ライフサイエンスコーパス: Plasmodium vivax

1 of studies conducted in humans infected with Plasmodium vivax.

2 PMV isolated from Plasmodium falciparum and Plasmodium vivax.

3 n and factors affecting rosette formation in Plasmodium vivax.

4 gle and mixed infection of P. falciparum and Plasmodium vivax.

5 the life cycle of Plasmodium falciparum and Plasmodium vivax.

6 ver, RDTs are known to perform less well for Plasmodium vivax.

7 known entry point for the malarial parasite Plasmodium vivax.

8 which mediates invasion of reticulocytes by Plasmodium vivax.

9 Iraq with life-threatening infection due to Plasmodium vivax.

10 liver stage hypnozoites after infection with Plasmodium vivax.

11 ers protection against malarial infection by Plasmodium vivax.

12 not found in individuals infected only with Plasmodium vivax.

13 est children and for the non-lethal parasite Plasmodium vivax.

14 asymptomatic human individuals infected with Plasmodium vivax.

15 and radical cure, and relapse prevention of Plasmodium Vivax.

16 most widespread form of malaria is caused by Plasmodium vivax.

17 he transmission of Plasmodium falciparum and Plasmodium vivax.

18 ria caused by both Plasmodium falciparum and Plasmodium vivax.

19 Anopheles gambiae, Plasmodium falciparum and Plasmodium vivax.

20 Also present were Plasmodium vivax (14.3%), Plasmodium falciparum (10.5%)

21 stem measures presence of antibodies against Plasmodium vivax, a causing agent for malaria.

22 enetic diversity and population structure of Plasmodium vivax, a debilitating and highly prevalent ma

23 Plasmodium vivax, a major agent of malaria in both tempe

24 ticulocyte binding protein 2-P1 (RBP2-P1) of Plasmodium vivax, a member of the reticulocyte binding p

25 Plasmodium vivax accounts for 65% of all cases of malari

26 ck transmission of Plasmodium falciparum and Plasmodium vivax across distantly related anopheline spe

27 We now report crystal structures of Plasmodium vivax ADA in complex with adenosine, guanosin

28 y and efficacy of DB289 for the treatment of Plasmodium vivax and acute, uncomplicated P. falciparum

29 ions of the human genome, and the genomes of Plasmodium vivax and Arabidopsis thaliana show that Evig

30 ic affinity of the malaria causing parasites Plasmodium vivax and falciparum in historic southern Eur

31 examine the association between relapses of Plasmodium vivax and febrile infectious diseases.

32 s, has been identified in the human parasite Plasmodium vivax and homologues (yir) of this family exi

33 Despite biochemical similarities between Plasmodium vivax and human NMTs, our recent research dem

34 nomic databases of Plasmodium falciparum and Plasmodium vivax and investigated as candidate antigens

35 rapid diagnostic tests (RDTs) for diagnosing Plasmodium vivax and nonfalciparum malaria in endemic ar

36 from P. knowlesi, Plasmodium falciparum, and Plasmodium vivax and outcomes following introduction of

37 Plasmodium vivax and P. cynomolgi produce numerous caveo

38 tibodies to the dominant surface antigens of Plasmodium vivax and P. falciparum following controlled

39 Plasmodium vivax and P. falciparum, the parasites respon

40 etectable hypnozoite reservoir for relapsing Plasmodium vivax and P. ovale malarias presents a major

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

42 ear space, while this was less pronounced in Plasmodium vivax and Plasmodium berghei, and absent in P

43 Cambodia, in which both Plasmodium vivax and Plasmodium falciparum are endemic,

44 ents containing the VWA and TSR domains from Plasmodium vivax and Plasmodium falciparum in different

45 iMAL (Flow Inc., Portland, Oreg.), to detect Plasmodium vivax and Plasmodium falciparum malaria durin

46 dept at transmitting malarial pathogens (eg, Plasmodium vivax and Plasmodium falciparum), A stephensi

47 d in volunteers experimentally infected with Plasmodium vivax and Plasmodium falciparum.

