ライフサイエンスコーパス: P. vivax

1 P. vivax binds the Duffy blood group antigen through its

2 P. vivax exclusively invades reticulocytes that is media

3 P. vivax IgG acquisition is not associated with recent e

4 P. vivax merozoite surface protein 3alpha (PvMSP3alpha)

5 P. vivax parasites were eliminated in all patients by da

6 P. vivax recurrences (all after day 35) occurred in 80/6

7 P. vivax shows a trend of regional adaptations that pose

8 P. vivax-infected patients were treated radically with c

9 on clinical samples (5 P. falciparum and 10 P. vivax samples).

10 ingle-cell gene expression profiles of 9,215 P. vivax parasites from bloodstream infections of Aotus

11 Among the 260 P. vivax patients (61% males [159/260]; age range 3-60)

12 We measured IgG antibody responses to 342 P. vivax proteins in longitudinal clinical cohorts condu

13 criteria was found in P. falciparum (9.4%), P. vivax (7.7%), P. ovale (5.3%), P. malariae (3.3%), an

14 ) and 100% for the Plasmodium genus (52/52), P. vivax (20/20), P. ovale (9/9), and P. malariae (6/6).

15 c mean parasite densities were similar; 5601 P. vivax parasites/mL and 5158 P. falciparum parasites/m

16 and splenectomized monkeys, we identified 67 P. vivax genes whose expression was spleen dependent.

17 an [range] 0.42 [0.33-0.66], PfVAR2CSA 0.69; P. vivax rho = 0.19 [0.09-0.3]).

18 Using genomic data on 88 P. vivax samples from western Thailand, we identified pv

19 We conducted a P. vivax volunteer infection study to characterise the a

20 We describe here a P. vivax recombinant modular chimera based on MSP1 (PvRM

21 However, a P. vivax vaccine has remained elusive by the scarcity of

22 al antibodies in protective immunity against P. vivax malaria.

23 Ab levels correlate with protection against P. vivax malaria.

24 vax and monoclonal antibodies raised against P. vivax Duffy binding protein (PvDBP).

25 emical properties and further tested against P. vivax and Plasmodium falciparum (P. falciparum) NMTs.

26 be exploited to develop therapeutics against P. vivax malaria.

27 DBP-based vaccines and therapeutics against P. vivax.

28 In this study, we analyzed P. vivax DMFA (PvDMFA) data from 22,236 mosquitoes teste

29 to bind Duffy-null erythrocytes, we analyzed P. vivax parasites obtained from two Duffy-null individu

30 crosatellite loci for P. falciparum (26) and P. vivax (11), respectively.

31 found in 11, P. knowlesi was found in 8, and P. vivax and P. cynomolgi were both found in 2.

32 ies independent, marking both P. berghei and P. vivax infected cells, and that MUC13 can be used to i

33 or 110 (11%), 45 (6%), and 23 (1%) cases and P. vivax accounted for 61 (6%), 17 (2%), and 8 (0.4%) ca

34 gG levels were measured to P. falciparum and P. vivax antigens in 201 postpartum and 201 controls ove

35 areas co-endemic for both P. falciparum and P. vivax are unknown.

36 Our P. falciparum and P. vivax assays exhibited 100% sensitivity and specifici

37 gainst multiple strains of P. falciparum and P. vivax in vitro, is efficacious against P. falciparum

38 ivation increased in early P. falciparum and P. vivax infection and preceded changes in the endotheli

39 rimentally induced Plasmodium falciparum and P. vivax infection.

40 Microscopically confirmed P. falciparum and P. vivax infections during follow-up were associated wit

41 tackling the reservoir of P. falciparum and P. vivax infections.

42 nhibitory activity against P. falciparum and P. vivax IspD and prevent the growth of P. falciparum in

43 istrict, Ethiopia, Plasmodium falciparum and P. vivax malaria patients and controls were examined, to

44 7.8%) mixed infection with P. falciparum and P. vivax.

45 he human parasites Plasmodium falciparum and P. vivax: P. chabaudi and P. falciparum infect red blood

46 te-stimulator for Plasmodium falciparum- and P. vivax-IRBC.

47 At thresholds for HRP2, pan LDH, and P. vivax LDH of 2.3 pg/ml, 47.8 pg/ml, and 75.1 pg/ml, r

48 m both P. falciparum ( Pf-M1 and Pf-M17) and P. vivax ( Pv-M1 and Pv-M17).

49 ge mass spectrometry, mutational mapping and P. vivax invasion studies.

