ライフサイエンスコーパス: Plasmodium

1 Plasmodium berghei Yop1 (PbYop1) is a REEP5 homolog in P

2 Plasmodium falciparum (Pf) relies solely on the salvage

3 Plasmodium falciparum gametocytes, the sexual stage resp

4 Plasmodium falciparum in pregnancy is a major cause of a

5 Plasmodium falciparum is a causative agent of human mala

6 Plasmodium falciparum is the causative agent of the dead

7 Plasmodium falciparum isolates (n = 914) from 2 randomiz

8 Plasmodium falciparum malaria is widespread in the tropi

9 Plasmodium falciparum parasites resistant to chloroquine

10 Plasmodium falciparum vaccine RTS,S/AS01 is based on the

11 Plasmodium falciparum, P. malariae and P. ovale sporozoi

12 Plasmodium falciparum-infected erythrocytes bind to spec

13 Plasmodium homopolare (Family Plasmodiidae, Order Haemos

14 Plasmodium invasion of mosquito midguts is a mandatory s

15 Plasmodium invasion of red blood cells involves malaria

16 Plasmodium malariae is considered a minor malaria parasi

17 Plasmodium parasite-specific antibodies are critical for

18 Plasmodium parasites contain various virulence factors t

19 Plasmodium parasites experience significant bottlenecks

20 Plasmodium sporozoites express circumsporozoite protein

21 Plasmodium spp. parasites are the causative agents of ma

22 Plasmodium spp., the causative agent of malaria, have a

23 Plasmodium vivax gene regulation remains difficult to st

24 Plasmodium vivax is an important cause of malaria, assoc

25 Plasmodium vivax is the most widely distributed human ma

26 Plasmodium vivax, the most widely distributed human mala

27 We sequence 2537 Plasmodium falciparum infections, including a nationally

28 nanomolar antiplasmodial compounds against a Plasmodium falciparum CQ-resistant Dd2 strain, with exce

29 We found that a Plasmodium-specific lysine-rich insertion within the cat

30 h, to experimental time-series data of acute Plasmodium chabaudi infection across doses spanning seve

31 PIMMS43 genetic structure across African Plasmodium falciparum populations indicates allelic adap

32 million small molecules for activity against Plasmodium vivax (P. vivax) NMT.

33 ocking intervention (TBI) candidates against Plasmodium falciparum and vivax.

34 anaplacide) and GNF179 are effective against Plasmodium symptomatic asexual blood-stage infections, a

35 ting reliable and effective immunity against Plasmodium falciparum parasites remains an elusive goal

36 lived and effective humoral immunity against Plasmodium takes many years and multiple rounds of infec

37 g of the protective humoral response against Plasmodium falciparum (Pf) circumsporozoite protein (PfC

38 The RTS,S/AS01 vaccine against Plasmodium falciparum malaria infection completed phase

39 efforts, a highly effective vaccine against Plasmodium falciparum remains elusive.

40 ears, an efficacious subunit vaccine against Plasmodium falciparum remains to be licensed and deploye

41 PV5 inactivation in the human malaria agent Plasmodium falciparum causes excessive multidirectional

42 Here we report incidence of all Plasmodium species in Sabah, including zoonotic P. knowl

43 ion channel PIEZO1 were shown to ameliorate Plasmodium parasite growth, blood-brain barrier dysfunct

44 anomolar potency versus Plasmodium DHODH and Plasmodium parasites were identified with good pharmacol

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

46 URFIN), exported protein family 1 (EPF1) and Plasmodium Helical Interspersed Sub-Telomeric (PHIST) ge

47 valent activity on Plasmodium falciparum and Plasmodium vivax DHODH.

48 er, while cases of Plasmodium falciparum and Plasmodium vivax have decreased substantially, the incid

49 l and experimental Plasmodium falciparum and Plasmodium vivax infections as well as during immunizati

50 For both P. falciparum and Plasmodium vivax, there is a solid evidence that antibod

51 cuses on studies using Toxoplasma gondii and Plasmodium spp. as the best studied apicomplexans; howev

52 ses from Plasmodium falciparum (PfA-M17) and Plasmodium vivax (Pv-M17) function as catalytically acti

53 relationship between placental pathology and Plasmodium falciparum infection in the placenta with PE

54 s of malaria (Plasmodium falciparum [Pf] and Plasmodium vivax [Pv]) as well as with multiple clones o

55 comparative analysis between Toxoplasma and Plasmodium scRNA-seq results reveals concerted expressio

56 ties and further tested against P. vivax and Plasmodium falciparum (P. falciparum) NMTs.