48 biochemical properties of PMT orthologs from Plasmodium vivax and Plasmodium knowlesi and show that b

49 Anopheles near costai G1, was infected with Plasmodium vivax and Plasmodium malariae, reported herei

50 pt that hypnozoites give rise to relapses in Plasmodium vivax and Plasmodium ovale malaria has become

51 se of primaquine is used for radical cure of Plasmodium vivax and Plasmodium ovale malaria only.

52 tivation of quiescent hepatic hypnozoites of Plasmodium vivax and Plasmodium ovale, hinder global eff

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

54 Studies of the interaction between Plasmodium vivax and the Duffy antigen provide the clear

55 Plasmodium vivax and the related simian malarial parasit

56 Tackling relapsing Plasmodium vivax and zoonotic Plasmodium knowlesi infect

57 is caused by a distinct Plasmodium species, Plasmodium vivax, and it has become increasingly apparen

58 uch as the Duffy blood group, a receptor for Plasmodium vivax, and the Gerbich-negative modification

59 one separately for Plasmodium falciparum and Plasmodium vivax, and the limitations of the approach we

60 distributions for Plasmodium falciparum and Plasmodium vivax, and the proportions of undetected infe

61 enic clearance of the rheologically impaired Plasmodium vivax- and Plasmodium falciparum-infected RBC

62 e MBC, and their levels correlated with both Plasmodium vivax- and Plasmodium falciparum-specific pla

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

64 smodium malariae, Plasmodium ovale spp., and Plasmodium vivax are less severe than P. falciparum, tre

65 The parasites Plasmodium falciparum and Plasmodium vivax are responsible for the majority of hum

66 asmodium falciparum (asexual and sexual) and Plasmodium vivax (asexual) as well as oral in vivo effic

67 Plasmodium vivax bench research greatly lags behind Plas

68 d CD71 largely overlap with arenaviruses and Plasmodium vivax binding regions in the apical part of t

69 es show the importance of the bone marrow in Plasmodium vivax biology by proving the preferential inf

70 Estimation of Plasmodium vivax biomass based on circulating biomarkers

71 hrocyte receptor is critical for maintaining Plasmodium vivax blood-stage infections, making DBP an a

72 binding protein (DBP) is a vital ligand for Plasmodium vivax blood-stage merozoite invasion, making

73 were assessed for Plasmodium falciparum and Plasmodium vivax by means of microscopy, rapid diagnosti

74 Plasmodium vivax can be associated with placental infect

75 enign disease, it is now becoming clear that Plasmodium vivax can cause significant morbidity.

76 tively, with correct identification of all 5 Plasmodium vivax cases.

77 Plasmodium vivax causes 25-40% of malaria cases worldwid

78 Plasmodium vivax causes the most geographically widespre

79 te increasing evidence of the development of Plasmodium vivax chloroquine (CQ) resistance, there have

80 apled" lipid vesicles carrying a recombinant Plasmodium vivax circumsporozoite antigen, VMP001, both

81 In areas where Plasmodium falciparum and Plasmodium vivax coexist and treatments for the 2 specie

82 piens/Mus musculus and Plasmodium falciparum/Plasmodium vivax comparisons).

83 inical illness with Plasmodium falciparum or Plasmodium vivax compromises the function of dendritic c

84 Plasmodium vivax contains the largest number of such ant

85 The recent research efforts to establish a Plasmodium vivax continuous, long-term blood-stage cultu

86 nsible for most imported infections (66.7%); Plasmodium vivax contributed 15.1%, Plasmodium malariae

87 m and Plasmodium berghei sporozoites by anti-Plasmodium vivax CSP serum samples.

88 ction from clinical vivax malaria or reduced Plasmodium vivax density, including Southeast Asian oval

89 FN-gamma-mediated restriction of liver-stage Plasmodium vivax depends only on the downstream autophag

90 valent activity on Plasmodium falciparum and Plasmodium vivax DHODH.