50 P. vivax allelic variants (VK210, VK247 and P. vivax-like) and of the C-terminal region (shared by a

51 of all ages (RBC generalist); P. yoelii and P. vivax preferentially infect young RBCs (RBC specialis

52 ghput screening to prime and accelerate anti-P. vivax drug discovery efforts.

53 free from recurrence at 6 months, defined as P. vivax clearance without recurrent parasitemia.

54 A 2-year prospective cohort study to assess P. vivax morbidity after radical cure treatment and rela

55 100-fold), but the reservoir of asymptomatic P. vivax infections was reconstituted within 3 months, p

56 development of a highly protective CSP-based P. vivax vaccine, a virus-like particle (VLP) known as R

57 rall, 83% of infections were predicted to be P. vivax infections, 13% were predicted to be P. falcipa

58 ed the known amount of heterogeneity between P. vivax schizont transcriptomes from individual patient

59 ramework for generating new tools that block P. vivax blood stage infection.

60 Both P. vivax and P. falciparum density distributions were un

61 r-stage infection has been achieved for both P. vivax and P. falciparum, controlled human transmissio

62 ing the burden of Plasmodium falciparum, but P. vivax has been more refractory.

63 ion of Plasmodium parasitaemia, dominated by P. vivax, was shown to cluster at both household and com

64 e immature reticulocytes (CD71+) targeted by P. vivax invasion are enzymatically normal, even in hemi

65 We hypothesise that a candidate P. vivax vaccine with low efficacy against primary infec

66 en who received PQ were less likely to carry P. vivax gametocytes (IRR = 0.27 [95% CI 0.19, 0.38], p

67 ponses to eight P. vivax proteins classified P. vivax infections in the previous 9 months with 80% se

68 e associated with a reduced risk of clinical P. vivax malaria in rural Amazonians.

69 multifaceted intervention approach to combat P. vivax in the region.

70 nzyme deficiency; all patients had confirmed P. vivax parasitemia.

71 522 patients with microscopically confirmed P. vivax infection (>100 to <100,000 parasites per micro

72 ocytes is considered critical for continuous P. vivax growth in vitro.

73 We found that delaying P. vivax recurrence was associated with a small but sign

74 duals with high levels residing in different P. vivax-endemic areas worldwide competed with mAbs, sug

75 dium vivax transmission or eliminate dormant P. vivax liver-stage parasites will be essential for mal

76 that PvMSP3alpha antibodies acquired during P. vivax infection can mediate complement fixation and s

77 on of inhibitory receptors on T cells during P. vivax malaria impairs parasite-specific T-cell effect

78 shown that circulating microparticles during P. vivax acute attacks are indirectly associated with se

79 This study thus shows that during P. vivax infections, parasites are always present in the

80 to the development of a global and effective P. vivax vaccine.

81 appear as potential targets for efficacious P. vivax neutralization.

82 omon Islands and antibody responses to eight P. vivax proteins classified P. vivax infections in the

83 collected before and after CHMI with either P. vivax (n = 18) or P. falciparum (n = 18), were tested

84 oximately 1 month following CHMI with either P. vivax or P. falciparum, >60% of subjects seroconverte

85 approaches that may be required to eliminate P. vivax globally.

86 luding some that are specific to the elusive P. vivax male gametocytes, and will be useful for analyz

87 Using ZFNs specific to the gene encoding P. vivax dihydrofolate reductase (pvdhfr), we transfecte

88 rum, which can invade all aged erythrocytes, P. vivax is restricted to reticulocytes.

89 Compared to other eukaryotes, P. vivax genes tend to have unusually long 5' untranslat

90 ogenetic analysis of the eradicated European P. vivax mtDNA genome indicates that the European isolat

91 e linear B-cell epitope in naturally exposed P. vivax patient was identified at three linear epitopes

92 ing we generate a transgenic line expressing P. vivax Duffy binding protein (PvDBP), a lead vaccine c

93 sted for IgG to antigens from P. falciparum, P. vivax and other infectious diseases.

94 To gain more insights, we expressed five P. vivax spleen-dependent genes as recombinant proteins,

95 2016 to be 0.171 (95% CI = 0.165, 0.178) for P. vivax cases and 0.089 (95% CI = 0.076, 0.103) for P.

96 creased 3-fold for P. falciparum and 29% for P. vivax from 2010 to 2014.

97 The AHR was 7.8 (95% CI: 5.0-12.3) for P. vivax and 3.0 (95% CI: 1.7-5.4) for P. falciparum (bo

98 sponse and a promising vaccine candidate for P. vivax malaria.

