ライフサイエンスコーパス: berghei

1 falciparum ) and in vivo (against Plasmodium berghei ).

2 life cycle using the rodent malaria model P. berghei.

3 ays blood schizonticidal activity against P. berghei.

4 <15 mpk x 3 in mice infected with Plasmodium berghei.

5 ally deficient in AQP4 were infected with P. berghei.

6 RecA homolog during sporogony in Plasmodium berghei.

7 nfection with the rodent malaria parasite P. berghei.

8 me-wide knockout and tagging programs for P. berghei.

9 infected with the rodent parasite Plasmodium berghei.

10 RNAi makes mosquitoes more susceptible to P. berghei.

11 GAP50, GAPM1-3) of both P. falciparum and P. berghei.

12 ding motility in the rodent malaria model P. berghei.

13 eight flagellated microgametes in Plasmodium berghei.

14 es in the rodent malaria parasite Plasmodium berghei.

15 s during infection by the rodent parasite P. berghei.

16 rval: 3.3-4.9 mg/kg) and 13 mg/kg against P. berghei (95% confidence interval: 11-16 mg/kg).

17 designed to modify the genome of Plasmodium berghei, a malaria parasite of rodents, which can be req

18 ng forms to sexual development in Plasmodium berghei, a malaria parasite of rodents.

19 e in the rodent malaria parasite, Plasmodium berghei, ablating the protein that converts ADP to ATP.

20 displayed anti-P. falciparum and Plasmodium berghei activity in vitro and in vivo, respectively.

21 is a secreted octamer that binds to both P. berghei and clinically circulating P. falciparum from ma

22 deficient mutants of the rodent-infecting P. berghei and human-infecting P. falciparum parasites, we

23 sing activity against liver stage Plasmodium berghei and moderate antimethicillin-resistant Staphyloc

24 he rodent parasites P. yoelii and Plasmodium berghei and on the human malaria parasite Plasmodium fal

25 atios, and higher antibody levels against P. berghei and P. chabaudi antigens than P. berghei-infecte

26 Host PC is taken up by both P. berghei and P. falciparum and is necessary for correct l

27 th the hepatic and erythrocytic stages of P. berghei and P. falciparum infection, suggesting inclusio

28 tes (mean ex vivo IC50 64 nM), and murine P. berghei and P. falciparum infections (day 4 ED90 0.34 an

29 ment in P. berghei, oocyst development in P. berghei and P. falciparum, and the liver stage of P. yoe

30 lso showed parasiticidal activity against P. berghei and P. knowlesi Hence, our data establish PfCLK3

31 rns are species independent, marking both P. berghei and P. vivax infected cells, and that MUC13 can

32 ways are known to be induced upon Plasmodium berghei and Plasmodium falciparum infection, respectivel

33 ificantly blocked transmission of Plasmodium berghei and Plasmodium vivax to Anopheles gambiae and An

34 ytic forms were observed for both Plasmodium berghei and Plasmodium yoelii, two different rodent mala

35 ral administration of WM382 cured mice of P. berghei and prevented blood infection from the liver.

36 zyme for normal physiological function in P. berghei and suggest that drugs that specifically inhibit

37 genome-scale knockout screens in Plasmodium berghei and Toxoplasma gondii, in which pooled transfect

38 ronounced in Plasmodium vivax and Plasmodium berghei, and absent in Plasmodium yoelii In Plasmodium k

39 e stages of Toxoplasma gondii and Plasmodium berghei, and apical positioning of TgGAC depends on an a

40 s follows: Plasmodium falciparum, Plasmodium berghei, and Plasmodium knowlesi.