91 Contrary to Plasmodium vivax, direct evidence for this hypothesis is

92 It is likely that Plasmodium vivax diverged approximately 2 million years

93 hennai, 56 in Nadiad, 101 in Rourkela), with Plasmodium vivax dominating in Chennai (70.8%) and Nadia

94 Plasmodium vivax Duffy binding protein (DBP) is a conser

95 Plasmodium vivax Duffy binding protein (DBP) is a merozo

96 Antibodies to the cysteine-rich domain II of Plasmodium vivax Duffy binding protein (PvDBP) can inhib

97 Plasmodium vivax Duffy Binding Protein (PvDBP) is the mo

98 The Plasmodium vivax Duffy-binding protein (DBP) is a prime

99 A major gap in the Plasmodium vivax elimination toolkit is the identificati

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

101 Analysis of Plasmodium vivax epidemic data indicates that local mala

102 Plasmodium vivax exacts a significant toll on health wor

103 against a farnesyl diphosphate synthase from Plasmodium vivax, finding a poor correlation between enz

104 for which long term culture is possible, and Plasmodium vivax, for which no long-term culture is feas

105 Plasmodium vivax forms long-lasting hypnozoites in the l

106 ssion of vivax malaria requires knowledge of Plasmodium vivax gametocyte dynamics.

107 Studies of Plasmodium vivax gene expression are complicated by the

108 Plasmodium vivax gene regulation remains difficult to st

109 rstanding of the structure and regulation of Plasmodium vivax genes is limited by our inability to gr

110 llelic combinations - were identified in the Plasmodium vivax genome by Siegel et al.

111 Here, an update on the Plasmodium vivax genome sequencing project is presented,

112 d and characterized a novel parasite ligand, Plasmodium vivax GPI-anchored micronemal antigen (PvGAMA

113 The human malaria parasite Plasmodium vivax has been shown to regulate the transcri

114 Controversially, it is also thought that Plasmodium vivax has driven the recent selection of G6PD

115 dence and range of endemic malaria caused by Plasmodium vivax has expanded during the past 30 years.

116 Plasmodium vivax has received less attention and study t

117 The evolutionary history of Plasmodium vivax has recently been addressed in terms of

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

119 th Ki values as low as 0.08 and 0.01 muM for Plasmodium vivax HGPRT (PvHGPRT).

120 me diversity of the important human pathogen Plasmodium vivax, however, remains essentially unknown.

121 ne is the only licensed drug for eradicating Plasmodium vivax hypnozoites and, therefore, preventing

122 er stages for both Plasmodium falciparum and Plasmodium vivax in a microscale human liver platform co

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

124 A high prevalence of chloroquine-resistant Plasmodium vivax in Indonesia has shifted first-line tre

125 t primaquine is the first-line treatment for Plasmodium vivax in malarious areas, but artemether-lume

126 Malaria is increasingly imported, caused by Plasmodium vivax in settings outside sub-Saharan Africa,

127 n of Africa harbors the largest reservoir of Plasmodium vivax in the continent.

128 Evidence of the presence of Plasmodium vivax in the placenta is scarce and inconclus

129 idence that challenges the current view that Plasmodium vivax-infected erythrocyte (Pv-iE) are unable

130 an important cause of hospitalization among Plasmodium vivax-infected individuals, leading to life-t

131 fected patients were lower than those in the Plasmodium vivax-infected patients, which, in turn, were

132 effectiveness of previous regimens to treat Plasmodium vivax infection have been hampered by complia

133 Prevention of relapse of Plasmodium vivax infection is a key treatment goal in ma

134 Severe disease attributable to Plasmodium vivax infection is already well described wor

135 mplicated P falciparum or mixed P falciparum/Plasmodium vivax infection of between 1000 and 200,000 p

136 es and endothelial cells and is required for Plasmodium vivax infection of erythrocytes.

137 receptor for chemokines that is required for Plasmodium vivax infection of erythroid cells.

138 espread distribution and relapsing nature of Plasmodium vivax infection present major challenges for

139 halassemia may facilitate so-called "benign" Plasmodium vivax infection to act later in life as a "na

140 We treated Cambodians who had acute Plasmodium vivax infection with PQ0.75 and a 3-day cours

141 xed infections, 3.73 (95% CI, 3.51-3.97) for Plasmodium vivax infection, and 2.16 (95% CI, 1.78-2.63)

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

143 7 (2%) with Plasmodium falciparum infection, Plasmodium vivax infection, Plasmodium malariae/Plasmodi

144 Plasmodium vivax infection, the predominant cause of mal

145 group-believed to confer resistance against Plasmodium vivax infection-was recently introduced to Pa

146 rred by the Duffy-negative phenotype against Plasmodium vivax infection.

