ライフサイエンスコーパス: merozoite

1 ole for CyRPA in erythrocyte invasion by the merozoite.

2 pressed at high levels at the surface of the merozoite.

3 otein family, anchored at the surface of the merozoite.

4 rhoptry secretory organelles of the invasive merozoite.

5 phenotype and failed to form exoerythrocytic merozoites.

6 me wild-type liver stages mature and release merozoites.

7 rythrocyte invasion and the proliferation of merozoites.

8 he fine-scale invasion preference of P vivax merozoites.

9 changes in the strength of its clearance of merozoites.

10 ge and erythrocyte invasion by P. falciparum merozoites.

11 pattern and apical localization in P. vivax merozoites.

12 ion and to dense granules of sporozoites and merozoites.

13 resent intracellularly in late schizonts and merozoites.

14 mystifying work on hypnozoites and quiescent merozoites.

15 ence staining localized CyRPA at the apex of merozoites.

16 reside within the dense granules of invasive merozoites.

17 se of 10-300 fold compared to wild-type (WT) merozoites.

18 dly reduce the expected contributions of the merozoite actomyosin motor to invasion.

19 ulocyte binding protein homolog 5 (PfRH5), a merozoite adhesin required for erythrocyte invasion, is

20 te membrane wrapping alone, as a function of merozoite adhesive and shape properties, is sufficient t

21 rane deformations are crucial for successful merozoite alignment and require interaction strengths co

22 membrane rigidity is found to result in poor merozoite alignment, which can be a possible reason for

23 ally the importance of RBC deformability for merozoite alignment.

24 ater, with a schizont releasing newly formed merozoites, all committed to either continued asexual re

25 The merozoite, an extracellular stage of the parasite lifecy

26 th invasion by a single, asexually committed merozoite and ends, 48 hours later, with a schizont rele

27 Well classified merozoite and erythrocytic antigens were strongly reacti

28 tion formation between the apical end of the merozoite and the RBC surface to initiate invasion.

29 GLURP-specific antibodies recognized merozoites and also mediated OP activity.

30 ear to be located on the surface of iRBC and merozoites and are therefore well placed to interact wit

31 e the strength of the adhesive force between merozoites and erythrocytes, and to probe the cellular m

32 ep linked to the formation of a pore between merozoites and erythrocytes.

33 apped the binding site in FH that recognizes merozoites and identified Pf92, a member of the six-cyst

34 alciparum, including the release of infected merozoites and infection of overlaid erythrocytes, as we

35 antigens of infected erythrocytes (IEs) and merozoites and levels of opsonizing IgG to IEs were meas

36 g STEVOR and RIFIN are expressed in invasive merozoites and on the infected erythrocyte surface.

37 We show that in merozoites and ookinetes, additional expression does not

38 d red blood cells (RBCs), background loss of merozoites and parasitised RBCs, RBC age preference, RBC

39 wing processes: adaptive immune clearance of merozoites and parasitised red blood cells (RBCs), backg

40 highlights the complex relationship between merozoites and the complement system.

41 with both the surface of intra-erythrocytic merozoites and the inner aspect of erythrocyte membranes

42 _0355) are extrinsically associated with the merozoite, and both have a DBL domain in each protein.

43 zonts, be localized at the apical end of the merozoite, and preferentially bind reticulocytes over no

44 against a chimeric parasite line encoding a merozoite antigen from P. falciparum.

45 ixation in response to Plasmodium falciparum merozoite antigens (erythrocyte-binding antigen [EBA] 17

46 lines FCR3, E8B, and R29, and antibodies to merozoite antigens AMA-1 and MSP2.