41 ation in vivo in mice, using the parasite P. berghei, and show that it is possible to create mutant p

42 zoa, e.g., Trichomonas vaginalis, Plasmodium berghei, and sporozoites and blood-stage forms of Plasmo

43 in an experimental CM model using Plasmodium berghei, and we provide strong evidence that the absence

44 the brains of mice infected with Plasmodium berghei ANKA (PbA) compared to uninfected controls and t

45 The murine Plasmodium berghei ANKA (PbA) infection model has helped to identif

46 We have used the Plasmodium berghei ANKA (PbA) model in which mice develop experimen

47 s required for the development of Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria

48 fection with the rodent parasite, Plasmodium berghei ANKA (PbANKA) has been extensively used to study

49 )-lactose into mice-infected with Plasmodium berghei ANKA (PbANKA) to block galectins and found signi

50 CD47-deficient mice infected with Plasmodium berghei ANKA and in vitro phagocytosis of P. falciparum-

51 that AhR-knockout (KO) mice infected with P. berghei Anka displayed increased parasitemia, earlier mo

52 gene (Cnr2(-/-)) inoculated with Plasmodium berghei ANKA erythrocytes exhibited enhanced survival an

53 knockout (KO) mice infected with Plasmodium berghei ANKA had significantly delayed mortality compare

54 tion in brain cortex subjected to Plasmodium berghei ANKA infection compared to asymptomatic, anemic,

55 significantly reduced survival following P. berghei ANKA infection compared to those receiving KO bo

56 ific cellular sources of IFN-gamma during P. berghei ANKA infection have not been investigated, and i

57 dy-mediated blockade of the IL-10R during P. berghei ANKA infection in ECM-resistant BALB/c mice lead

58 al malaria (ECM) using the murine Plasmodium berghei ANKA infection model.

59 Plasmodium berghei ANKA infection of C57BL/6 mice is a widely used

60 tal cerebral malaria (ECM) during Plasmodium berghei ANKA infection of C57BL/6 mice.

61 Plasmodium berghei Anka infection of mice recapitulates many featur

62 ression of SOCS3 in spleen and brain, and P. berghei Anka infection resulted in enhanced expression o

63 hogenic effects of IL-10R blockade during P. berghei ANKA infection were reversible by depletion of T

64 lls promote the development of ECM during P. berghei ANKA infection.

65 Using the Plasmodium berghei ANKA murine model of ECM and mice deficient for

66 or parasite growth, we generated a mutant P. berghei ANKA parasite with a reduced CD36-mediated adher

67 ated them, and challenged their pups with P. berghei ANKA parasites to assess the impact of maternal

68 Irbc of the rodent parasite Plasmodium berghei ANKA sequester in a fashion analogous to P. falc

69 sistant to ECM when infected with Plasmodium berghei ANKA sporozoites, the liver-infective form of th

70 = 5) mice were infected with the Plasmodium berghei ANKA strain from May 2016 to July 2018.

71 Additionally, mice with patent Plasmodium berghei ANKA strain infection treated with a single dose

72 malaria and in mice infected with Plasmodium berghei ANKA with or without the arginase gene.

73 c cells that were inoculated with Plasmodium berghei ANKA, a murine model of cerebral malaria.

74 he neuroinflammatory process triggered by P. berghei ANKA, an experimental model of cerebral malaria.

75 itidis serogroup B, Candida albicans, and P. berghei ANKA, and against colonic pathology in a model o

76 urified Plasmodium falciparum and Plasmodium berghei ANKA, and by spleen macrophages and DCs from Pla

77 vity in vitro and in vivo against Plasmodium berghei ANKA, comparable to artesunate and artemether.

78 single cohort of semisynchronous, Plasmodium berghei ANKA- or Plasmodium yoelii 17XNL-parasitized red

79 lation of immune responses during Plasmodium berghei ANKA-induced experimental cerebral malaria (ECM)

80 c T. gondii infection can prevent Plasmodium berghei ANKA-induced experimental cerebral malaria (ECM)

81 of IL-4 against fatal malaria in Plasmodium berghei ANKA-infected C57BL/6J mice, an experimental CM

82 However, P. berghei ANKA-infected Card9(-/-) mice succumbed to neuro

83 ascular inflammation and protects Plasmodium berghei ANKA-infected mice from CM.