57 by the parasite species Plasmodium vivax and Plasmodium ovale, which can arrest growth at an early, a

58 l new targets and strategies to improve anti-Plasmodium humoral immunity.

59 gonist, halofenozide, is able to induce anti-Plasmodium immune responses that limit Plasmodium ookine

60 The deadly symptoms of malaria occur as Plasmodium parasites replicate within blood cells.

61 ically important protozoan parasites such as Plasmodium, Entamoeba, Toxoplasma, and Leishmania secret

62 ria with those patients who had asymptomatic Plasmodium infection.

63 A live-attenuated Plasmodium falciparum (Pf) sporozoite (SPZ) vaccine (PfS

64 after repeated administration of attenuated Plasmodium falciparum sporozoite vaccine.

65 The interactions between Plasmodium parasites and human erythrocytes are prime ta

66 l for improving research on organisms beyond Plasmodium.

67 oes of inherited symbiotic microbes to block Plasmodium transmission.

68 Malaria caused by Plasmodium falciparum manifests in many organ-specific f

69 Malaria caused by Plasmodium falciparum remains the leading single-agent c

70 st severe form of human malaria is caused by Plasmodium falciparum.

71 Malaria, a parasitic infection caused by Plasmodium parasites and transmitted through the bite of

72 of malaria, an infectious disease caused by Plasmodium parasites.

73 s a prominent vector-borne illness caused by Plasmodium parasites.

74 Malaria infection by Plasmodium falciparum continues to afflict millions of p

75 hrocyte proteins by P. falciparum but not by Plasmodium knowlesi, which does not export FIKK kinases.

76 n is an additional evasion mechanism used by Plasmodium vivax to escape humoral immunity targeting Pv

77 attenuated, aseptic, purified, cryopreserved Plasmodium falciparum (Pf) sporozoites (PfSPZ Vaccine) a

78 attenuated, aseptic, purified, cryopreserved Plasmodium falciparum [Pf] sporozoites [SPZ]) has been w

79 reverse genetics can be scaled in culturable Plasmodium species.

80 nd Jensen established a method for culturing Plasmodium falciparum, a breakthrough for malaria resear

81 ythrocytic phase of the parasite life cycle, Plasmodium falciparum invades red blood cells, where it

82 nostic tests (mRDTs), which generally detect Plasmodium falciparum via its abundant histidine-rich pr

83 when present in infected humans, developing Plasmodium falciparum gametocytes may express proteins o

84 nto the development of CD4+ Tfh cells during Plasmodium infection and highlights the heterogeneity of

85 modelling to track memory development during Plasmodium infection and treatment.

86 ced (Ag-exp) CD4(+) T cell exhaustion during Plasmodium yoelii nonlethal infection occurs alongside t

87 ortunity to study the immune response during Plasmodium falciparum infection.

88 Our results provide evidence that during Plasmodium male gametogony, this divergent cyclin/CDK pa

89 Efforts to eradicate Plasmodium vivax malaria are hampered by the presence of

90 Erythrocytic Plasmodium parasite forms refractory to enrichment remai

91 Since then, multiple attempts to establish Plasmodium vivax in continuous culture have failed.

92 In Adama district, Ethiopia, Plasmodium falciparum and P. vivax malaria patients and

93 ne responses during natural and experimental Plasmodium falciparum and Plasmodium vivax infections as

94 ne responses during natural and experimental Plasmodium infections can enhance our understanding of m

95 emiology of malaria, we intensively followed Plasmodium falciparum infections in a cohort in a malari

96 development and transmission bottlenecks for Plasmodium.

97 The dry season is a major challenge for Plasmodium falciparum parasites in many malaria endemic

98 rotocol, followed by SHERLOCK for 60 min for Plasmodium species-specific detection via fluorescent or

99 ite stimulation, as a rosette-stimulator for Plasmodium falciparum- and P. vivax-IRBC.