47 nance of antibodies to Plasmodium falciparum merozoite antigens and infected erythrocytes (IEs), incl

48 ntibody levels to P. falciparum and P. vivax merozoite antigens and the pregnancy-specific PfVAR2CSA

49 antibodies (IgM, IgG, and IgG subclasses) to merozoite antigens and their relationship to the prospec

50 othesis, we compared antibody levels to four merozoite antigens from the P. falciparum 3D7 clone (api

51 ibody responses to several vaccine candidate merozoite antigens in relation to the infecting parasite

52 unity, such as young children, antibodies to merozoite antigens may act as biomarkers of malaria expo

53 ts demonstrate that conserved domains within merozoite antigens targeted by opsonization generate str

54 after adjustment for responses to all other merozoite antigens tested, while those against MSP-2, MS

55 alciparum are mostly focused on well-studied merozoite antigens that induce immune responses after na

56 electrophoresis and measured antibodies to 7 merozoite antigens using a multiplex assay.

57 uccessful antibody induction against leading merozoite antigens using protein-in-adjuvant or viral ve

58 immunoglobulin G (IgG) antibodies against 24 merozoite antigens was determined at the baseline of an

59 Between settings, seroprevalences for merozoite antigens were similar between Ungoye and Mfang

60 globulin G (IgG) levels to schizont extract, merozoite antigens, and VAR2CSA-DBL5epsilon were measure

61 psonizing antibodies to VSA, and antibody to merozoite antigens.

62 ate vaccine approaches targeting blood-stage merozoite antigens.

63 nhancing the acquisition of IgG responses to merozoite antigens.

64 ic merozoite-red-cell interactions align the merozoite apex in preparation for penetration.

65 distinct phylogenetic clade with Plasmodium merozoite apical erythrocyte-binding ligand (MAEBL) prot

66 ns hampered by the short-period of time that merozoites are invasive.

67 maturation into infectious exo-erythrocytic merozoites as well as the formation and persistence of h

68 ete within 1 min, and shortly thereafter the merozoites, at least in in vitro culture, lose their inv

69 d phosphorylation of erythrocyte proteins on merozoite attachment, including modification of the cyto

70 antigen PvTRAg38, which is expressed by its merozoites, binds to host erythrocytes, and interferes w

71 ized erythrocyte releases not only infective merozoites, but also the digestive vacuole (DV), a membr

72 n), while antibodies targeting STEVOR in the merozoite can effectively inhibit invasion.

73 The association with merozoite contact but not active entry demonstrates that

74 or failure of protection, against P. berghei merozoites could guide the development of an efficacious

75 Antibodies promoting opsonic phagocytosis of merozoites declined rapidly (half-life, 0.15 years).

76 e, showing that newly released P. falciparum merozoites, delivered via optical tweezers to a target e

77 o be directly sporozoite-derived rather than merozoite-derived.

78 In contrast, complement-fixing antibodies to merozoites did not decline and antibodies to IE surface

79 Because the entrapped merozoites die when prevented from escaping their host e

80 n late liver-stage growth arrest and lack of merozoite differentiation.

81 vacuoles, and independently interfering with merozoite disaggregation.

82 The series targets both merozoite egress and erythrocyte invasion, but crucially

83 At the same time, merozoite egress and invasion required a threshold ionic

84 analysis to detect and automatically record merozoite egress events in 100% of the 40 egress-invasio

85 ated genes are predominantly associated with merozoite egress functions.

86 that the same Syk kinase inhibitors suppress merozoite egress near the end of the parasite's intraery

87 es, where it remained throughout maturation, merozoite egress, and host cell invasion.

88 allenges, requiring multiple observations of merozoite egress-invasion sequences in live cultures und

89 We show that although merozoite entry does not involve erythrocyte actin reorg

90 However, these DeltaPfMSP3.1 merozoites exhibit enhanced invasion of RBCs in the pres

91 ryptophan-rich antigens (PvTRAgs), including merozoite expressed PvTRAg38, from this noncultivable hu

92 n suggested that after the initial adhesion, merozoites facilitate their proper alignment by inducing

93 When bound to merozoites, FH retains cofactor activity, a key function

94 licited antibody at opsonizing P. falciparum merozoites for phagocytosis.

