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 gametocyte carriage mirrors asexual-stage infec

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

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

6 parum clinical isolates from Tanzania and 10 P. vivax strains and 96 P. vivax clinical isolates from

7 eteroduplex tracking assay, we genotyped 107 P. vivax infections in individuals from Cambodia, 45 of

8 Recombinant proteins of 15 P. vivax tryptophan-rich antigens (PvTRAgs) were express

9 tween the resistance phenotypes for these 16 P. vivax alleles and previously observed resistance data

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

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

12 ected high multiplicities of infection in 63 P. vivax infections in Cambodia.

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

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

15 from Tanzania and 10 P. vivax strains and 96 P. vivax clinical isolates from Venezuela, and we have v

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

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

18 The within-host model is embedded in a P. vivax transmission model to demonstrate the build-up

19 In order to produce a P. vivax vaccine for global use, we have previously repo

20 port that vaccination of mice with VMP001, a P. vivax CSP vaccine candidate, reduces, not enhances, P

21 monoclonal and polyclonal antibodies against P. vivax CSP strongly inhibit parasite infection and thu

22 second-generation vaccine candidate against P. vivax malaria.

23 ans that may provide some protection against P. vivax infection and severity, is taken into account t

24 aluating protective immune responses against P. vivax vaccines based on CSP.

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

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

27 train-transcending candidate vaccine against P. vivax.

28 e efficacy of new candidate vaccines against P. vivax using a fully infectious transgenic Plasmodium

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

30 37,554, mean = 9.47 [95% CI 9.44-9.50]), and P. vivax (n = 19,858, mean = 9.53 [95% CI 9.49-9.57]); p

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

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

33 tocols were able to detect P. falciparum and P. vivax at higher densities, but these assays may not r

34 Plasmodium falciparum and P. vivax cases were actively identified by monthly rapid

35 ethod for the detection of P. falciparum and P. vivax in conventional or multiplex PCR platforms.

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

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

38 o high endemicity for both P. falciparum and P. vivax infections.

39 igh levels of both Plasmodium falciparum and P. vivax infections.

40 ortant differences between P. falciparum and P. vivax is the formation of P. vivax latent-stage paras

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

42 r the treatment of Plasmodium falciparum and P. vivax malaria.

43 Antibody levels to P. falciparum and P. vivax merozoite antigens and the pregnancy-specific P

44 inhibitor of both Plasmodium falciparum and P. vivax NMT and displays activity in vivo against a rod

45 ection of Plasmodium spp., P. falciparum and P. vivax targets in order to produce an assay amenable t

46 have mined the genomes of P. falciparum and P. vivax to identify species-specific, repetitive sequen

47 Antibodies to P. falciparum and P. vivax were highly variable over time, and maintenance

48 the major human pathogens P. falciparum and P. vivax, and inhibit liver-stage hypnozoites in the sim

49 sequence data for Plasmodium falciparum and P. vivax, the majority of PCR-based methods still rely o

50 d the Plasmodium pathogens P. falciparum and P. vivax.

51 h RF Borrelia from Plasmodium falciparum and P. vivax.

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

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

54 ups of monkeys generated high titers of anti-P. vivax IgG antibodies, as detected by enzyme-linked im

55 ent against human-malaria parasites, such as P. vivax and P. ovale, which develop inside reticulocyte

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 protective allele is not understood because P. vivax is believed to have originated in Asia.

59 The P. berghei-P. vivax chimeric strain develops normally in mosquitoes

60 posed to the bites of as few as 3 P. berghei-P. vivax-infected mosquitoes.

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

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

63 fied compounds that selectively inhibit both P. vivax and falciparum Kinesin-5 motor domains but, as

64 Whole-genome sequencing of both P. vivax and Plasmodium cynomolgi and characterization o

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

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

67 Monoinfection by P. vivax and Plasmodium falciparum was detected by qPCR

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

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

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

71 15 genes was also determined among clinical P. vivax isolates.

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

73 and the risk of having at least one clinical P. vivax episode (HR = 0.25 [95% CI 0.11, 0.61], p = 0.0

74 We show complete P. vivax liver stage development, including maturation i

75 polymerase chain reaction (qPCR) to confirm P. vivax infection and rule out coinfection with other P

76 inized samples of spleen and lung to confirm P. vivax monoinfection.

