 infected with the human parasite Plasmodium falciparum.

19 or HRP2 by bead-based immunoassay and for P. falciparum 18S rDNA by photo-induced electron transfer p

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

21 pants were infected by bites from Plasmodium falciparum 3D7-infected mosquitoes (MB, n=12) or by indu

22 stablished a method for culturing Plasmodium falciparum, a breakthrough for malaria research worldwid

23 In the human malaria parasite Plasmodium falciparum, a unicellular eukaryotic pathogen, little is

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

25 h to the malaria-causing parasite Plasmodium falciparum, an organism that has resisted conventional s

26 ty and specificity on clinical samples (5 P. falciparum and 10 P. vivax samples).

27 tro culture of the human parasite Plasmodium falciparum and in vivo infections of laboratory animals

28 nant cytosine DNA modification pathway in P. falciparum and opens up exciting avenues for gene regula

29 lemented in human malaria species such as P. falciparum and P. knowlesi, in part because the extent t

30 Our P. falciparum and P. vivax assays exhibited 100% sensitivit

31 endothelial activation increased in early P. falciparum and P. vivax infection and preceded changes i

32 ocesses in experimentally induced Plasmodium falciparum and P. vivax infection.

33 In Adama district, Ethiopia, Plasmodium falciparum and P. vivax malaria patients and controls we

34 nzymes and equivalent activity on Plasmodium falciparum and Plasmodium vivax DHODH.

35 However, while cases of Plasmodium falciparum and Plasmodium vivax have decreased substanti

36 s during natural and experimental Plasmodium falciparum and Plasmodium vivax infections as well as du

37 For both P. falciparum and Plasmodium vivax, there is a solid eviden

38 r instance, the malarial parasite Plasmodium falciparum and the Lyme disease spirochete Borrelia burg

39 caused by the protozoan parasite Plasmodium falciparum and underscores the urgent need for new drugs

40 rvention (TBI) candidates against Plasmodium falciparum and vivax.

41 f P. vivax, how the parasite differs from P. falciparum, and the key features that render it more dif

42 tion, as a rosette-stimulator for Plasmodium falciparum- and P. vivax-IRBC.

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

44 Vaccines based on Plasmodium falciparum apical membrane antigen 1 (AMA1) have failed

45 in and partner-drug resistance in Plasmodium falciparum are major threats to malaria control and elim

46 cytosine-like (5hmC-like) modification in P. falciparum asexual blood stages using a suite of biochem

47 n addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and preve

48 d to be benign bystanders, potently kills P. falciparum at low exogenous concentrations.

49 n of a systems genetics approach to study P. falciparum biology.

50 hosphorylation of erythrocyte proteins by P. falciparum but not by Plasmodium knowlesi, which does no

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

52 ctinonin kills malaria parasites (Plasmodium falciparum) by interfering with apicoplast function.

53 Unfortunately, P. vivax, unlike P. falciparum, cannot be cultivated continuously in vitro,

54 tor gametocyte production in asymptomatic P. falciparum carriers allowing early detection and treatme

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

56 vation in the human malaria agent Plasmodium falciparum causes excessive multidirectional crystal bra

57 efficiently and accurately translated in P. falciparum cells.

58 The Plasmodium falciparum chloroquine resistance transporter (PfCRT) is

59 e, or piperaquine harbor mutations in the P. falciparum chloroquine resistance transporter (PfCRT), a

60 The Plasmodium falciparum circumsporozoite protein (PfCSP) is a sporozo

61 l antibodies (mAbs) targeting the Plasmodium falciparum circumsporozoite protein (PfCSP) on sporozoit

62 tested for immunoglobulin G antibodies to P. falciparum circumsporozoite protein (PfCSP) using enzyme

63 target, the repeat region of the Plasmodium falciparum circumsporozoite protein (PfCSP), plateaued a