95 es from the infected erythrocyte and priming merozoites for subsequent erythrocyte invasion.

96 te the effect of Dantu on the ability of the merozoite form of the malaria parasite Plasmodium falcip

97 odium falciparum involves interaction of the merozoite form through proteins on the surface coat.

98 LS schizonts exhibited exoerythrocytic merozoite formation and merosome release.

99 phospholipids necessary for exoerythrocytic merozoite formation.

100 mosquito and egress of Plasmodium falciparum merozoites from infected human erythrocytes.

101 Release (egress) of malaria merozoites from the host erythrocyte is a highly regulat

102 lood stage by enabling egress of the progeny merozoites from the infected erythrocyte and priming mer

103 candidate site on CR1 by which P. falciparum merozoites gain access to human erythrocytes in a non-si

104 The blood stage malaria parasite, the merozoite, has a small window of opportunity during whic

105 d that P. falciparum histones extracted from merozoites (HeH) directly stimulated the production of I

106 bodies to different AMA1 and MSP2 alleles of merozoites, IE surface antigens, and antibody functional

107 cell membranes eventually rupture, releasing merozoites in a process called egress.

108 line) schizonts produce variable numbers of merozoites in all erythrocyte types tested, with median

109 The first is concerned with whether latent merozoites in the lymphatic system can give rise to rela

110 a 95% decrease in the proportion of released merozoites in vitro (P < 0.0001).

111 d stage involves invasion of erythrocytes by merozoites, in which they grow and divide to release dau

112 ing was not apparent in blood-stage invasive merozoites, indicating that the apical complex is differ

113 invasive blood-stage malaria parasite - the merozoite - induces rapid morphological changes to the t

114 -like protein family functions after initial merozoite interaction by binding via the Duffy binding-l

115 add to our understanding of the erythrocyte-merozoite interactions that occur during invasion, and d

116 Successful invasion of merozoites into host erythrocytes is dependent on this p

117 rmation and release of thousands of invasive merozoites into the bloodstream.

118 asexual blood stages of malarial infection, merozoites invade erythrocytes and replicate within a pa

119 The mechanism by which P. falciparum merozoites invade human erythrocytes is complex, involvi

120 -stage parasites, which are established when merozoites invade human erythrocytes.

121 this study, we show that whereas P cynomolgi merozoites invade monkey red blood cells indiscriminatel

122 fected erythrocyte (IE) surface at 30 h post-merozoite invasion (PMI), concomitant with extensive oli

123 emonstrate that PMX is a master modulator of merozoite invasion and direct maturation of proteins req

124 h) family of proteins play a pivotal role in merozoite invasion and hence are important targets of im

125 Inhibition of merozoite invasion by CyRPA-specific mAbs in vitro and i

126 he deformability of erythrocytes and inhibit merozoite invasion by directly inhibiting the phosphoryl

127 ough soluble cytotoxic mediators, abrogating merozoite invasion capacity.

128 hibitor of this interaction that also blocks merozoite invasion in genetically distinct parasites by

129 derstanding the underlying mechanisms behind merozoite invasion into the protected niche inside the h

130 ular changes in the host cell that accompany merozoite invasion is lacking.

131 A key step in merozoite invasion is the essential binding of PfRh5/CyR

132 known erythrocyte receptor for the P. vivax merozoite invasion ligand, Duffy binding protein 1 (DBP1

133 inhibiting receptor-binding functions of key merozoite invasion ligands.

134 The West African Merozoite Invasion Network (WAMIN) has been formed to me

135 Malaria vaccines targeting merozoite invasion of erythrocytes have long held appeal

136 Merozoite invasion of RBCs requires interaction between

137 The ability to target merozoite invasion proteins with specific small inhibito

138 e find a strong link between RBC tension and merozoite invasion, and identify a tension threshold abo

139 ital ligand for Plasmodium vivax blood-stage merozoite invasion, making the molecule an attractive va

140 es in a non-sialic acid-dependent pathway of merozoite invasion.