99 is the most promising vaccine candidate for P. vivax malaria.

100 hat were undertaken in regions coendemic for P. vivax between 1 January 1960 and 5 January 2018.

101 nature but is convincingly demonstrated for P. vivax.

102 ted with a high risk of malaria, greater for P. vivax than P. falciparum.

103 However, for P. vivax, the most widely distributed and difficult to t

104 identification has therapy implications for P. vivax and P. ovale, which have dormant liver stages r

105 space-time clusters of malaria incidence for P. vivax and P. falciparum corresponded to the pre- and

106 rved antigen lactate dehydrogenase (LDH) for P. vivax and other malaria species.

107 lations in nonhuman primates, as methods for P. vivax cloning and in vitro cultivation remain unavail

108 -chimeric (huHep) FRG KO mice as a model for P. vivax infection.

109 unique biology, and proposes priorities for P. vivax research and control efforts.

110 at compared different treatment regimens for P. vivax malaria, patients with a normal standard NADPH

111 may encode potential ligands responsible for P. vivax infections of Duffy-negative Africans.

112 MSP1P-19 suggesting the species-specific for P. vivax.

113 ther clinical development as a treatment for P. vivax malaria.

114 n the next generation of potent vaccines for P. vivax malaria.

115 T-seq" to sequence the transcriptome of four P. vivax field isolates that were cultured for a short p

116 Finally, the protein fragments derived from P. vivax containing well-known antigen sequences were ca

117 osatellite genotyping showed relatively high P. vivax genetic diversity (mean heterozygosity, 0.843 [

118 on of genetically heterologous or homologous P. vivax infection recurrence following receipt of chlor

119 However, P. vivax infections have been documented in Duffy-negati

120 immunoassay for the quantification of HRP2, P. vivax LDH, and all-malaria LDH (pan LDH) was develope

121 Indeed, we show that Salvador (Sal) I P. vivax infects Squirrel monkeys independently of DBP1

122 This review discusses recent advances in P. vivax research, current knowledge of its unique biolo

123 nvolvement of complement receptor 1 (CR1) in P. vivax invasion.

124 -fold reduction suggests a recent decline in P. vivax transmission intensity and, thus, a substantial

125 small-to-moderate spatial scales differed in P. vivax parasite prevalence, and multilevel Poisson reg

126 revious reports of high genomic diversity in P. vivax relative to the more virulent Plasmodium falcip

127 vivax and P. falciparum, and were higher in P. vivax infection.

128 -19 sequences showed limited polymorphism in P. vivax worldwide isolates.

129 In contrast, alternative splicing is rare in P. vivax but its association with the late schizont stag

130 otection, thus prompting a paradigm shift in P. vivax biology toward deeper studies of the spleen dur

131 ocyte preference of a large number of Indian P. vivax isolates.

132 g-inhibitory antibodies (BIAbs) also inhibit P. vivax invasion of reticulocytes in vitro.

133 hat block DBPII-DARC interaction and inhibit P. vivax reticulocyte invasion, and Ab levels correlate

134 We also found that mAbs inhibited P. vivax entry into reticulocytes in vitro.

135 ding radical cure of short- and long-latency P. vivax malaria in Nepal.

136 lower limits of detection for HRP2, pan LDH, P. vivax LDH, and CRP were 0.2 pg/ml, 9.3 pg/ml, 1.5 pg/

137 ce has been replaced with either full-length P. vivax VK210 or the allelic VK247 csp that additionall

138 recent years, cases of severe and high-level P. vivax parasitemia have been reported, challenging the

139 vailability on the surface of RBCs modulates P. vivax invasion.

140 Most P. vivax studies must therefore rely on patient samples,

141 ntimalarial drug efficiently eliminates most P. vivax parasite stages but, in contrast to P. falcipar

142 Our results show that transcription of most P. vivax genes occurs during short periods of the intrae

143 asmodium falciparum while largely neglecting P. vivax.

144 turally acquired human antibodies neutralize P. vivax by targeting the binding site for Duffy antigen

145 , infectivity, and transmissibility of a new P. vivax isolate.

146 age at last P. falciparum infection, but not P. vivax infection, was positively associated with antib

147 Genetically related P. falciparum, but not P. vivax infections showed strong clustering within hous

148 hree and eight copies) in the two Duffy-null P. vivax infections suggests that an expansion of DBP1 m

149 analyses also indicate that more than 10% of P. vivax genes encode multiple, often undescribed, prote

150 f merozoite surface protein 1 (MSP-1(42)) of P. vivax and P. falciparum using an enzyme-linked immuno

151 006 to 2010; 72% of P. falciparum and 87% of P. vivax infections were submicroscopic in 2014.