64 Artemisinin resistance (delayed P. falciparum clearance following artemisinin-based combina

65 We analysed 1218 P. falciparum clinical isolates, and the results show that

66 ditional mutants, we demonstrate that the P. falciparum Clp protease (PfClpP) has robust enzymatic ac

67 The human malaria parasite, Plasmodium falciparum, contains an essential plastid called the api

68 Malaria infection by Plasmodium falciparum continues to afflict millions of people world

69 caused by the protozoan parasite Plasmodium falciparum continues to impose significant morbidity and

70 n has been achieved for both P. vivax and P. falciparum, controlled human transmission to mosquitoes

71 ol 3-phosphate (PI(3)P) levels in Plasmodium falciparum correlate with tolerance to cellular stresses

72 ntiplasmodial compounds against a Plasmodium falciparum CQ-resistant Dd2 strain, with excellent selec

73 reases gametocyte quantity and quality in P. falciparum culture.

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

75 It is now well established that Plasmodium falciparum emerged following the transmission of a goril

76 mber of the antigenically variant Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) famil

77 ail to provide optimal protection against P. falciparum, especially submicroscopic infections.

78 infection of the malaria parasite Plasmodium falciparum exhibits a 48-hour developmental cycle that c

79 n events in 119 progeny from four Plasmodium falciparum experimental crosses, using long-read data on

80 other human-infecting Plasmodium species, P. falciparum exports a family of 18 FIKK serine/threonine

81 n participants following inoculation with P. falciparum For both species, the most pronounced increas

82 nd to erythrocytes that are infected with P. falciparum for diagnostic purposes, to disrupt host-para

83 asite densities covering eight strains of P. falciparum from different geographical areas.

84 parasite Toxoplasma gondii and implicated P. falciparum FtsH1 as a likely target in malaria parasites

85 The Plasmodium falciparum gametocyte surface protein, Pfs48/45, is a po

86 fected An. arabiensis tested negative for P. falciparum gametocytes and, on experimental infection wi

87 nt in infected humans, developing Plasmodium falciparum gametocytes may express proteins on the surfa

88 Plasmodium falciparum gametocytes, the sexual stage responsible for

89 ny with host rhythms; (iii) 6% of Plasmodium falciparum genes show 24 h rhythms in expression under f

90 cells, we report 5hmC-like levels in the P. falciparum genome of 0.2-0.4%, which are significantly h

91 ost, high throughput interrogation of the P. falciparum genome, and can be tailored to simultaneously

92 e P. falciparum parasites(2), we identify P. falciparum glutamic-acid-rich protein (PfGARP) as a para

93 tested either alone or in combinations in P. falciparum growth inhibition assay to determine Bliss' a

94 antimalarial-resistant strains of Plasmodium falciparum (half maximal inhibitory concentration [IC50]

95 used by the apicomplexan parasite Plasmodium falciparum has served as a strong evolutionary force thr

96 tricate interactions the parasite Plasmodium falciparum has with its host allows it to grow and multi

97 tions capable of blocking the more lethal P. falciparum have not succeeded in malarious zones.

98 ilized three targets of interest (Plasmodium falciparum, Hepatitis C virus and T-cells) to demonstrat

99 uencing were identified, representing the P. falciparum heterozygome.

100 out a functional analysis of the Plasmodium falciparum homolog of Protein Phosphatase 1 (PfPP1), a u

101 pressed between the isolates lack Plasmodium falciparum homologs and are predicted to be involved in

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

103 an estimated 18-19% prevalence of Plasmodium falciparum in children 2-10 years in 2015-2016.

104 agnostic tests (RDTs) identifying Plasmodium falciparum in clinical and community settings.

105 to reactive case detection strategies for P. falciparum in Ethiopia.

106 he growth of the malaria parasite Plasmodium falciparum in human blood causes all the symptoms of mal

107 Plasmodium falciparum in pregnancy is a major cause of adverse preg

108 e is safe and induces sterile immunity to P. falciparum in some recipients, but a single 45 mg dose o

109 in and partner drug resistance in Plasmodium falciparum in the Greater Mekong Subregion (GMS).