77 o all cases with parasitologically confirmed P. vivax infections.

78 rghei parasites expressing the corresponding P. vivax antigens in mice.

79 ry tract infections (LRTIs) with low-density P. vivax on BS; 2 received a diagnosis of P. vivax malar

80 Immunohistofluorescence was used to detect P. vivax parasitized red blood cells (RBCs).

81 risk of having at least one qPCR-detectable P. vivax or P. ovale infection during 8 mo of follow-up

82 The primers detected P. vivax in the clinical samples with 94.59% sensitivity

83 y developed for the LAMP method in detecting P. vivax.

84 be necessary for protection against diverse P. vivax strains.

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

86 to define the role of these molecules during P. vivax malaria.

87 vestigated beta-thalassaemia, haemoglobin E, P. vivax malaria, or pregnancy-associated malaria.

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

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

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

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

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

93 models constitutes an obstacle in examining P. vivax liver stage infection and drug efficacy.

94 vivax vaccine which simultaneously expresses P. vivax circumsporozoite protein (PvCSP) and P25 (Pvs25

95 genic Plasmodium berghei parasite expressing P. vivax TRAP to allow studies of vaccine efficacy and p

96 ecombinant ChAd63 and MVA vectors expressing P. vivax TRAP (PvTRAP) and show their ability to induce

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

98 ts during acute uncomplicated P. falciparum, P. vivax, and convalescent P. falciparum infections.

99 evere anaemia associated with P. falciparum, P. vivax, and P. malariae were 2.11 (95% CI 2.00-2.23),

100 3 (9.7%), and 4 of 151 (2.6%) P. falciparum, P. vivax, and P. malariae/P. knowlesi notifications resp

101 were assembled that contained P. falciparum, P. vivax, P. malariae, and P. ovale; DBSs contained eith

102 specifically identify Plasmodium falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi.

103 The first P. vivax relapses of life are usually genetically homolo

104 econdary outcome measures were time to first P. vivax infection (by qPCR), time to first clinical epi

105 apses cause approximately four of every five P. vivax infections and at least three of every five P.

106 for P. falciparum, 89.5% (75.2 to 97.1%) for P. vivax, 94.1% (71.3 to 99.9%) for P. ovale, and 100% (

107 %) for P. falciparum, 99% (84.8 to 100%) for P. vivax, 98.4% (94.4 to 99.8%) for P. ovale, and 99.3%

108 (49/63) for P. falciparum, 91.7% (11/12) for P. vivax, 83.3% (10/12) for P. malariae, and 70% (7/10)

109 of the real-time PCR primers were 94.2% for P. vivax (49/52) and 100% for P. falciparum (51/51), P.

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

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

112 cted a 42-day efficacy study of AL or CQ for P. vivax in Oromia Regional State, Ethiopia.

113 ow present across most countries endemic for P. vivax.

114 d across most countries that are endemic for P. vivax.

115 and/or a more stable demographic history for P. vivax relative to P. falciparum, which is thought to

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

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

118 lciparum assay and 0.127 parasite/microl for P. vivax assay.

119 l for P. malariae and 5 parasites/microl for P. vivax using the genus specific primer set.

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

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

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

123 dicted to be a highly effective strategy for P. vivax elimination.

124 and CQ were effective and well-tolerated for P. vivax malaria, but high rates of recurrent parasitemi

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

126 sequenced and annotated the genomes of four P. vivax strains collected from disparate geographic loc

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

128 UB1 with bacterial subtilisins and generated P. vivax SUB1 three-dimensional models.

129 lts (of whom 20 had P. falciparum and 20 had P. vivax infections), alongside samples from 16 patients

130 ren (of whom 15 had P. falciparum and 36 had P. vivax infections) and 162 afebrile adults (of whom 20

131 In areas of high P. vivax diversity, targeted deep sequencing can help de

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

133 All extant human P. vivax parasites are derived from a single ancestor th

134 These findings indicate that human P. vivax is of African origin and likely selected for th

135 parasites that are closely related to human P. vivax.

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

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

138 f antimalarial efficacy is essential, but in P. vivax infections the assessment of treatment efficacy

139 reement with common polymorphic DHFR data in P. vivax, from which this quadruple mutant is missing.