84 Plasmodium berghei ANKA-infected mice served as the positive contro

85 anemia in Plasmodium yoelii- and Plasmodium berghei ANKA-infected mice, similar to our previous obse

86 ompared MP proteins from non-infected and P. berghei ANKA-infected mice.

87 from Plasmodium yoelii 17NXL-infected and P. berghei ANKA-infected mice.

88 susceptible phenotype if challenged with P. berghei ANKA-infected red blood cells that bypass the li

89 ECM resistance in P. berghei ANKA-infected Themis(I23N) mice is associated wi

90 ch C57BL/6 mice are infected with Plasmodium berghei ANKA.

91 C57BL/6J mice were infected with Plasmodium berghei ANKA.

92 ia (ECM) caused by infection with Plasmodium berghei ANKA.

93 ntal CM in Ifnar1(-/-) mice infected with P. berghei ANKA.

94 with the rodent malaria parasite Plasmodium berghei ANKA.

95 sistant IFN-gamma(-/-) mice infected with P. berghei ANKA.

96 ability of lead HHQs to suppress Plasmodium berghei blood-stage parasite proliferation.

97 parum and rodent malaria parasite Plasmodium berghei by up to 98%.

98 alent dose of the oral parent drug in the P. berghei causal prophylaxis model.

99 We show that Plasmodium berghei CDK-related kinase 5 (CRK5), is a critical regul

100 rasitemia and longer survival following a P. berghei challenge compared to pups born to control dams.

101 ancy protects their offspring from lethal P. berghei challenge.

102 ion (95%) in BALB/c mice required Plasmodium berghei circumsporozoite protein (CS(252-260))-specific

103 we conducted PGP gene knockout studies in P. berghei, confirming that this conserved metabolic proofr

104 Combinatorial complementation of Plasmodium berghei CP genes with the orthologs from Plasmodium falc

105 Furthermore, P. berghei CS(252)-specific CD8 T cells exhibit reduced pro

106 monoclonal antibody (mAb) 3D11 binding to P. berghei CSP (PbCSP) using molecular dynamics simulations

107 dent P. berghei parasite lines, where the P. berghei csp gene coding sequence has been replaced with

108 e we confirm a failure to protect against P. berghei, despite successful antibody induction against l

109 ood stage development and impairs Plasmodium berghei development inside hepatocytes, both in vitro an

110 We also demonstrated that Plasmodium berghei DHFR promoter is recognized and functional in B.

111 f 35 orphan transport proteins of Plasmodium berghei during its life cycle in mice and Anopheles mosq

112 ambiae (G3) mosquitoes were infected with P. berghei, encapsulation was strongly correlated with the

113 Because P. berghei ENT1 (PbENT1) shares only 60% amino acid sequenc

114 Visualizing the Plasmodium berghei ER during liver stage development, we found that

115 development of P. falciparum and Plasmodium berghei expressing PfCelTOS in Anopheles gambiae mosquit

116 Using transgenic Plasmodium berghei expressing the repeat region of P. falciparum CS

117 ne protein P47, known to be important for P. berghei female gamete fertility, is shown to serve a dif

118 We selected two vital Plasmodium berghei G-actin-binding proteins, C-CAP and profilin, in

119 (2)(+) signals that mediate activation of P. berghei gametocytes in the mosquito and egress of Plasmo

120 anslationally repressed in female Plasmodium berghei gametocytes, is activated translationally during

121 or CD8(+) T cell responses to the Plasmodium berghei GAP5040-48 epitope in mice expressing the MHC cl

122 s because we could not delete the Plasmodium berghei gene encoding GatA in blood stage parasites in v

123 for effective modification of the Plasmodium berghei genome.

124 ating a high-integrity library of Plasmodium berghei genomic DNA (>77% A+T content) in a bacteriophag

125 prime-boost immunization against Plasmodium berghei glideosome-associated protein 5041-48-, sporozoi

126 nd 2 are important for robust liver-stage P. berghei growth.