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

111 derivative inhibits the growth of Plasmodium falciparum in vitro in the nanomolar range (IC(50) = 74

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

113 t emergence of drug resistance in Plasmodium falciparum increases the urgency to genetically validate

114 lunteer infection study using the Plasmodium falciparum induced blood-stage malaria model consisting

115 ant mosquito proteins interacted with the P. falciparum-infected cell lysates.

116 ansport system operates in the cytosol of P. falciparum-infected erythrocytes as a cholesterol import

117 Plasmodium falciparum-infected erythrocytes bind to specific endoth

118 It is expressed on the surface of Plasmodium falciparum-infected host red blood cells and binds to sp

119 ed control participants underwent Plasmodium falciparum-infected mosquito challenge (controlled human

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

121 ars in sub-Saharan Africa on prevalence of P falciparum infection and anaemia, clinical malaria, and

122 s a common presentation of severe Plasmodium falciparum infection and remains an important cause of d

123 ing prediction that mutations which block P. falciparum infection are most likely to be found in popu

124 explain the rarity of strain-transcending P. falciparum infection blocking adaptations in humans; (ii

125 Mosquito-transmitted Plasmodium falciparum infection can cause human cerebral malaria (H

126 utcomes of interest included prevalence of P falciparum infection detected by microscopy, anaemia (st

127 cy is a particularly high-risk period for P. falciparum infection during pregnancy, especially for th

128 p between placental pathology and Plasmodium falciparum infection in the placenta with PE is underexp

129 young age and those with a submicroscopic P. falciparum infection prior to pregnancy were at signific

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

131 and erythrocytic stages of P. berghei and P. falciparum infection, suggesting inclusion of ivermectin

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

133 study the immune response during Plasmodium falciparum infection.

134 populations of unconventional T cells to P. falciparum infection.

135 ts were more likely to have qPCR detected P. falciparum infections (22.0%, 9/41) compared to individu

136 ly associated with an increased number of P. falciparum infections (adjusted incidence rate ratio [aI

137 a cross-sectional survey of asymptomatic P. falciparum infections across all ages in Bongo District,

138 The incidence rate of submicroscopic P. falciparum infections during pregnancy was 12.7 per 100

139 luencing submicroscopic (and microscopic) P. falciparum infections during the 3 trimesters of pregnan

140 re quantified in 161 PCR-positive Plasmodium falciparum infections from a cross-sectional survey in P

141 malaria, we intensively followed Plasmodium falciparum infections in a cohort in a malaria endemic a

142 ing revealed a marked temporal cluster of P. falciparum infections, almost exclusively comprised of c

143 The majority of Plasmodium falciparum infections, constituting the reservoir in all

144 r 17 weeks of gestation, on the number of P. falciparum infections, focusing on submicroscopic infect

145 We sequence 2537 Plasmodium falciparum infections, including a nationally representa

146 Screening for P. falciparum infections, using both microscopy- and polyme

147 malaria species and low parasite density P. falciparum infections.

148 omains, mostly in children with documented P falciparum infections.

149 egions to characterize polyclonal Plasmodium falciparum infections.

150 ly with respect to submicroscopic Plasmodium falciparum infections.

151 n is being paid to submicroscopic Plasmodium falciparum infections.

152 After P. falciparum initially acquired free cholesterol or inner

153 phase of the parasite life cycle, Plasmodium falciparum invades red blood cells, where it catabolizes

154 fresh insight into why the efficiency of P. falciparum invasion might vary across the heterogenous p

155 ut proteins that interact with and affect P. falciparum invasion.