152 mutations in DBP1 resulted in the ability of P. vivax to bind Duffy-null erythrocytes, we analyzed P.

153 s in DBP1 did not account for the ability of P. vivax to infect Duffy-null Africans.

154 data also greatly improve the annotations of P. vivax gene untranslated regions, providing an importa

155 trophozoites and that the asynchronicity of P. vivax infections is therefore unlikely to confound ge

156 Understanding the basis of P. vivax chloroquine resistance (CQR) will inform drug d

157 icle reviews the epidemiology and biology of P. vivax, how the parasite differs from P. falciparum, a

158 relapse prevention through the clearance of P. vivax parasitemia and hypnozoites, termed "radical cu

159 Cocrystallization of P. vivax NMT with one compound revealed peptide binding

160 is emerging research field in the context of P. vivax.

161 blish a system for the continuous culture of P. vivax.

162 uine showed efficacy for the radical cure of P. vivax malaria, although tafenoquine was not shown to

163 ntly been registered for the radical cure of P. vivax.

164 odels suitable to support the development of P. vivax vaccines candidates.

165 densities and the frequency distribution of P. vivax malaria attacks experienced by each individual

166 nity against some of the virulent effects of P. vivax malaria may be built up over the course of many

167 ve strategies for control and elimination of P. vivax.

168 14-month prospective cohort, 12 episodes of P. vivax and 6 episodes of P. falciparum were observed i

169 Eradication of P. vivax hypnozoites using primaquine (radical cure) and

170 laria pathology and support the existence of P. vivax-adherent parasite subpopulations in the microva

171 Specific biological features of P. vivax, particularly invasion of reticulocytes, occurr

172 the morphological and phenotypic features of P. vivax.

173 PQ also reduced the molecular force of P. vivax blood-stage infection in the first 3 mo of foll

174 n of the PVM with LC3 promotes the fusion of P. vivax compartments with lysosomes and subsequent kill

175 Here we investigate the genetics of P. vivax CQR by a cross of parasites differing in drug r

176 95% CI 0.48-0.49]), whereas the incidence of P. vivax malaria fell from 331 to 239 per 1,000 py (IRR

177 chemokines (DARC) and the dimer interface of P. vivax DBP.

178 he first population genomic investigation of P. vivax from the region, comparing the genomes of 24 Et

179 e authors injected a unique human isolate of P. vivax that reached high gametocyte density within wee

180 te invasion by multiple clinical isolates of P. vivax.

181 terventions has been hindered by the lack of P. vivax in vitro culture and could be accelerated by a

182 ria in a population exposed to low levels of P. vivax transmission, we measured total levels of immun

183 function of RBP2-P1 as an invasion ligand of P. vivax was evaluated.

184 A substantial number of P. vivax recurrences, mainly submicroscopic (SM) and asy

185 falciparum species; regional populations of P. vivax exhibited greater diversity than the global P.

186 omparing drug efficacy for the prevention of P. vivax infection relapse.

187 multivariable analyses, the highest rate of P. vivax parasitaemia over 42 days of follow-up was in p

188 ine, ACT administered, and PQ on the rate of P. vivax recurrence between days 7 and 42 after starting

189 the end of follow-up, the incidence rate of P. vivax was 2.2 episodes/person-year for patients treat

190 Rates of homologous recurrence of P. vivax infection appear to be clinically useful for co

191 Freedom from recurrence of P. vivax parasitemia at 6 months was the primary efficac

192 as a reduction in homologous recurrences of P. vivax infection as drug doses were increased.

193 was evident for heterologous recurrences of P. vivax infection.

194 this meta-analysis, we found a high risk of P. vivax parasitaemia after treatment of P. falciparum m

195 The risk of P. vivax parasitaemia at days 42 and 63 and associated r

196 The primary endpoints were the risk of P. vivax recurrence at day 28 and at day 42.

197 In this study, we observed the risk of P. vivax recurrence at day 42 to be significantly lower

198 ne resulted in a significantly lower risk of P. vivax recurrence than placebo in patients with phenot

199 a role in mediating host cell selectivity of P. vivax.

200 inhibited invasion of all tested strains of P. vivax.

201 rent guidelines for clinical drug studies of P. vivax malaria need to be revised.