127 The rodent parasite Plasmodium berghei has served as a model for human malaria transmis

128 In this study, the Plasmodium berghei homologues of antigens CSP and TRAP are combined

129 Deregulation of PV5 expression renders P. berghei hypersensitive to the antimalarial drugs artesun

130 , a systematic knockout screen in Plasmodium berghei identified ten ApiAP2 genes that were essential

131 tion, transmission-based study of Plasmodium berghei in Anopheles stephensi to assess the impact of a

132 etect the rodent malaria parasite Plasmodium berghei in blood.

133 CSP-derived epitope SYIPSAEKI of Plasmodium berghei in both sporozoite- and vaccine-induced protecti

134 lciparum strains, inhibits development of P. berghei in hepatocytes, and at doses up to 100 mg/kg als

135 vivo Thompson test results using Plasmodium berghei in mice showed that these 4(1H)-quinolones were

136 itro and in vivo activity against Plasmodium berghei in the Thompson test.

137 Synergy is also observed against Plasmodium berghei in vivo.

138 etic tool in the rodent malaria parasite, P. berghei, in which endogenous proteins engineered to cont

139 Plasmodium chabaudi-infected mice and the P. berghei-induced experimental cerebral malaria (ECM).

140 om P. berghei infected An. stephensi, and P. berghei infected An. gambiae more similar to the P. berg

141 berghei infected Anopheles stephensi, and P. berghei infected An. gambiae.

142 parum infected An. gambiae differing from P. berghei infected An. stephensi, and P. berghei infected

143 infected An. gambiae more similar to the P. berghei infected An. stephensi.

144 parum infected Anopheles gambiae, Plasmodium berghei infected Anopheles stephensi, and P. berghei inf

145 to mice and suppressed parasite growth in P. berghei infected mice following subcutaneous administrat

146 Parasitemia was reduced by over 90% in P. berghei infected mice in 3/6 derivatives following oral

147 Additional in vivo experiments using P. berghei infected mice showed that administration of 6h a

148 in two 60-day survival studies of Plasmodium berghei infected mice.

149 ated for antimalarial efficacy in Plasmodium berghei infected mice.

150 When evaluated in P. berghei -infected mice, compound 4 was completely curati

151 rial activity when administered orally to P. berghei -infected mice.

152 Red cells from P. chabaudi/P. berghei-infected animals had increased surface IgG and C

153 P. chabaudi/P. berghei-infected animals had more intense splenic hemato

154 py showed that red cells from P. chabaudi/P. berghei-infected animals were removed at an accelerated

155 lso showed remarkable in vivo activity in P. berghei-infected mice (ED(50) ~ 0.5 mg/kg) when administ

156 n two different mouse models for malaria, P. berghei-infected mice and P. falciparum-infected NOD-sci

157 temia in Plasmodium chabaudi- and Plasmodium berghei-infected mice and the 48-hour in vitro cycle of

158 Children with cerebral malaria and P. berghei-infected mice demonstrated depletion of plasma a

159 P. chabaudi/P. berghei-infected mice had an initial 9- to 10-day phase

160 One of the lead analogues cured P. berghei-infected mice in the Peters 4 day-suppressive te

161 g/kg of mefloquine hydrochloride, Plasmodium berghei-infected mice survived on average 29.8 days afte

162 Compound 15 completely cured Plasmodium berghei-infected mice with a single oral dose of 30 mg/k

163 Treatment of P. berghei-infected mice with recombinant IL-12 significant

164 In P. berghei-infected mice, oral administration of 1o drastic

165 iparum parasites and in vivo with Plasmodium berghei-infected mice.

166 and T cell infiltration in the brains of P. berghei-infected mice.

167 opheles stephensi fed on non-infected and P. berghei-infected mice.

168 was upregulated in the livers of Plasmodium berghei-infected mice; hepatic activin B was also upregu

169 P. berghei and P. chabaudi antigens than P. berghei-infected or P. chabaudi-recovered animals.

170 urative with all mice surviving a Plasmodium berghei infection after 30 days.