147 nd confers partial resistance to blood-stage Plasmodium vivax infection.

148 Plasmodium falciparum and Plasmodium vivax infections are important causes of adve

149 Unlike the case in Asia and Latin America, Plasmodium vivax infections are rare in sub-Saharan Afri

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

151 Challenges in classifying recurrent Plasmodium vivax infections constrain surveillance of an

152 Plasmodium vivax infections often recur due to relapse o

153 Asymptomatic, low-density Plasmodium vivax infections pose a significant challenge

154 Plasmodium vivax infections remain a major source of mal

155 Asymptomatic P. falciparum and Plasmodium vivax infections were cleared by MDA.

156 ositive infections in Asia and the Americas, Plasmodium vivax infections were more likely to be submi

157 Plasmodium vivax invasion into human reticulocytes is a

158 Plasmodium vivax invasion of human erythrocytes requires

159 Plasmodium vivax invasion of reticulocytes relies on dis

160 Plasmodium vivax is a major cause of malaria morbidity w

161 Plasmodium vivax is a major public health burden, respon

162 Plasmodium vivax is a serious health concern in many reg

163 Here, we tested whether infection with Plasmodium vivax is an alternative mechanism of acquisit

164 Plasmodium vivax is an important cause of malaria, assoc

165 Erythrocyte invasion by Plasmodium vivax is completely dependent on binding to t

166 Plasmodium vivax is considered to be absent from Central

167 However, the proportion of cases due to Plasmodium vivax is increasing, accounting for up to 90-

168 Chloroquine (CQ)-resistant Plasmodium vivax is increasingly reported throughout sou

169 BACKGROUNDThe biology of Plasmodium vivax is markedly different from that of P. f

170 Plasmodium vivax is one of four Plasmodium species that

171 The human malaria parasite Plasmodium vivax is responsible for 25-40% of the approx

172 Plasmodium vivax is the leading cause of human malaria i

173 Plasmodium vivax is the main cause of malaria in Nepal.

174 Plasmodium vivax is the major cause of malaria outside s

175 Plasmodium vivax is the most prevalent parasite species

176 Plasmodium vivax is the most widely distributed human ma

177 Plasmodium vivax is the most widespread species of Plasm

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

179 Plasmodium vivax is the world's most widely distributed

180 r reinfection with Plasmodium falciparum and Plasmodium vivax is unknown.

181 morphic microsatellite markers to analyze 74 Plasmodium vivax isolates, which we collected in cross-s

182 d host invasion by Plasmodium falciparum and Plasmodium vivax--major causative organisms of human mal

183 expression in a rhesus monkey model of human Plasmodium vivax malaria (P. cynomolgi in Macaca mulatta

184 e used for the radical curative treatment of Plasmodium vivax malaria and can cause haemolysis in G6P

185 on spatio-temporal epidemiological cases of Plasmodium vivax malaria and land-use irrigation from re

186 ylactic regimens fail to prevent relapses of Plasmodium vivax malaria and review available options.

187 DARC acts as a receptor for Plasmodium vivax malaria and the DARC-null genotype has

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

189 nts to development of vaccines and drugs for Plasmodium vivax malaria are the inability to culture th

190 The radial distribution of Plasmodium vivax malaria burden has evoked enormous conc

191 spective infant cohort, 21 infants developed Plasmodium vivax malaria during their first year.

192 Mainstay treatment for Plasmodium vivax malaria has long relied on chloroquine

193 erapy (ACT) is recommended for uncomplicated Plasmodium vivax malaria in areas of emerging chloroquin

194 Chloroquine is the first-line treatment for Plasmodium vivax malaria in most endemic countries, but

195 Plasmodium vivax malaria increased the odds of stillbirt

196 the nonperipheral blood origin of recurrent Plasmodium vivax malaria is both hypnozoites (relapse so

197 Plasmodium vivax malaria is characterized by periodic re

198 Pathogenesis of severe Plasmodium vivax malaria is poorly understood.

199 e and fatal infections; however, the risk of Plasmodium vivax malaria is unknown.