202 was reduced to a greater extent than that of P. vivax malaria.

203 Here, we characterize the transcriptomes of P. vivax parasites from 26 malaria patients.

204 reproducible, and efficient transmission of P. vivax gametocytes from humans to mosquitoes, and have

205 Use of P. vivax genotyping in a multicenter, double-blind, rand

206 Circumsporozoite protein (CSP) variants of P. vivax, besides having variations in the protein repet

207 stages of P. falciparum and the activity on P. vivax have the potential to meet the specific profile

208 ater impact on Plasmodium falciparum than on P. vivax in areas where both species are coendemic.

209 f enrolled individuals, 47% had at least one P. vivax parasitaemia and 10% P. falciparum, by qPCR, bo

210 T cell responses induced by P. falciparum or P. vivax vaccine candidates based on MSP119 have not bee

211 study and eradication of the human parasite P. vivax.

212 We conclude that P. vivax Sal I and perhaps P. vivax in Duffy-null patients may have adapted to use

213 To identify potential P. vivax ligands, we compared parasite gene expression i

214 ategy for specific single epitope to prevent P. vivax invasion.

215 leads to increased mRNA levels and protects P. vivax in vitro against invasion inhibitory human mono

216 pable of classifying individuals with recent P. vivax infections who have a high likelihood of harbor

217 Recently, P. vivax infections in Duffy-null Africans have been doc

218 sis of pooled patient data on 1441 recurrent P. vivax infections in 1299 patients on the Thailand-Mya

219 t 820 of 3883 patients (21.1%) had recurrent P. vivax malaria before 2010, compared with 22 of 886 (2

220 The risk of recurrent P. vivax at day 42 was significantly higher in the 384 p

221 The risk of recurrent P. vivax infection at day 28 was 4.0% (95% CI 1.5%-10.4%

222 ration (MDA) for the prevention of recurrent P. vivax infections.

223 out primaquine (PQ) on the risk of recurrent P. vivax.

224 testing and treatment strategy could reduce P. vivax prevalence by 59-69%.

225 highly efficacious intervention for reducing P. vivax and P. ovale transmission.

226 In this region of frequent relapsing P. vivax, failure rates after supervised high-dose prima

227 ious endemic regions, however, have reported P. vivax infections in Duffy-negative individuals, sugge

228 exhibited high efficacy against CQ resistant P. vivax and is an adequate alternative in the study are

229 High-grade CQ-resistant P. vivax is prevalent in eastern Malaysia.

230 Despite evidence of CQ-resistant P. vivax, the risk of recurrence in this study was great

231 (pvmdr1) may select for mefloquine-resistant P. vivax Surveillance is not undertaken routinely owing

232 Some P. vivax-exposed individuals acquired Abs to DBPII that

233 ased in volunteers infected with blood-stage P. vivax and P. falciparum, and were higher in P. vivax

234 re intravenously inoculated with blood-stage P. vivax and subsequently received a single oral 200 mg

235 FN-gamma mediates the control of liver-stage P. vivax by inducing a noncanonical autophagy pathway re

236 sphate dehydrogenase status with symptomatic P. vivax mono-infection were enrolled and randomly assig

237 Effective control strategies targeting P. vivax malaria is hindered by our limited understandin

238 We conclude that P. vivax Sal I and perhaps P. vivax in Duffy-null patien

239 arefully staging the parasites, we find that P. vivax schizonts are largely missing in peripheral blo

240 First, we observed that P. vivax invasion of reticulocytes was consistently redu

241 een documented, raising the possibility that P. vivax, a virulent pathogen in other parts of the worl

242 Our results show that P. vivax isolates significantly vary in their level of r

243 Our data suggest that P. vivax antimalarial drug resistance is likely overesti

244 Signals of natural selection suggest that P. vivax is evolving in response to antimalarial drugs a

245 dividuals throughout Africa, suggesting that P. vivax may use ligands other than DBP1 to invade Duffy

246 The P. vivax entomological inoculation rate was reduced by 1

247 The P. vivax prevalence decreased from 42% in 2006 to 13% in

248 Critically, antibodies raised against the P. vivax antigen potently inhibit proliferation of this

249 ever, this is only part of the story, as the P. vivax intraerythrocytic life cycle is complex.