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

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

142 estigated antimalarial treatment efficacy in P. vivax malaria.

143 o undertake studies previously impossible in P. vivax that will facilitate a better understanding of

144 rocessing pattern and apical localization in P. vivax merozoites.

145 r, placental inflammation is not observed in P. vivax monoinfections, suggesting other causes of poor

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

147 predicted to cause substantial reductions in P. vivax transmission as individuals with the most hypno

148 hese observations prompt a paradigm shift in P. vivax biology and open avenues to investigate the rol

149 ings warrant a deeper survey of variation in P. vivax to equip disease interventions targeting the di

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

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

152 the most important strategy for interrupting P. vivax transmission.

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

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

155 use of severe anemia in early infancy, mixed P. vivax/P. falciparum infections are associated with a

156 the treatment of uncomplicated monoinfection P. vivax malaria in North Sumatera, Indonesia.

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

158 g the transmission patterns of the neglected P. vivax malaria parasite.

159 asmodium falciparum while largely neglecting P. vivax.

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

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

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

163 006 to 2010; 72% of P. falciparum and 87% of P. vivax infections were submicroscopic in 2014.

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

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

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

167 understanding of the blood-stage biology of P. vivax.

168 he contribution of relapses to the burden of P. vivax and P. ovale infection, illness, and transmissi

169 ntribute substantially to the high burden of P. vivax disease observed in young Papua New Guinean chi

170 How much they contribute to the burden of P. vivax malaria in children living in highly endemic ar

171 blood in order to unravel the complexity of P. vivax and P. falciparum infections.

172 sed on the circumsporozoite protein (CSP) of P. vivax.

173 we describe new primers for the detection of P. vivax using the RealAmp method.

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

175 patient deaths with a clinical diagnosis of P. vivax infection occurred in a tertiary care center in

176 ty P. vivax on BS; 2 received a diagnosis of P. vivax malaria on the basis of RDT but BSs were negati

177 tochondrial and nuclear genetic diversity of P. vivax parasites isolated from great apes in Africa an

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

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

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

181 falciparum and P. vivax is the formation of P. vivax latent-stage parasites (hypnozoites) that can c

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

183 he Duffy antigen, the portal of infection of P. vivax, would be a novel and potentially effective app

184 A single isolate of P. vivax obtained from a febrile patient with clinical m

185 y detected laboratory-maintained isolates of P. vivax from different parts of the world.

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

187 The T lymphocytes of P. vivax exposed individuals expressed higher level of C

188 The majority of P. vivax patients (75.7%-100%, n = 33) produced IgG anti

189 tional variation in the global population of P. vivax.

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

191 rable effect irrespective of the presence of P. vivax blood-stage infection at the time of treatment

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

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

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

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

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

197 arasites bearing the type I repeat region of P. vivax circumsporozoite protein (CSP).

198 tterns of incubation periods and relapses of P. vivax, variation in treatment, and seasonal abundance

199 th artesunate-primaquine reduced the risk of P. vivax episodes by 28% (P = .042) and 33% (P = .015) c

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

201 Clinical samples of P. vivax and other human-infecting malaria parasite spec

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

203 Hypnozoites are an important source of P. vivax infection and contribute substantially to the h

204 hment of small forms in late liver stages of P. vivax.

205 ate it against data from tropical strains of P. vivax.

206 ola-vesicle complexes, a unique structure of P. vivax-infected erythrocytes.

207 dministration of primaquine for treatment of P. vivax malaria needs to be urgently considered to prev

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

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

210 alone, would have only a transient effect on P. vivax transmission levels, while MDA that includes li

211 ed in view of the recent, increased focus on P. vivax and liver stages of Plasmodium.

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

213 more relapses and contribute more to onwards P. vivax transmission.

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

215 d with either P. falciparum (22 patients) or P. vivax (70 patients) , the most prevalent human malari

216 In Papua P. vivax is the dominant cause of severe anemia in early

217 nce to CQ in the important malarial parasite P. vivax.