100 ovo mutation events in 119 progeny from four Plasmodium falciparum experimental crosses, using long-r

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

102 24 participants were infected by bites from Plasmodium falciparum 3D7-infected mosquitoes (MB, n=12)

103 Applied to whole-genome sequence data from Plasmodium parasites, Anopheles mosquitoes, and global h

104 we demonstrate that plasma-derived EVs from Plasmodium vivax patients (PvEVs) are preferentially upt

105 ally, the incidence of zoonotic malaria from Plasmodium knowlesi continues to increase, presenting a

106 re of the extracellular domain of a PIR from Plasmodium chabaudi We use structure-guided sequence ana

107 being found diversely in male gametes (e.g., Plasmodium falciparum microgametocytes and human and Dro

108 Parasites from the genus Plasmodium are the causative agents of malaria.

109 us disease caused by a parasite of the genus Plasmodium, and the emergence of parasites resistant to

110 ection of humans with parasites of the genus Plasmodium.

111 uine induces protection against a homologous Plasmodium falciparum sporozoite (PfSPZ) challenge, but

112 e marrow and provide further insights on how Plasmodium parasites interfere with erythropoiesis and c

113 f the most deadly form of malaria in humans, Plasmodium falciparum, RIFINs form the largest family of

114 ed rapid diagnostic tests (RDTs) identifying Plasmodium falciparum in clinical and community settings

115 on of a 20E agonist can significantly impact Plasmodium infection outcomes, reducing oocyst numbers a

116 ia MB) in the An. gambiae complex can impair Plasmodium transmission.

117 onic and blood stage development and impairs Plasmodium berghei development inside hepatocytes, both

118 As a microbe that impairs Plasmodium transmission that is non-virulent and vertica

119 ponsible for Duffy negativity, which impedes Plasmodium vivax infection, has reached high frequencies

120 In Plasmodium, IZPs inhibit protein trafficking, block the

121 berghei Yop1 (PbYop1) is a REEP5 homolog in Plasmodium.

122 tidylinositol 3-phosphate (PI(3)P) levels in Plasmodium falciparum correlate with tolerance to cellul

123 c potential of IL-4 against fatal malaria in Plasmodium berghei ANKA-infected C57BL/6J mice, an exper

124 ociated with clinical outcomes of malaria in Plasmodium-infected individuals.

125 isen through convergent de novo mutations in Plasmodium falciparum parasite populations in Southeast

126 d samples and for 0.006-1.5% parasitemias in Plasmodium-infected cultured red blood cells, and discri

127 tral role that erythrocyte invasion plays in Plasmodium falciparum survival and reproduction makes th

128 ene regulation and life cycle progression in Plasmodium spp.

129 Previous reports in Plasmodium knowlesi, another parasite species shown to i

130 Artemisinin and partner-drug resistance in Plasmodium falciparum are major threats to malaria contr

131 f artemisinin and partner drug resistance in Plasmodium falciparum in the Greater Mekong Subregion (G

132 he recurrent emergence of drug resistance in Plasmodium falciparum increases the urgency to genetical

133 A contributing to antimalarial resistance in Plasmodium falciparum, the most virulent human malaria p

134 genetic underpinnings of drug resistance in Plasmodium falciparum.

135 ersus in vitro samples serve unique roles in Plasmodium research.

136 facilitated genome-scale knockout screens in Plasmodium berghei and Toxoplasma gondii, in which poole

137 ne proteins in apicomplexans such as TRAP in Plasmodium and MIC2 in Toxoplasma.

138 superfamily, and whether the family includes Plasmodium falciparum variant surface proteins, such as

139 of these processes in experimentally induced Plasmodium falciparum and P. vivax infection.

140 Unlike other human-infecting Plasmodium species, P. falciparum exports a family of 18

141 evolutionary history of all human-infective Plasmodium species, the time and circumstances of their

142 vectors of the disease, ivermectin inhibits Plasmodium falciparum sporogonic and blood stage develop

143 we have utilized three targets of interest (Plasmodium falciparum, Hepatitis C virus and T-cells) to

144 BACKGROUNDInterventions that interrupt Plasmodium vivax transmission or eliminate dormant P. vi

145 ) is a key antimalarial drug thought to kill Plasmodium parasites by blocking protein translation in

146 entially expressed between the isolates lack Plasmodium falciparum homologs and are predicted to be i

147 anti-Plasmodium immune responses that limit Plasmodium ookinetes.

148 RTS,S is based on the major Plasmodium falciparum sporozoite surface antigen, circum

149 t more severe disease in a model of malaria (Plasmodium chabaudi chabaudi AS).