156 Plasmodium falciparum is a causative agent of human malaria.

157 ynthesis of the malaria parasite, Plasmodium falciparum is a key process for its survival and its inh

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

159 Plasmodium falciparum is the causative agent of the deadliest human

160 Plasmodium falciparum isolates (n = 914) from 2 randomized clinical

161 ned to determine the frequency of Plasmodium falciparum isolates with histidine-rich protein 2 (pfhrp

162 caused by the protozoan parasite Plasmodium falciparum Its life cycle is regulated by a cGMP-depende

163 Here we genotyped the P. falciparum K13 (Pfkelch13) propeller domain, mutations i

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

165 Infection with Plasmodium falciparum leads to severe malaria and death in approxim

166 mmarizes the human-relevant stages of the P. falciparum life cycle and describes how licensed antimal

167 gated combining two liver-stage antigens, P. falciparum LSA1 (PfLSA1) and PfLSAP2, and investigated t

168 with severe (N = 101) or acute uncomplicated falciparum malaria (N = 83) were recruited from 2 hospit

169 aged 2-65 years, with acute, uncomplicated P falciparum malaria alone or mixed with non-falciparum sp

170 cardiac function and volume status in severe falciparum malaria and its prognostic significance.

171 , we recruited patients with uncomplicated P falciparum malaria at 18 hospitals and health clinics in

172 with Epstein-Barr virus (EBV) and Plasmodium falciparum malaria coinfections.

173 hy participants, patients with uncomplicated falciparum malaria had shorter QT intervals (-61.77 mill

174 essfully reduced the incidence of Plasmodium falciparum malaria in many areas, there has been a consi

175 The RTS,S/AS01 vaccine against Plasmodium falciparum malaria infection completed phase III trials

176 load and the clinical severity of Plasmodium falciparum malaria infections.

177 Plasmodium falciparum malaria is widespread in the tropical and sub

178 Transmission of Plasmodium falciparum malaria parasites occurs when nocturnal Anoph

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

180 remaining safe and effective treatments for falciparum malaria that can be deployed rapidly in the G

181 ted to identify studies on severe Plasmodium falciparum malaria that included information on treatmen

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

183 Using a mathematical model of P. falciparum malaria transmission and RTS,S vaccine impact

184 identified efficacy studies of uncomplicated falciparum malaria treated with ACT that were undertaken

185 am infection and 35 children with Plasmodium falciparum malaria were analyzed using protein microarra

186 ated, and safe treatments of uncomplicated P falciparum malaria, including in areas with artemisinin

187 In severe falciparum malaria, unlike sepsis, hypotension on admiss

188 during, and after infection with Plasmodium falciparum malaria.

189 survival among children hospitalised with P falciparum malaria.

190 um vivax parasitaemia following treatment of falciparum malaria.

191 d children with microscopically confirmed P. falciparum malaria.

192 opment of coma and lactic acidosis in severe falciparum malaria.

193 h among children admitted to hospital with P falciparum malaria.

194 has one of the largest global burdens of P. falciparum malaria.

195 e revolutionized the treatment of Plasmodium falciparum malaria; however, resistance threatens to und

196 Malaria caused by Plasmodium falciparum manifests in many organ-specific fatal pathol

197 The mechanism by which P. falciparum merozoites invade human erythrocytes is compl

198 diversely in male gametes (e.g., Plasmodium falciparum microgametocytes and human and Drosophila mel

199 le membrane-bound ABC transporter PfMDR1 (P. falciparum multidrug resistance 1 transporter).

200 ing inoculation with P. vivax (n = 16) or P. falciparum (n = 15), with the angiopoietin-2 level also

201 ainst P. vivax and Plasmodium falciparum (P. falciparum) NMTs.

202 h translated into in vivo efficacy in the P. falciparum NOD-scid IL-2Rgamma(null) (NSG) mouse model.

203 ssessed the impact of exposure to Plasmodium falciparum on parasite kinetics, clinical symptoms, and

204 rther tested against P. vivax and Plasmodium falciparum (P. falciparum) NMTs.

205 Plasmodium falciparum, P. malariae and P. ovale sporozoite infectio

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

207 h convergent de novo mutations in Plasmodium falciparum parasite populations in Southeast Asia and So

208 lay a key role in determining the rate of P. falciparum parasite proliferation and malaria virulence.