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

201 e is the only widely used drug that prevents Plasmodium vivax malaria relapses, but adherence to the

202 Plasmodium vivax malaria requires a 2-week course of pri

203 Treatment of Plasmodium vivax malaria requires the clearing of asexua

204 is is a common cause of complications during Plasmodium vivax malaria treatment in individuals with g

205 Chloroquine (CQ)-resistant Plasmodium vivax malaria was first reported 12 years ago

206 Radical cure of Plasmodium vivax malaria with 8-aminoquinolines (primaqu

207 on the Thailand-Myanmar border had recurrent Plasmodium vivax malaria within 63 days, compared with 1

208 A successful vaccine against Plasmodium vivax malaria would significantly improve the

209 maquine is necessary for the radical cure of Plasmodium vivax malaria, but the optimum duration of tr

210 Tafenoquine, a single-dose therapy for Plasmodium vivax malaria, has been associated with relap

211 es in patients with Plasmodium falciparum or Plasmodium vivax malaria.

212 tes might not be the only cause of recurrent Plasmodium vivax malaria.

213 taemia, or pregnancy-associated malaria, and Plasmodium vivax malaria.

214 y 3.3 billion people live with the threat of Plasmodium vivax malaria.

215 fixing antibodies remain uncharacterized for Plasmodium vivax malaria.

216 and the spleen has been reported in cases of Plasmodium vivax malaria.

217 pLDH from Plasmodium vivax, malariae, and ovale exhibit 90-92% ide

218 The Plasmodium vivax merozoite Duffy binding protein (DBP) c

219 The interaction between the Plasmodium vivax merozoite Duffy binding protein region

220 Plasmodium vivax merozoite invasion is totally dependent

221 206) who acquire high antibody levels to two Plasmodium vivax merozoite proteins, Duffy binding prote

222 The Plasmodium vivax merozoite surface protein 1 (MSP-1) 42-

223 mbinant protein containing the C terminus of Plasmodium vivax merozoite surface protein 1 and two T-h

224 Using a newly developed Plasmodium vivax merozoite surface protein 1 gene (Pvmsp

225 Two recombinant protein subunits of the Plasmodium vivax merozoite surface protein 1 have been s

226 The Plasmodium vivax merozoite surface protein 1 paralog (Pv

227 heteroduplex tracking assay used to genotype Plasmodium vivax merozoite surface protein 1 was adapted

228 Plasmodium vivax merozoites only invade reticulocytes, a

229 usly reported a method for the production of Plasmodium vivax MSP-1(42) (PvMSP-1(42)) as a soluble pr

230 iparum (n = 47 uncomplicated, n = 8 severe), Plasmodium vivax (n = 37), or Plasmodium malariae (n = 1

231 port the successful discovery of a series of Plasmodium vivax NMT inhibitors by high-throughput scree

232 s allele has been the target of selection by Plasmodium vivax or some other infectious agent.

233 b-Saharan Africa has been used to argue that Plasmodium vivax originated on that continent.

234 Plasmodium vivax (P. vivax) is one of the most important

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

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

237 ence and micro-geographical heterogeneity of Plasmodium vivax parasitaemia in communities of the Peru

238 Relapses arising from dormant liver-stage Plasmodium vivax parasites (hypnozoites) are a major cau

239 rasite development of both P. falciparum and Plasmodium vivax parasites in five different species of

240 Plasmodium vivax parasites preferentially invade reticul

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

242 nd differentiation of Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malar

243 Two new studies confirm that Plasmodium vivax populations are more diverse than Plasm

244 e is known about allelic variants of dhfr in Plasmodium vivax populations.

245 The most widespread Plasmodium species, Plasmodium vivax, poses a significant public health thre

246 Plasmodium vivax preferentially invades reticulocytes, w

247 ctive against the dormant relapsing forms of Plasmodium vivax, primaquine is the sole effective treat

248 To evaluate whether the recently cloned Plasmodium vivax proteins Pvs25 and Pvs28 are candidates

249 These results are combined with those for Plasmodium vivax (published separately) to form the mala

250 bitors of the Plasmodium falciparum (Pf) and Plasmodium vivax (Pv) 6-oxopurine phosphoribosyltransfer

251 Plasmodium vivax (Pv) is a major cause of human malaria

252 inhibitors of Plasmodium falciparum (Pf) and Plasmodium vivax (Pv) NMT.