250 nvades reticulocytes that is mediated by the P. vivax reticulocyte-binding proteins (PvRBPs) specific

251 Here we established the P. vivax transcriptome of the Intraerythrocytic Developm

252 the only known erythrocyte receptor for the P. vivax merozoite invasion ligand, Duffy binding protei

253 ptides representing the allelic forms of the P. vivax CSP were also recognized to a similar extent re

254 rough a process requiring interaction of the P. vivax Duffy binding protein (PvDBP) with its human re

255 t of the highly polymorphic domain II of the P. vivax Duffy-binding protein (DBPII) with the erythroc

256 terventions targeting multiple stages of the P. vivax life cycle.TRIAL REGISTRATIONACTRN1261400093068

257 ccine candidates, the 19 kDa fragment of the P. vivax Merozoite Surface Protein 1 (PvMSP119) is one o

258 equencing at a highly variable region of the P. vivax merozoite surface protein 1 gene revealed impre

259 aphic history and selective pressures on the P. vivax genome by sequencing 182 clinical isolates samp

260 These P. vivax infections are likely attributable to relapses

261 e slave trade and evolved adaptively in this P. vivax malaria-endemic region.

262 proteins corresponding to each of the three P. vivax allelic variants (VK210, VK247 and P. vivax-lik

263 Thus, P. vivax-infected FRG KO huHep mice are a model to inves

264 does not bind to Saimiri erythrocytes; thus, P. vivax Sal I must invade Saimiri erythrocytes independ

265 -infecting species phylogenetically close to P. vivax, was briefly reported in the early 1980s, but n

266 Such aspects must be considered to P. vivax vaccine development.

267 increase in the proportion of malaria due to P. vivax in regions where both parasites coexist.

268 ds, the overall proportion of malaria due to P. vivax rose from 44.1% (30,444/69,098) to 53.3% (29,93

269 usion in a vaccine to prevent malaria due to P. vivax.

270 regnant Colombians and Brazilians exposed to P. vivax and monoclonal antibodies raised against P. viv

271 sequilibrium in human populations exposed to P. vivax malaria compared with unexposed populations.

272 What do reticulocytes offer to P. vivax that is not present in mature erythrocytes?

273 the role of antibody-mediated resistance to P. vivax infection and discuss current progress in vacci

274 for the Duffy antigen are not susceptible to P. vivax infections.

275 g work that establishes a system to transmit P. vivax gametocytes from humans to mosquitoes.

276 AQ) versus CQ for treatment of uncomplicated P. vivax infection in Manaus, Brazil.

277 Clinical efficacy studies of uncomplicated P. vivax treated with DP or AL and published between Jan

278 Patients with uncomplicated P. vivax malaria on the Thailand-Myanmar border were ran

279 orts need to address this largely undetected P. vivax transmission by simultaneously tackling the res

280 Unfortunately, P. vivax, unlike P. falciparum, cannot be cultivated con

281 After this uptake, P. vivax-infected reticulocytes obtained from patients s

282 cules for activity against Plasmodium vivax (P. vivax) NMT.

283 All mAbs were P. vivax strain transcending and targeted known binding

284 A critical question remains why P. vivax selectively invades reticulocytes?

285 Plasma from children and adults with P. vivax malaria in Sabah, Malaysia, were collected duri

286 Immuno-precipitation experiments with P. vivax Reticulocyte Binding Proteins showed no evidenc

287 ) memory B cell activity in individuals with P. vivax strain-transcending Abs to DBPII display a limi

288 and Aotus monkey erythrocytes infected with P. vivax Salvador I (Sal I).

289 alciparum and >85% among those infected with P. vivax.

290 larly marked in participants inoculated with P. vivax, where the osteoprotegerin level correlated wit

291 n = 2; Study 2, n = 24) were inoculated with P. vivax-infected red blood cells to initiate infection,

292 d in participants following inoculation with P. vivax (n = 16) or P. falciparum (n = 15), with the an

293 3.1%-34.5%) after initial monoinfection with P. vivax and 29.2% (95% CI 28.1%-30.4%) after mixed-spec

294 CI -0.34 to -0.07]) but not in patients with P. vivax malaria (0.28% [21/7,545] versus 0.23% [28/12,3

295 We enrolled 40 patients with P. vivax malaria in northeastern Cambodia, where >17% tr

296 Patients with P. vivax malaria were randomized to receive chloroquine

297 The risk of re-presentation with P. vivax malaria was higher in children 1 to <5 years of

298 As for P. falciparum, CHMI studies with P. vivax will provide a platform for early proof-of-conc

299 he colocalization of lysosomal vesicles with P. vivax compartments.

300 proved understanding of the diversity within P. vivax transcriptomes will be essential for the priori