141 zont stage to form rosettes and in promoting merozoite invasion.

142 s process is unlikely to directly facilitate merozoite invasion.

143 les that of proteins known to be involved in merozoite invasion.

144 Red blood cell (RBC) invasion by malaria merozoites involves formation of a parasitophorous vacuo

145 Invasion of erythrocytes by Plasmodial merozoites is a composite process involving the interpla

146 rythrocyte invasion by Plasmodium falciparum merozoites is a highly intricate process in which Plasmo

147 rythrocyte invasion by Plasmodium falciparum merozoites is an essential step for parasite survival an

148 rythrocyte invasion by Plasmodium falciparum merozoites is an essential step for parasite survival an

149 Invasion of erythrocytes by merozoites is an essential step for the survival and pro

150 in schizogony/merogony, and its location in merozoites is distinct from, and anterior to, that of a

151 The most abundant protein on the surface of merozoites is merozoite surface protein 1 (MSP1), which

152 ion of erythrocytes by Plasmodium falciparum merozoites is necessary for malaria pathogenesis and is

153 d cells (RBCs) by Plasmodium falciparum (Pf) merozoites is the binding of rhoptry neck protein 2 (RON

154 gue that the innate immune response clearing merozoites is the most likely, but not necessarily the o

155 ocessed MSP1 mutant show delayed egress, and merozoites lacking surface-bound MSP1 display a severe e

156 odium falciparum gamma-irradiated long-lived merozoite (LLM) line was developed and investigated.

157 essed in Plasmodium falciparum schizonts and merozoites: MSPDBL1 (also termed MSP3.4) and MSPDBL2 (MS

158 In extracellular ookinetes, sporozoites, and merozoites, MyoA was located at the parasite periphery.

159 cR-dependent effector mechanisms, we produce merozoite-neutralizing and non-neutralizing anti-PfRH5 c

160 ts address the controversy regarding whether merozoite-neutralizing antibody can cause protection aga

161 a strong association between protection and merozoite-neutralizing antibody responses following vacc

162 Blood-stage merozoites of P. falciparum invade erythrocytes, and thi

163 Ags expressed by merozoites of Plasmodium falciparum are likely to be imp

164 Merozoites of the protozoan parasite responsible for the

165 Plasmodium vivax merozoites only invade reticulocytes, a minor though het

166 is located in the IMC in all three invasive (merozoite, ookinete-, and sporozoite) stages of developm

167 MyoB is expressed in all invasive stages (merozoites, ookinetes, and sporozoites) of the life cycl

168 arasite strains strongly supports the use of merozoite opsonization as a correlate of immunity for fi

169 We have provided the first evidence that merozoite opsonization is predominantly strain transcend

170 ibit in vitro parasite growth and had strong merozoite opsonizing capacity, suggesting that protectio

171 In this study, we investigated whether merozoite-opsonizing antibodies are associated with prot

172 arasite protein, which we name P. falciparum Merozoite Organizing Protein (PfMOP), as essential for c

173 sient expression of PfMSP8 on the surface of merozoites, PfMSP8-specific rabbit IgG did not inhibit t

174 wever, the discovery that the members of the merozoite PfRH5-PfCyRPA-PfRipr (RCR) complex are capable

175 e of IgG3, complement-fixing antibodies, and merozoite phagocytosis vary according to transmission in

176 Papua New Guinea with our validated assay of merozoite phagocytosis.

177 isin-like serine protease SUB1 of Plasmodium merozoites plays a dual role in egress from and invasion

178 In addition, owing to merozoite preference for young erythrocytes, iron supple

179 that recruitment of FH affords P. falciparum merozoites protection from complement-mediated lysis.

