ライフサイエンスコーパス: Plasmodium

1 development and transmission bottlenecks for Plasmodium.

2 l for improving research on organisms beyond Plasmodium.

3 ection of humans with parasites of the genus Plasmodium.

4 onal antibodies in mosquito sexual stages of Plasmodium.

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

6 ributing to both pathogenesis and control of Plasmodium.

7 hich is caused by the intracellular parasite Plasmodium.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 to ookinetes in the rodent malaria parasite Plasmodium berghei.

25 functions of the parasitophorous vacuole of Plasmodium blood stages.

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

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

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

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

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

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

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

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

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

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

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

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

38 Plasmodium falciparum (Pf) relies solely on the salvage

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

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

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

42 24 participants were infected by bites from Plasmodium falciparum 3D7-infected mosquitoes (MB, n=12)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 The Plasmodium falciparum chloroquine resistance transporter

58 The Plasmodium falciparum circumsporozoite protein (PfCSP) i

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

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

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

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

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

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

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

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

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

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

69 The Plasmodium falciparum gametocyte surface protein, Pfs48/

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

71 Plasmodium falciparum gametocytes, the sexual stage resp

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

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

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

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

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

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

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

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

80 Plasmodium falciparum in pregnancy is a major cause of a

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

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

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

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

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

86 Mosquito-transmitted Plasmodium falciparum infection can cause human cerebral

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

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

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

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

91 The majority of Plasmodium falciparum infections, constituting the reser

92 We sequence 2537 Plasmodium falciparum infections, including a nationally

93 h genomic regions to characterize polyclonal Plasmodium falciparum infections.

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

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

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

97 Plasmodium falciparum is a causative agent of human mala

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

99 Plasmodium falciparum is the causative agent of the dead

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

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

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

103 Infection with Plasmodium falciparum leads to severe malaria and death

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

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

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

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

108 Plasmodium falciparum malaria is widespread in the tropi

109 Transmission of Plasmodium falciparum malaria parasites occurs when noct

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

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

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

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

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

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

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

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

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

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

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

121 Plasmodium falciparum parasites resistant to chloroquine

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

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

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

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

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

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

128 Infection with Plasmodium falciparum results in immune dysfunction char

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

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

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

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

133 after repeated administration of attenuated Plasmodium falciparum sporozoite vaccine.

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

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

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

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

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

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

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

141 Multidrug-resistant Plasmodium falciparum undermines the efficacy of current

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 Plasmodium falciparum-infected erythrocytes bind to spec

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

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

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

165 genetic underpinnings of drug resistance in Plasmodium falciparum.

166 itoes to transmit the human malaria parasite Plasmodium falciparum.

167 erythrocyte signaling during infection with Plasmodium falciparum.

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

169 ic screen against the human malaria parasite Plasmodium falciparum.

170 needed by the lethal human malaria parasite Plasmodium falciparum.

171 rythrocytes infected with the human parasite Plasmodium falciparum.

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

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

174 Plasmodium homopolare (Family Plasmodiidae, Order Haemos

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 ria with those patients who had asymptomatic Plasmodium infection.

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

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

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

193 Plasmodium invasion of mosquito midguts is a mandatory s

194 Plasmodium invasion of red blood cells involves malaria

195 In Plasmodium, IZPs inhibit protein trafficking, block the

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

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

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

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

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

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

202 Plasmodium malariae is considered a minor malaria parasi

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

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

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

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

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

208 anti-Plasmodium immune responses that limit Plasmodium ookinetes.

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

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

211 Erythrocytic Plasmodium parasite forms refractory to enrichment remai

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

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

214 Plasmodium parasite-specific antibodies are critical for

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

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

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

218 Plasmodium parasites contain various virulence factors t

219 Plasmodium parasites experience significant bottlenecks

220 Asymptomatic carriers of Plasmodium parasites hamper malaria control and eradicat

221 Research on Plasmodium parasites has driven breakthroughs in reducin

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

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

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

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

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

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

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

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

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

231 nfection of red blood cells with unicellular Plasmodium parasites.

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

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

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

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

236 The Plasmodium species that cause malaria are obligate intra

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

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

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

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

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

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

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

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

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

246 reverse genetics can be scaled in culturable Plasmodium species.

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

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

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

250 Plasmodium sporozoites express circumsporozoite protein

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

252 ene regulation and life cycle progression in Plasmodium spp.

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

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

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

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

257 Plasmodium spp. parasites are the causative agents of ma

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

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

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

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

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

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

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

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

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

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

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

269 oes of inherited symbiotic microbes to block Plasmodium transmission.

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

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

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

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

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

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

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

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

278 valent activity on Plasmodium falciparum and Plasmodium vivax DHODH.

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

280 Plasmodium vivax gene regulation remains difficult to st

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

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

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

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

285 Plasmodium vivax is an important cause of malaria, assoc

286 Plasmodium vivax is the most widely distributed human ma

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

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

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

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

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

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

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

294 Plasmodium vivax, the most widely distributed human mala

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

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

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

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

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

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