150 oinfected with different species of malaria (Plasmodium falciparum [Pf] and Plasmodium vivax [Pv]) as

151 We focus on malaria (Plasmodium) parasites which exhibit developmental rhythm

152 A putative new Plasmodium species widespread in chimpanzees, gorillas,

153 alaria parasites, we reveal that: (i) 57% of Plasmodium chabaudi genes exhibit daily rhythms in trans

154 -of-synchrony with host rhythms; (iii) 6% of Plasmodium falciparum genes show 24 h rhythms in express

155 The apicoplast of Plasmodium falciparum parasites is believed to rely on t

156 Asymptomatic carriers of Plasmodium parasites hamper malaria control and eradicat

157 However, while cases of Plasmodium falciparum and Plasmodium vivax have decrease

158 ributing to both pathogenesis and control of Plasmodium.

159 The radical cure of Plasmodium vivax and P. ovale requires treatment with pr

160 The complex life cycle of Plasmodium parasites is shared between two hosts, with i

161 mastine treatment leads to disorientation of Plasmodium mitotic spindles during the asexual reproduct

162 The genomic diversity of Plasmodium malariae malaria parasites is understudied, p

163 le of TLR3 in promoting the establishment of Plasmodium yoelii infection through delayed clearance of

164 y was designed to determine the frequency of Plasmodium falciparum isolates with histidine-rich prote

165 ane proteins expressed in the gametocytes of Plasmodium yoelii and identify that GEP1 is required for

166 ost active derivative inhibits the growth of Plasmodium falciparum in vitro in the nanomolar range (I

167 A clinical hallmark of Plasmodium infection, the paroxysm, is driven by pyrogen

168 s have successfully reduced the incidence of Plasmodium falciparum malaria in many areas, there has b

169 mical classes specific for the inhibition of Plasmodium NMTs over human NMTs, including multiple nove

170 y of a collection of selective inhibitors of Plasmodium NMT and serve as a starting point for subsequ

171 The majority of Plasmodium falciparum infections, constituting the reser

172 , gorillas, and bonobos places the origin of Plasmodium malariae in Africa.

173 infectivity, and ultimately pathogenesis of Plasmodium falciparum rely on a macromolecular complex,

174 The presence of Plasmodium vivax malaria parasites in the human bone mar

175 lawi, with an estimated 18-19% prevalence of Plasmodium falciparum in children 2-10 years in 2015-201

176 Unusually high rates of Plasmodium sporozoite infections were detected in An. fu

177 lution in mammals against the CSP repeats of Plasmodium sporozoites.

178 There is a high risk of Plasmodium vivax parasitaemia following treatment of fal

179 l parasite load and the clinical severity of Plasmodium falciparum malaria infections.

180 resent a method for separating all stages of Plasmodium-infected erythrocytes through lysis and remov

181 onal antibodies in mosquito sexual stages of Plasmodium.

182 he parasite growth rate of the 3D7 strain of Plasmodium falciparum using data from 177 subjects from

183 f multiple antimalarial-resistant strains of Plasmodium falciparum (half maximal inhibitory concentra

184 le antigens, is a well-described strategy of Plasmodium and other parasites to evade host immunity.

185 It is expressed on the surface of Plasmodium falciparum-infected host red blood cells and

186 unodominant CSP-derived epitope SYIPSAEKI of Plasmodium berghei in both sporozoite- and vaccine-induc

187 Transmission of Plasmodium falciparum malaria parasites occurs when noct

188 source of human-to-mosquito transmission of Plasmodium falciparum.

189 isinins have revolutionized the treatment of Plasmodium falciparum malaria; however, resistance threa

190 functions of the parasitophorous vacuole of Plasmodium blood stages.

191 mammalian enzymes and equivalent activity on Plasmodium falciparum and Plasmodium vivax DHODH.

192 Vaccines based on Plasmodium falciparum apical membrane antigen 1 (AMA1) h

193 Research on Plasmodium parasites has driven breakthroughs in reducin

194 is approaching elimination of the human-only Plasmodium species.

195 Gametocytes are the only Plasmodium life stage infectious to mosquitoes.

196 ern of gene expression is conserved in other Plasmodium species.

197 sis of antibody-mediated inhibition of other Plasmodium species via CSP binding remains unclear.

198 icacy of SWGA on mixed infections with other Plasmodium spp.

199 Malaria caused by the apicomplexan parasite Plasmodium falciparum has served as a strong evolutionar

200 his approach to the malaria-causing parasite Plasmodium falciparum, an organism that has resisted con

201 tems, in vitro culture of the human parasite Plasmodium falciparum and in vivo infections of laborato

202 rythrocytes infected with the human parasite Plasmodium falciparum.

203 hich is caused by the intracellular parasite Plasmodium.