180 b responses to a comprehensive repertoire of merozoite proteins and investigate whether they are targ

181 ade human erythrocytes is complex, involving merozoite proteins as well as erythrocyte surface protei

182 dy levels to Circumsporozoite Protein and 10 merozoite proteins increased at different rates with age

183 ng evidence suggests that antibodies against merozoite proteins involved in Plasmodium falciparum inv

184 has demonstrated the significant role of the merozoite proteome during erythrocyte invasion, while id

185 ria is both hypnozoites (relapse source) and merozoites (recrudescence source), not hypnozoites only.

186 rief preinvasion period during which dynamic merozoite-red-cell interactions align the merozoite apex

187 m species antigens accessible at the time of merozoite release are likely targets of biologically fun

188 diversity of confluent processes leading to merozoite release.

189 vel in vitro assay to quantify the number of merozoites released from an individual schizont, termed

190 nal antibodies against Plasmodium falciparum merozoites remain largely unexplored and, more important

191 st key step of the invasion process, that of merozoite reorientation to its apex and tight adhesive l

192 eviously reported a significant reduction in merozoite replication and oocyst shedding in E. tenella

193 th measles (457 years), and much shorter for merozoite responses (0.8-7.6 years), compared with PfVAR

194 y be able to circumvent vaccine-induced anti-merozoite responses.

195 secreted polymorphic antigen associated with merozoite (SPAM) domain characteristic of MSP-3 family m

196 ntibody levels in the neonate (P. falciparum merozoite, spearman rho median [range] 0.42 [0.33-0.66],

197 by anti-MSP3 antibodies were attached to the merozoite surface and also associated with erythrocyte m

198 recombinant form of the relatively conserved merozoite surface antigen, PfRH5.

199 The major merozoite surface antigens of Babesia canis have been de

200 L) domain-containing proteins located on the merozoite surface but whose function remains unknown.

201 rm for display of MSPDBL1 and MSPDBL2 on the merozoite surface for binding to receptors on the erythr

202 e-binding homologue protein 4 (PfRh4) on the merozoite surface interacting with complement receptor t

203 ate that interactions between SUB1-processed merozoite surface MSP1 and the spectrin network of the e

204 ssed 91 recombinant proteins, located on the merozoite surface or within invasion organelles, and scr

205 . falciparum erythrocyte membrane protein 1, merozoite surface protein (MSP) 10, MSP2, liver-stage an

206 ic mouse model with T cells specific for the merozoite surface protein (MSP)-1 of Plasmodium chabaudi

207 ite Plasmodium falciparum, genotyping of the merozoite surface protein (MSP1/2) genes is a standard m

208 ite protein (CSP) and the 42-kDa fragment of merozoite surface protein 1 (MSP-1(42)) of P. vivax and

209 The C-terminal 19-kDa domain of merozoite surface protein 1 (MSP1(1)(9)) is the target o

210 igen 175 (EBA-175), and the 19-kDa region of merozoite surface protein 1 (MSP1(19)).

211 ow that the 33-kDa fragment of P. falciparum merozoite surface protein 1 (MSP1(33)), an abundant prot

212 lood-stage malaria vaccine targets, that is, merozoite surface protein 1 (MSP1) and apical membrane A

213 or-transgenic mouse recognizing a peptide of merozoite surface protein 1 (MSP1) injected into BALB/c

214 Merozoite surface protein 1 (MSP1) is a target for malar

215 dant protein on the surface of merozoites is merozoite surface protein 1 (MSP1), which consists of fo

216 fusion of the C-terminal 19-kDa fragment of merozoite surface protein 1 (MSP119) to P. falciparum MS

217 pecimens from Mozambique: 19-kDa fragment of merozoite surface protein 1 (MSP119), erythrocyte bindin

218 C-terminal fragment of Plasmodium falciparum merozoite surface protein 1 (MSP142) and the risk of (re

219 minal 19-kDa domain of Plasmodium falciparum merozoite surface protein 1 (PfMSP119) is an established