209 P. falciparum parasites express Pfs47 haplotypes compatible

210 eviously documented compatibility between P. falciparum parasites expressing different Pfs47 haplotyp

211 Ts allows detection and quantification of P. falciparum parasites from asymptomatic patients with par

212 y season is a major challenge for Plasmodium falciparum parasites in many malaria endemic regions, wh

213 The apicoplast of Plasmodium falciparum parasites is believed to rely on the import o

214 Here we show that low levels of P. falciparum parasites persist in the blood of asymptomati

215 le and effective immunity against Plasmodium falciparum parasites remains an elusive goal in malaria

216 Plasmodium falciparum parasites resistant to chloroquine, amodiaqui

217 of this work, BH267.meta, killed cultured P. falciparum parasites with nanomolar efficacy and did not

218 od to analyse the proteome of blood-stage P. falciparum parasites(2), we identify P. falciparum gluta

219 s related strongly to the total burden of P. falciparum parasites.

220 al 3D7 (chloroquine-sensitive) strains of P. falciparum parasites.

221 ls of the major TRiC substrate tubulin in P. falciparum parasites.

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

223 ividuals living in households of clinical P. falciparum patients were more likely to have qPCR detect

224 S01 - the leading malaria vaccine against P. falciparum (Pf) - has been associated with the humoral r

225 otective humoral response against Plasmodium falciparum (Pf) circumsporozoite protein (PfCSP).

226 Plasmodium falciparum (Pf) relies solely on the salvage pathway for

227 A live-attenuated Plasmodium falciparum (Pf) sporozoite (SPZ) vaccine (PfSPZ Vaccine)

228 aseptic, purified, cryopreserved Plasmodium falciparum (Pf) sporozoites (PfSPZ Vaccine) and protecti

229 ith different species of malaria (Plasmodium falciparum [Pf] and Plasmodium vivax [Pv]) as well as wi

230 aseptic, purified, cryopreserved Plasmodium falciparum [Pf] sporozoites [SPZ]) has been well tolerat

231 The M17 aminopeptidases from Plasmodium falciparum (PfA-M17) and Plasmodium vivax (Pv-M17) funct

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

233 sing a newly generated transgenic line of P. falciparum (PfGCaMP3) that expresses constitutively the

234 t with the human malaria parasite Plasmodium falciparum played a key role in determining the genetic

235 hts into the pfhrp2 gene deletion amongst P. falciparum population from Sudan.

236 genetic structure across African Plasmodium falciparum populations indicates allelic adaptation to s

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

238 le and male gametocytes per 2.5 uL blood, P. falciparum-positive individuals detected exclusively by

239 on model fitted to our data predicted 16% P. falciparum-positive individuals that are likely to trans

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

241 ed DV destabilization in PI(3)P-deficient P. falciparum precedes cell death and is reversible after w

242 we found treatment significantly decreased P falciparum prevalence (adjusted RR [ARR] 0.46, 95% CI 0.

243 reatment was associated with reductions in P falciparum prevalence (risk ratio [RR] 0.27, 95% CI 0.17

244 hool-aged children significantly decreases P falciparum prevalence, anaemia, and risk of subsequent c

245 y, and ultimately pathogenesis of Plasmodium falciparum rely on a macromolecular complex, called the

246 easured invasion of laboratory strains of P. falciparum relying on distinct invasion pathways into re

247 highly effective vaccine against Plasmodium falciparum remains elusive.

248 Malaria caused by Plasmodium falciparum remains the leading single-agent cause of mor

249 ficacious subunit vaccine against Plasmodium falciparum remains to be licensed and deployed.