218 In 13 of 17 deceased patients, P. vivax infection was the plausible cause of death.

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

220 dults with asymptomatic, microscopy-positive P. vivax or P. falciparum infection increased or retaine

221 hain reaction- and light microscopy-positive P. vivax reinfections by 44% (P < .001) and 67% (P < .00

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

223 Recombinant P. vivax tryptophan-rich antigens (PvTRAgs) were used to

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

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

226 /107) in the CQ arm presented with recurrent P. vivax infection, with the median number of days to re

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

228 the only licensed drug to prevent relapses, P. vivax may be highly prevalent; (iii) the mean age at

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

230 global surveillance of chloroquine-resistant P. vivax, which is now present across most countries end

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

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

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

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

235 We systematically reviewed P. vivax malaria treatment efficacy studies to establish

236 Recently, we have described several P. vivax tryptophan-rich antigens (PvTRAgs), including m

237 These results herald the era of stable P. vivax genetic modifications.

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

239 FRG KO huHep mice support P. vivax sporozoite infection, liver stage development,

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

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

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

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

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

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

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

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

248 nclude two AP2 transcription factors and the P. vivax multidrug resistance-associated protein (PvMRP1

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 results were observed when we expressed the P. vivax alleles in a transgenic bacterial system.

253 accharomyces cerevisiae model expressing the P. vivax DHFR enzyme, we assayed growth rate and resista

254 We characterize here the P. vivax SUB1 enzyme and show that it displays a typical

255 re specific immune responses to minimize the P. vivax infection.

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

257 man erythrocytes requires interaction of the P. vivax Duffy binding protein (PvDBP) with its host rec

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

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

260 ssful high level inducible expression of the P. vivax orthologue, PvCRT, and compare CQ hypersensitiv

261 a recombinant chimeric protein based on the P. vivax CSP (PvCSP).

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

263 We show that the P. vivax sequences from parasites of great apes form a c

264 from a conserved DNA sequence unique to the P. vivax genome.

265 The relationship between this P. vivax clade in great apes and the human isolates is d

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

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

268 ent parasitemia, representing the first time P. vivax variants associated with a higher risk of relap

269 rates of chloroquine resistance according to P. vivax malaria recurrence rates by day 28 whole-blood

270 3 revealed that death could be attributed to P. vivax infection; in the remaining 4, acute diseases o

271 n, a lesser protection of G6PD deficiency to P. vivax infection, and a shorter latent period of hypno

272 enetic restriction of the immune response to P. vivax CSP.

273 We applied amplicon deep sequencing to P. vivax isolates from 78 Cambodian volunteers, nearly o

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

275 The lack of tractable P. vivax animal models constitutes an obstacle in examin

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

277 od-stage parasite clearance of uncomplicated P. vivax malaria.

278 uential cohorts of adults with uncomplicated P. vivax malaria (10 patients) or P. falciparum malaria

279 sitemia rapidly in adults with uncomplicated P. vivax or P. falciparum malaria.

280 This full-genome sequence of an uncultured P. vivax isolate shows that the same regions with low nu

281 P. ovale infection during 8 mo of follow-up (P. vivax: PQ arm 0.63/y versus PL arm 2.62/y, HR = 0.18

282 Plasmodium vivax (P. vivax) is one of the most important human malaria spe

283 rmation is relevant to understanding whether P. vivax affects placental function and how it may contr

284 ) with P. falciparum, and 7 of 43 (16%) with P. vivax.

285 es of poor delivery outcomes associated with P. vivax infection.

286 Individuals with P. vivax monoinfection were enrolled.

287 influence the number of humans infected with P. vivax and the mean age at infection of humans in trop

288 that: (i) the number of humans infected with P. vivax may increase when an incubation period of paras

289 impact on the number of humans infected with P. vivax.

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

291 3.1%-34.5%) after initial monoinfection with P. vivax and 29.2% (95% CI 28.1%-30.4%) after mixed-spec

292 A total of 492 patients with P. vivax infections from Thailand and 476 patients (162

293 le range, 0.85 to 1.14) in the patients with P. vivax malaria and 0.90 hours (range, 0.68 to 1.64; in

294 artile range, 8 to 16 hours in patients with P. vivax malaria and 10 to 16 hours in those with P. fal

295 By histology, 3 placentas with P. vivax monoinfection showed parasitized erythrocytes i

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

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

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

299 was collected from a 49-year-old woman with P. vivax infection, characterized, and used in an experi

300 Seven of the 8 women with P. vivax placental monoinfection were negative in periph