220 didates, the 19 kDa fragment of the P. vivax Merozoite Surface Protein 1 (PvMSP119) is one of the mos

221 A recombinant malaria vaccine antigen, the merozoite surface protein 1 (rMSP1), was conjugated to I

222 s found that antibodies to 5 proteins of the Merozoite Surface Protein 1 complex were differentially

223 of the system by targeting the P. falciparum merozoite surface protein 1 gene (msp1), which has previ

224 Using a newly developed Plasmodium vivax merozoite surface protein 1 gene (Pvmsp1) heteroduplex t

225 at a highly variable region of the P. vivax merozoite surface protein 1 gene revealed impressive div

226 The Plasmodium vivax merozoite surface protein 1 paralog (PvMSP1P), which has

227 king assay used to genotype Plasmodium vivax merozoite surface protein 1 was adapted to a capillary e

228 titers against circumsporozoite protein and merozoite surface protein 1 were significantly higher in

229 clone (apical membrane antigen 1, AMA1-3D7; merozoite surface protein 1, MSP1-3D7; 175 kDa erythrocy

230 ed from the circumsporozoite protein and the merozoite surface protein 1.

231 y-acquired and vaccine-induced antibodies to merozoite surface protein 2 (MSP2) are associated with r

232 erythrocyte-binding antigen [EBA] 175RIII-V, merozoite surface protein 2 [MSP-2], and MSP-142) and op

233 n-based genotyping of the highly polymorphic merozoite surface protein 2 gene was performed on blood

234 erythrocyte-binding antigen, EBA175-3D7; and merozoite surface protein 2, MSP2-3D7) in a cohort of 10

235 s that belong to tryptophan-rich antigen and merozoite surface protein 3 (MSP3) families that were mo

236 n fused in frame to the C-terminal region of merozoite surface protein 3 (MSP3).

237 We identified PfMSP3.1, a member of the merozoite surface protein 3 family of merozoite surface

238 Merozoite surface protein 3 of Plasmodium falciparum, a

239 P. vivax merozoite surface protein 3alpha (PvMSP3alpha) is a targ

240 we focused on the use of highly immunogenic merozoite surface protein 8 (MSP8) as a vaccine carrier

241 9) (PyMSP1(1)(9)) with full-length P. yoelii merozoite surface protein 8 (MSP8).

242 19) fused to the N terminus of P. falciparum merozoite surface protein 8 that lacked its low-complexi

243 in LLMs and further characterized the major merozoite surface protein complex.

244 Two unusual members of the MSP-3 family, merozoite surface protein duffy binding-like (MSPDBL)1 a

245 (2) 18S rDNA PCR positive; (3) positive for merozoite surface protein genes by PCR or positive by lo

246 Here, we identify P113 as a merozoite surface protein that directly interacts with R

247 The most abundant merozoite surface protein, MSP1, is synthesized as a lar

248 circumsporozoite protein (CSP) and P. yoelii merozoite surface protein-1 (MSP-1) showed encouraging r

249 didates SE36 and 42-kDa region of the 3D7 Pf merozoite surface protein-1 (MSP-1), and tetanus toxoid

250 cting with a major invasion-related protein, merozoite surface protein-1 (MSP-1).

251 ules anchored to the parasite surface is the merozoite surface protein-1 (MSP1).

252 ge antigen-1, apical membrane antigen-1, and merozoite surface protein-1 do not to predict protection

253 sponse and demonstrated improved efficacy of merozoite surface protein-1 protein vaccines against a P

254 responses against Plasmodium falciparum (Pf) merozoite surface protein-3 and glutamate-rich protein.