204 on of PIMMS43 in the rodent malaria parasite Plasmodium berghei triggers robust complement activation

205 to ookinetes in the rodent malaria parasite Plasmodium berghei.

206 age of the infection of the malaria parasite Plasmodium falciparum exhibits a 48-hour developmental c

207 The growth of the malaria parasite Plasmodium falciparum in human blood causes all the symp

208 carried out with the human malaria parasite Plasmodium falciparum played a key role in determining t

209 ids are more diverse in the malaria parasite Plasmodium falciparum than previously postulated as we u

210 f the merozoite form of the malaria parasite Plasmodium falciparum to invade red blood cells (RBCs).

211 In the human malaria parasite Plasmodium falciparum, a unicellular eukaryotic pathogen

212 In the malaria parasite Plasmodium falciparum, the switch from asexual multiplic

213 itoes to transmit the human malaria parasite Plasmodium falciparum.

214 ic screen against the human malaria parasite Plasmodium falciparum.

215 needed by the lethal human malaria parasite Plasmodium falciparum.

216 e aspartic proteases in the malaria parasite Plasmodium Their functions are strikingly multifaceted,

217 For instance, the malarial parasite Plasmodium falciparum and the Lyme disease spirochete Bo

218 of malaria caused by the protozoan parasite Plasmodium falciparum and underscores the urgent need fo

219 Malaria caused by the protozoan parasite Plasmodium falciparum continues to impose significant mo

220 deaths are caused by the protozoan parasite Plasmodium falciparum Its life cycle is regulated by a c

221 l deregulation of PV5 in the rodent parasite Plasmodium berghei results in inordinate elongation of h

222 ized that an intrinsic clock in the parasite Plasmodium chabaudi underlies the 24-hour-based rhythms

223 The intricate interactions the parasite Plasmodium falciparum has with its host allows it to gro

224 olipid biosynthesis of the malaria parasite, Plasmodium falciparum is a key process for its survival

225 The human malaria parasite, Plasmodium falciparum, contains an essential plastid cal

226 le stages prompt the human malaria parasite, Plasmodium falciparum, to acquire sophisticated molecula

227 duced by infection with the rodent parasite, Plasmodium berghei ANKA (PbANKA) has been extensively us

228 ntibiotic actinonin kills malaria parasites (Plasmodium falciparum) by interfering with apicoplast fu

229 s that the most lethal of malaria parasites, Plasmodium falciparum, uses to sense nutrient levels and

230 The spreading of malaria parasites, Plasmodium falciparum, with resistance to all known drug

231 picomplexa, with a focus on three parasites: Plasmodium, Toxoplasma, and Cryptosporidium.

232 zoite surface protein designated as PIMMS43 (Plasmodium Infection of the Mosquito Midgut Screen 43) i

233 h genomic regions to characterize polyclonal Plasmodium falciparum infections.

234 etocytes were quantified in 161 PCR-positive Plasmodium falciparum infections from a cross-sectional

235 cule NMT inhibitor developed against related Plasmodium spp. is also functional in Toxoplasma.

236 ng regions of PbANKA and the closely related Plasmodium berghei NK65 (PbNK65), that does not cause EC

237 s of both sensitive and multi-drug-resistant Plasmodium falciparum strains.

238 Multidrug-resistant Plasmodium falciparum undermines the efficacy of current

239 l malaria is a common presentation of severe Plasmodium falciparum infection and remains an important

240 ally conducted to identify studies on severe Plasmodium falciparum malaria that included information

241 e cycle, CRK5 stably interacts with a single Plasmodium-specific cyclin (SOC2), although we obtained

242 urrent understanding of the unique solutions Plasmodium has evolved to these challenges and discuss t

243 is caused in humans by the parasite species Plasmodium vivax and Plasmodium ovale, which can arrest

244 active against both liver- and blood- stage Plasmodium parasites, including drug-resistant strains.

245 th, proliferation, and egress of blood-stage Plasmodium falciparum, yet our understanding of Ca(2+) s

246 dominate the acute response to a blood-stage Plasmodium infection and provide signals to direct B cel

247 cribing the role and function of blood-stage Plasmodium-induced plasmablasts but they also reveal new

248 nancy, mainly with respect to submicroscopic Plasmodium falciparum infections.

249 al attention is being paid to submicroscopic Plasmodium falciparum infections.