171 s the prevalence and intensity of Plasmodium berghei infection in adults, whereby Nishikoi Fish Pelle

172 ation of in vivo efficacy against Plasmodium berghei infection in mice on the basis of their improved

173 vaccine candidate, reduces, not enhances, P. berghei infection in mice.

174 timuli in vitro, and during the course of P. berghei infection in vivo.

175 sis of CM in vivo, we further investigated P berghei infection in VWF(-/-) C57BL/6J mice.

176 pathogenic response of mice to a Plasmodium berghei infection is dominated by a Vbeta8.1 T cell resp

177 STAg treatment 24 h post-P. berghei infection led to a rapid increase in serum level

178 P. berghei infection of mice is an animal model for human m

179 mbiae, and FREP1 is important for Plasmodium berghei infection of mosquitoes.

180 By 5 days after P. berghei infection, STAg-treated mice had reduced IFN-gam

181 hat plasma arginase flux was unchanged by P. berghei infection.

182 e also observed in murine plasma following P berghei infection.

183 studies in NMRI mice harboring the rodent P. berghei infection.

184 th P. chabaudi followed after recovery by P. berghei infection.

185 e itself is also an excellent liver stage P. berghei inhibitor (78: IC50 = 0.33 muM).

186 P chabaudi and P berghei iRBCs with apoptotic parasites (TdT(+)) exhibite

187 We discovered that the knock-out of HO in P. berghei is lethal; therefore, we investigated the functi

188 utility of this resource, we rescreen the P. berghei kinome, using published kinome screens for compa

189 h rates in mice of 2,578 barcoded Plasmodium berghei knockout mutants, representing >50% of the genom

190 ed MyoA expression throughout the Plasmodium berghei life cycle in both mammalian and insect hosts.

191 anscriptional atlas of the entire Plasmodium berghei life cycle.

192 PbVIT-deficient P. berghei lines (Pbvit(-)) show a reduction in parasite lo

193 s II molecules as determinants of Plasmodium berghei liver stage infection in mice.

194 than primaquine in vitro against Plasmodium berghei liver stage.

195 data by building a thermodynamic model of P. berghei liver-stage metabolism, which shows a major repr

196 ic compartments accumulate around Plasmodium berghei liver-stage parasites during development, and wh

197 oward HeLa cells and in vivo in a Plasmodium berghei malaria model as well as in the SCID mouse P. fa

198 l activity after oral administration in a P. berghei malaria model, although no complete parasite eli

199 ds showing excellent oral efficacy in the P. berghei malaria mouse model with ED90 values below 1 mg/

200 n-carrying line of sexual reproduction in P. berghei malaria.

201 ection, or failure of protection, against P. berghei merozoites could guide the development of an eff

202 , exhibits activity in the murine Plasmodium berghei model and efficacy comparable to that of the ref

203 In this study, using a Plasmodium berghei model compatible with tracking anti-blood stage

204 idation of this approach with the Plasmodium berghei model of murine malaria.

205 itoring liver stage burden in the Plasmodium berghei model.

206 ppresses parasites in vivo in the Plasmodium berghei model.

207 oral antimalarial activity in the Plasmodium berghei mouse malaria model associated with favorable ph

208 35 exhibited 98% activity in the in vivo P. berghei mouse model (4-day test by Peters) at 4 x 50 mg/

209 ith improved in vivo oral efficacy in the P. berghei mouse model and additional activity against para

210 promising in vivo efficacy in the Plasmodium berghei mouse model and will be further evaluated as pot

211 y, was completely curative in the Plasmodium berghei mouse model at 4 x 50 mg/kg po.

212 In contrast, efficacy in the Plasmodium berghei mouse model differed dramatically for some of th

213 mg/kg orally once a day for 4 days in the P. berghei mouse model of malaria.

214 d pharmacokinetics and oral activity in a P. berghei mouse model of malaria.

215 posure and better efficacy in the Plasmodium berghei mouse model of the disease than previously repor

216 exhibited in vivo activity in the Plasmodium berghei mouse model when administered orally.