250 Thus, the P. falciparum reservoir in all ages can contribute to the m

251 Infection with Plasmodium falciparum results in immune dysfunction characterized b

252 Members of the P. falciparum reticulocyte binding-like protein homolog (Pf

253 deadly form of malaria in humans, Plasmodium falciparum, RIFINs form the largest family of surface pr

254 low transmission or artemisinin-resistant P. falciparum, several single-site studies have been conduc

255 late erythroblasts as a new host cell for P falciparum sexual stages and show that gametocytes can f

256 d can support the intracellular growth of P. falciparum similar to wild-type cells.

257 P falciparum malaria alone or mixed with non-falciparum species, and a temperature of 37.5 degrees C

258 the disease, ivermectin inhibits Plasmodium falciparum sporogonic and blood stage development and im

259 s protection against a homologous Plasmodium falciparum sporozoite (PfSPZ) challenge, but whether blo

260 The whole Plasmodium falciparum sporozoite (PfSPZ) vaccine is being evaluated

261 RTS,S is based on the major Plasmodium falciparum sporozoite surface antigen, circumsporozoite

262 ated administration of attenuated Plasmodium falciparum sporozoite vaccine.

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

264 man malaria infection (CHMI) with Plasmodium falciparum sporozoites.

265 cytes and, on experimental infection with P. falciparum, sporozoites aren't detected in Microsporidia

266 a-naive adults upregulated PD-1 following P. falciparum stimulation in vitro Additionally, functional

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

268 ensitive and multi-drug-resistant Plasmodium falciparum strains.

269 hat erythrocyte invasion plays in Plasmodium falciparum survival and reproduction makes this process

270 P. falciparum susceptibility to heme-binding antimalarials

271 tify that clemastine binds to the Plasmodium falciparum TCP-1 ring complex or chaperonin containing T

272 e diverse in the malaria parasite Plasmodium falciparum than previously postulated as we uncovered ac

273 ing to antimalarial resistance in Plasmodium falciparum, the most virulent human malaria parasite.

274 In the malaria parasite Plasmodium falciparum, the switch from asexual multiplication to se

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

276 s and understanding growing resistance of P. falciparum to ART.

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

278 oite form of the malaria parasite Plasmodium falciparum to invade red blood cells (RBCs).

279 rompt the human malaria parasite, Plasmodium falciparum, to acquire sophisticated molecular mechanism

280 Dilution cloning of P. falciparum transfectants showed that individual clones p

281 their role in cytoadherence, two Plasmodium falciparum transgenic lines expressing two variant prote

282 AGAP008138, FREP1, and HPX15) facilitated P. falciparum transmission to mosquitoes.

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

284 Multidrug-resistant Plasmodium falciparum undermines the efficacy of currently deployed

285 most lethal of malaria parasites, Plasmodium falciparum, uses to sense nutrient levels and elicit cha

286 growth rate of the 3D7 strain of Plasmodium falciparum using data from 177 subjects from 14 induced

287 Plasmodium falciparum vaccine RTS,S/AS01 is based on the major NPNA

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

289 , and whether the family includes Plasmodium falciparum variant surface proteins, such as RIFINs and

290 s (mRDTs), which generally detect Plasmodium falciparum via its abundant histidine-rich protein 2 (HR

291 to infected RBCs and killed intracellular P. falciparum via the transfer of the granzymes, which was

292 We propose that P. falciparum virulence in areas of seasonal malaria transm

293 However, surface expression of the P. falciparum virulence protein PfEMP-1 was significantly r

294 tion may be related to impaired export of P. falciparum virulence proteins.

295 vivax parasitaemia following treatment of P. falciparum was 31.1% (95% CI 28.9-33.4) after AL, 14.1%

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

297 Unlike P. falciparum, which can invade all aged erythrocytes, P. v

298 ggest the presence of two Ca(2+) pools in P. falciparum with differential sensitivity to the sarcopla

299 e spreading of malaria parasites, Plasmodium falciparum, with resistance to all known drugs calls for

300 ration, and egress of blood-stage Plasmodium falciparum, yet our understanding of Ca(2+) signaling in