255 en 1, apical-membrane antigen 1 (AMA-1), and merozoite surface proteins (MSP) 1 and 3, in children in

256 ng evidence suggests that antibodies against merozoite surface proteins (MSPs) play an important role

257 mediated predominately via C1q fixation, and merozoite surface proteins 1 and 2 were identified as ma

258 enrichment in reticulocyte binding proteins, merozoite surface proteins and exported proteins with un

259 The merozoite surface proteins DBL1 and -2 (PfMSPDBL1 and Pf

260 We have shown that the peripheral merozoite surface proteins MSPDBL1 and MSPDBL2 are part

261 te that MSP1 interacts with other peripheral merozoite surface proteins to form a large complex.

262 of the merozoite surface protein 3 family of merozoite surface proteins, as the direct interaction pa

263 ternalisation and for correct functioning of merozoite surface proteins.

264 the mechanism by which it is anchored to the merozoite surface remains unknown because both PfRH5 and

265 n and suitably localized in abundance on the merozoite surface represents an ideal target for antimal

266 When bound to the merozoite surface, C1-INH retains its ability to complex

267 duced by human immunization with a candidate merozoite surface-protein vaccine.

268 RH5/PfRipr/CyRPA multiprotein complex on the merozoite surface.

269 eleasable mechanism for anchoring RH5 to the merozoite surface.

270 sis in schizonts, where ontogeny of daughter merozoites takes place, and in gametocytes that infect A

271 We investigated the merozoite targets and antibody-mediated mechanisms assoc

272 cates within erythrocytes, producing progeny merozoites that are released from infected cells via a p

273 r and infect hepatocytes prior to release of merozoites that initiate symptomatic blood-stage malaria

274 ion of erythrocytes and rapid death of those merozoites that invade.

275 P. falciparum merozoites that lack PfMSP3.1 showed a marked reduction

276 This stage is initiated when merozoites, the free invasive blood-stage form, invade c

277 article, we show that Plasmodium falciparum merozoites, the invasive form of blood stage malaria par

278 s report, we show that Plasmodium falciparum merozoites, the invasive form of the malaria parasites,

279 the speed of red blood cell invasion by the merozoite, thereby potentiating the effect of all neutra

280 and the consequent dissemination of released merozoites throughout the bloodstream, we decided to exp

281 ibodies promote complement deposition on the merozoite to mediate inhibition of erythrocyte invasion

282 analysis using dimensions for an archetypal merozoite to predict the respective contributions of the

283 gs support previous studies that found OP of merozoites to be associated with protection against mala

284 ti-PfRH5 Abs inhibit the tight attachment of merozoites to erythrocytes and are capable of blocking t

285 t cycle' prepares gene expression in nascent merozoites to initiate sexual development through a hith

286 ter mu, the ratio of background loss rate of merozoites to invasion rate of mature RBCs, needed to be

287 of AMA1 as the step that commits Plasmodium merozoites to RBC invasion and point to RON2 as a potent

288 ly marginal differences were observed in the merozoite transcriptomes.

289 smodium express a TRAP family protein called merozoite-TRAP (MTRAP) that has been implicated in eryth

290 Plasmodium falciparum merozoites use diverse alternative erythrocyte receptors

291 eins, leading to rational design of improved merozoite vaccines.

292 2], and MSP-142) and opsonic phagocytosis of merozoites were measured in a multinational trial assess

293 noglobulin G (IgG) antibodies against intact merozoites were quantified in the plasma of Ghanaian chi

294 abolism links PKG to egress of P. falciparum merozoites, where inhibition of PKG blocks hydrolysis of

295 d was located at the periphery of segmenting merozoites, where it remained throughout maturation, mer

296 Even spent merozoites, which had lost the ability to invade, retain

297 ich they grow and divide to release daughter merozoites, which in turn invade new erythrocytes perpet

298 stablished because the orientation of a free merozoite with respect to the RBC membrane is random whe

299 Interaction of SUB2-null merozoites with RBCs leads to either abortive invasion w

300 inhibited malaria parasite egress, trapping merozoites within infected erythrocytes.