217 in part curative activity in the Plasmodium berghei mouse model when administered perorally.

218 In the Plasmodium berghei mouse model, this series generally exhibited goo

219 g/kg once daily for 4 days in the Plasmodium berghei mouse model, which is superior to the activity s

220 hERG activity and in vivo efficacy in the P. berghei mouse model.

221 how that hepcidin upregulation in Plasmodium berghei murine malaria infection was accompanied by chan

222 Thus, the P. berghei murine malaria model may be useful to evaluate t

223 gap, we followed more than 1,300 barcoded P. berghei mutants through the life cycle.

224 in vivo by evolution of resistant Plasmodium berghei mutants.

225 By contrast, the nonneurotropic P. berghei NK65 (PbN) causes severe malarial disease in C57

226 o mice infected with the non-neurotrophic P. berghei NK65 (PbN).

227 of PbANKA and the closely related Plasmodium berghei NK65 (PbNK65), that does not cause ECM, differ i

228 reticulocyte-restricted parasite Plasmodium berghei NK65 1556Cl1.

229 In this study, using Plasmodium berghei NK65 as a model of a systemic, proinflammatory i

230 ole in suppressing protective immunity to P. berghei NK65 infection and that it is involved in inhibi

231 cient (WSX-1(-/-)) mice following Plasmodium berghei NK65 infection than in wild-type (WT) mice, ther

232 ficient (knockout [KO]) mice with Plasmodium berghei NK65.

233 /ED(90) of 1.87/4.72 mg/kg versus Plasmodium berghei (NS Strain) in a murine model of malaria when fo

234 odium falciparum, ookinete development in P. berghei, oocyst development in P. berghei and P. falcipa

235 ent melanization response against Plasmodium berghei ookinetes and exhibited significantly increased

236 aracterize a novel SPN protein of Plasmodium berghei ookinetes and sporozoites named G2 (glycine at p

237 Using the motility of Plasmodium berghei ookinetes as a signalling paradigm, we show that

238 alciparum erythrocytic stages and Plasmodium berghei ookinetes have identified proteolysis as a major

239 We also localized the Plasmodium berghei ortholog to the apicoplast in blood stage parasi

240 mice were challenged with double chimeric P. berghei-P. falciparum parasites expressing both PfUIS3 a

241 The P. berghei-P. vivax chimeric strain develops normally in mo

242 t are exposed to the bites of as few as 3 P. berghei-P. vivax-infected mosquitoes.

243 Here, we investigate the function of P. berghei P47 in Anopheles gambiae mosquito infections.

244 Our data establish a dual role of P. berghei P47 in vivo and reinforce the use of this parasi

245 icroglia from mice infected with a mutant P. berghei parasite (DeltaDPAP3), which does not cause ECM,

246 ing a fully infectious transgenic Plasmodium berghei parasite expressing P. vivax TRAP to allow studi

247 c receptor CD32b, nor against a Deltasmac P. berghei parasite line with a non-sequestering phenotype.

248 we generated two novel transgenic rodent P. berghei parasite lines, where the P. berghei csp gene co

249 Moreover, we determined that Plasmodium berghei parasites are heterogeneous for midgut invasion,

250 and characterization of chimeric Plasmodium berghei parasites bearing the type I repeat region of P.

251 essential for parasite growth as Plasmodium berghei parasites carrying a complete deletion of the fe

252 y isolating luciferase-expressing Plasmodium berghei parasites directly from the salivary glands of i

253 rotection against challenge with chimeric P. berghei parasites expressing PfUIS3.

254 Furthermore, we also developed chimeric P. berghei parasites expressing the cognate P. falciparum a

255 nd TB (82%) efficacies against transgenic P. berghei parasites expressing the corresponding P. vivax

256 ic T-cell responses, we generated Plasmodium berghei parasites expressing the model antigen ovalbumin

257 e malaria challenge models using chimeric P. berghei parasites expressing the relevant P. falciparum

258 They kill P. berghei parasites in 24-hour ex vivo culture.

259 Here we show that Plasmodium berghei parasites infecting hepatic cells rely on the PV

260 unction with recently produced transgenic P. berghei parasites that express P. falciparum sporozoite

261 otection against challenge with wild-type P. berghei parasites.