250 Interventions that effectively target Plasmodium vivax are critical for the future control and

251 ighlight the potential to selectively target Plasmodium TRiC-mediated protein folding for malaria int

252 New drugs that target Plasmodium species, the causative agents of malaria, are

253 We also demonstrated that Plasmodium berghei DHFR promoter is recognized and funct

254 It is now well established that Plasmodium falciparum emerged following the transmission

255 We show that Plasmodium berghei CDK-related kinase 5 (CRK5), is a cri

256 nally, using stalling reporters we show that Plasmodium cells evolved not to have a fully functional

257 The Plasmodium falciparum chloroquine resistance transporter

258 The Plasmodium falciparum circumsporozoite protein (PfCSP) i

259 The Plasmodium falciparum gametocyte surface protein, Pfs48/

260 The Plasmodium species that cause malaria are obligate intra

261 ese, the largest and most ubiquitous are the Plasmodium-interspersed repeat (PIR) proteins, with more

262 Together, our findings demonstrate the Plasmodium-tailored role of a lipocalin family member in

263 However, PI(3)P function during the Plasmodium stress response was unknown.

264 f systemic inflammation, septic shock in the Plasmodium chabaudi-infected mice and the P. berghei-ind

265 d in the DNA binding site of a member of the Plasmodium ApiAP2 transcription factor family, that we r

266 rs to a key target, the repeat region of the Plasmodium falciparum circumsporozoite protein (PfCSP),

267 We carried out a functional analysis of the Plasmodium falciparum homolog of Protein Phosphatase 1 (

268 ing WM382, that block multiple stages of the Plasmodium life cycle.

269 The complexity of the Plasmodium parasite and its life cycle poses a challenge

270 e clemastine inhibits multiple stages of the Plasmodium parasite that causes malaria, but the molecul

271 nfectious disease caused by parasites of the Plasmodium spp. that takes an estimated 435,000 lives ea

272 e-induced thermodynamic stabilization of the Plasmodium TRiC delta subunit, suggesting an interaction

273 n monoclonal antibodies (mAbs) targeting the Plasmodium falciparum circumsporozoite protein (PfCSP) o

274 ne and identify that clemastine binds to the Plasmodium falciparum TCP-1 ring complex or chaperonin c

275 en-label volunteer infection study using the Plasmodium falciparum induced blood-stage malaria model

276 We assessed the impact of exposure to Plasmodium falciparum on parasite kinetics, clinical sym

277 ntigen-specific CD4+ Tfh cells responding to Plasmodium infection in order to understand the generati

278 emory has been shown to occur in response to Plasmodium spp. in experimental model infections, and in

279 tly held views regarding B-cell responses to Plasmodium infections.

280 B-cell and antibody responses to Plasmodium spp., the parasite that causes malaria, are c

281 Mosquito-transmitted Plasmodium falciparum infection can cause human cerebral

282 African apes harbor at least twelve Plasmodium species, some of which have been a source of

283 o determine their role in cytoadherence, two Plasmodium falciparum transgenic lines expressing two va

284 unvaccinated control participants underwent Plasmodium falciparum-infected mosquito challenge (contr

285 nfection of red blood cells with unicellular Plasmodium parasites.

286 specific member of the antigenically variant Plasmodium falciparum erythrocyte membrane protein 1 (Pf

287 Compounds with nanomolar potency versus Plasmodium DHODH and Plasmodium parasites were identifie

288 ckets persist across the Amazon Basin, where Plasmodium vivax is the predominant infecting species.

289 ted understanding of the mechanisms by which Plasmodium parasites induce CM.

290 perhaps within the last 10,000 years, while Plasmodium vivax emerged earlier from a parasite lineage

291 The whole Plasmodium falciparum sporozoite (PfSPZ) vaccine is bein

292 l bloodstream infection and 35 children with Plasmodium falciparum malaria were analyzed using protei

293 ntrolled human malaria infection (CHMI) with Plasmodium falciparum sporozoites.

294 nga infection was negatively correlated with Plasmodium infection in the mosquito and wAnga influence

295 C57BL/6J mice were infected with Plasmodium yoelii yoelli 17XNL, and blood and tissues we

296 MCHC of healthy RBCs and RBCs infected with Plasmodium yoelii, a commonly studied rodent parasite mo

297 Infection with Plasmodium falciparum leads to severe malaria and death

298 sis before, during, and after infection with Plasmodium falciparum malaria.

299 Infection with Plasmodium falciparum results in immune dysfunction char

300 erythrocyte signaling during infection with Plasmodium falciparum.