253 inhibitors of Plasmodium falciparum (Pf) and Plasmodium vivax (Pv) SHMT with a pyrazolopyran core str

254 ial parasites Plasmodium falciparum (Pf) and Plasmodium vivax (Pv).

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

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

257 Here, the crystal structure of ADA from Plasmodium vivax (PvADA) in a complex with MT-coformycin

258 ed with the sexual-stage-specific antigen of Plasmodium vivax, Pvs25, as a negative control, and the

259 Plasmodium vivax relapse infections occur following acti

260 malaria in humans, Plasmodium falciparum and Plasmodium vivax, rely on two distinct host cell surface

261 The population structure of Plasmodium vivax remains elusive.

262 Plasmodium vivax, requires the Duffy blood group antigen

263 search: 2002 and Beyond, devoted entirely to Plasmodium vivax research.

264 Plasmodium vivax resistance to chloroquine (CQ) has been

265 isks of elimination are presented, including Plasmodium vivax, resistance in the parasite and mosquit

266 laria cases are caused by its distant cousin Plasmodium vivax, resulting in a daunting morbidity and

267 been identified by comparative analyses with Plasmodium vivax reticulocyte binding protein 2 (PvRBP-2

268 e binding protein 1 (PfNBP1), an ortholog of Plasmodium vivax reticulocyte binding protein-1.

269 Crucial gaps in our understanding of Plasmodium vivax reticulocyte invasion and protective im

270 ctures of PKG from Plasmodium falciparum and Plasmodium vivax, revealing how key structural component

271 onal antibody directed against a proprietary Plasmodium vivax-specific antigen, in addition to the an

272 Plasmodium vivax sporozoites consist of tachysporozoites

273 Plasmodium vivax synthesizes the largest number of 36 tr

274 parasites such as Plasmodium falciparum and Plasmodium vivax, the causative agents of malaria.

275 mprising HIV-1, the malaria-causing parasite Plasmodium vivax, the fungus Aspergillus niger, and the

276 The difficulty in controlling Plasmodium vivax, the most common cause of human malaria

277 Plasmodium vivax, the most widely distributed human mala

278 Plasmodium vivax, the most widely distributed human mala

279 it has a close phylogenetic relationship to Plasmodium vivax, the second most important species of h

280 he development of vaccine candidates against Plasmodium vivax-the most geographically widespread huma

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

282 ocked transmission of Plasmodium berghei and Plasmodium vivax to Anopheles gambiae and Anopheles diru

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

284 The ability of the malaria parasite Plasmodium vivax to invade erythrocytes is dependent on

285 The Plasmodium vivax TRAg (PvTRAg) family includes 36 member

286 spatial limits of Plasmodium falciparum and Plasmodium vivax transmission on a global scale.

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

288 Recently, we have characterized a Plasmodium vivax tryptophan-rich antigen PvTRAg38, which

289 Plasmodium vivax uses a single member of the Duffy bindi

290 we describe the development of a multistage Plasmodium vivax vaccine which simultaneously expresses

291 Later evolution of long latency in Plasmodium vivax was a necessary adaptation as early hom

292 laria symptoms, the prevalence was 87.6% and Plasmodium vivax was the most prevalent species (74.0%).

293 d 163,000 new cases (more than 80% caused by Plasmodium vivax) were recorded in the Brazilian Amazon

294 Dengue and malaria, predominantly Plasmodium vivax, were the most frequently identified sp

295 f coendemicity for Plasmodium falciparum and Plasmodium vivax where mefloquine is used to treat P. fa

296 In contrast to Plasmodium vivax, which has disappeared from West Africa

297 We present evidence from one such species, Plasmodium vivax, which has experienced sustained select

298 t widely distributed human malaria parasite, Plasmodium vivax, will be a major step towards malaria e

299 nt years, there has been renewed interest in Plasmodium vivax, with CHMI models developed by groups i

300 Plasmodium vivax, with its dormant liver stage, will be