262 d PfSHMT, blood-stage Pf, and liver-stage P. berghei (Pb) cells and a high selectivity when assayed a

263 Compound 12 was efficacious in the P. berghei (Pb) model of malaria.

264 pressed and purified homolog from Plasmodium berghei (Pb), leading to the identification of 2-phospho

265 cination of mice with recombinant Plasmodium berghei PbSEA-1 significantly reduced parasitemia and de

266 Plasmodium falciparum (PfVIT) and Plasmodium berghei (PbVIT).

267 e subtilisin-encoding genes SUB1 and SUB3 P. berghei PIMMS2 is specifically expressed in zygotes and

268 ites expressing a mutated form of Plasmodium berghei PKG or carrying a deletion of the CDPK4 gene are

269 Gene disruption analysis of P. berghei PPs reveals that half of the genes are likely es

270 port a functional analysis of the Plasmodium berghei protein phosphatome, which exhibits high conserv

271 ito midgut screen candidate 2), a Plasmodium berghei protein with structural similarities to subtilis

272 a single stage of its complex life cycle, P. berghei requires two-thirds of genes for optimal growth,

273 odent parasites P. falciparum and Plasmodium berghei, respectively.

274 ion of PV5 in the rodent parasite Plasmodium berghei results in inordinate elongation of hemozoin cry

275 However, increasing data suggest the P. berghei rodent malaria may be able to circumvent vaccine

276 to bite challenge with transgenic Plasmodium berghei rodent sporozoites that incorporate the P. falci

277 2), strongly inhibited midgut invasion by P. berghei (SM1-sensitive and SM1-resistant) and Plasmodium

278 cells exhibit reduced protection against P. berghei sporozoite challenge in the context of C57BL/6 a

279 l response in the liver following Plasmodium berghei sporozoite challenge.

280 model; (3) prevention of in vitro Plasmodium berghei sporozoite-induced development in human hepatocy

281 epatocytes; and (4) protection of in vivo P. berghei sporozoite-induced infection in mice.

282 exposures to radiation-attenuated Plasmodium berghei sporozoites (Pb gamma-spz) induce long-lasting p

283 tion of Plasmodium falciparum and Plasmodium berghei sporozoites by anti-Plasmodium vivax CSP serum s

284 ered functional activation on exposure to P. berghei sporozoites.

285 m infection with PfCSP transgenic Plasmodium berghei sporozoites.

286 y after lethal challenge with the Plasmodium berghei strain ANKA.

287 nization and challenge with the wild-type P. berghei strains ANKA or NK65, or against a chimeric para

288 hat were then coinfected with two Plasmodium berghei strains, only one of which could be recognized d

289 se model of Hb S confers host tolerance to P berghei, through inhibition of pathogenic CD8(+) T cells

290 th FBG achieved >75% blocking efficacy of P. berghei to A. gambiae without triggering immunopathology

291 of Anopheles gambiae to transmit Plasmodium berghei to mice.

292 43 in the rodent malaria parasite Plasmodium berghei triggers robust complement activation and ookine

293 in survival of mice infected with Plasmodium berghei was observed when compared to control.

294 essing sporozoites of the rodent parasite P. berghei we are able to robustly quantify parasite infect

295 a genetically targeted strain of Plasmodium berghei, we observed that the Plasmodium ortholog of mac

296 Using the rodent malaria parasite Plasmodium berghei, we show that CDPK1, which is known to be essent

297 Here, using conditional mutagenesis in P. berghei, we show that SUB1 plays an essential role at th

298 es expressing PfUIS3 as well as wild-type P. berghei; when this vaccine is combined with another part

299 male-deficient, self-infertile strain of P. berghei, which restored fertility and production of oocy

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