ライフサイエンスコーパス: berghei

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

2 RNAi makes mosquitoes more susceptible to P. berghei.

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

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

5 RecA homolog during sporogony in Plasmodium berghei.

6 GAP50, GAPM1-3) of both P. falciparum and P. 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 he rodent model malarial parasite Plasmodium berghei.

11 reaction in the malaria organism Plasmodium berghei.

12 t DHODH from P. falciparum, P. vivax, and P. berghei.

13 itical role of lymphocytes in immunity to P. berghei.

14 he growth of the rodent parasite, Plasmodium berghei.

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

16 eight flagellated microgametes in Plasmodium berghei.

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

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

19 ays blood schizonticidal activity against P. berghei.

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

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

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

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

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

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

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

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

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

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

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

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

32 Using rodent malaria models (Plasmodium berghei and P. yoelii), we were unable to show that sali

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

34 hibits oocyst development of both Plasmodium berghei and Plasmodium falciparum, suggesting that enola

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

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

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

38 on in the rodent malaria parasite Plasmodium berghei, and distinctive features of fertilization in bo

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

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

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

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

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

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

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

46 In the Plasmodium berghei ANKA (PbA) murine model, CM pathogenesis is asso

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

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

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

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

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

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

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

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

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

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

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

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

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

60 Plasmodium berghei Anka infection of mice recapitulates many featur

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

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

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

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

65 Using the Plasmodium berghei ANKA murine model of experimental cerebral malar

66 We used the Plasmodium berghei ANKA murine model of experimental cerebral malar

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

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

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

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

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

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

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

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

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

76 ndow in the murine model of CM by Plasmodium berghei ANKA, we show that murine CM is associated with

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

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

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

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

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

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

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

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

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

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

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

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

89 with the rodent malaria parasite Plasmodium berghei ANKA.

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

91 bral malaria mortality when infected with P. berghei ANKA.

92 murine cerebral malaria caused by Plasmodium berghei ANKA.

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

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

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

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

97 s by conditionally disrupting the Plasmodium berghei cGMP-dependent protein kinase in sporozoites.

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

99 PNPN)(2)D of the malaria parasite Plasmodium berghei circumsporozoite protein.

100 We show that P. berghei circumsporozoite-specific memory CD8 T cells und

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

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

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

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

105 asma exposure and reduced potency against P. berghei DHODH.

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

107 se, and ED(50) values in the 4-day murine P. berghei efficacy model of 13-21 mg/kg/day with oral twic

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

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

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

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

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

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

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

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

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

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

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

119 We built a pipeline for generating P. berghei genetic modification vectors at genome scale in

120 for effective modification of the Plasmodium berghei genome.

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

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

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

124 which are resistant partially to Plasmodium berghei, had higher fitness than non-transgenic mosquito

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

126 t the rodent malaria parasite orthologue, P. berghei hexose transporter (PbHT) gene, was similarly re

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

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

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

130 etect the rodent malaria parasite Plasmodium berghei in blood.

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

132 ifluoromethylphenyl, suppressed growth of P. berghei in mice after oral administration.

133 ere we show that lack of efficacy against P. berghei in mice resulted from a combination of poor plas

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

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

136 Synergy is also observed against Plasmodium berghei in vivo.

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

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

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

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

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

142 ated for antimalarial efficacy in Plasmodium berghei infected mice.

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

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

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

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

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

148 rotection in P. yoelii-infected BALB/c or P. berghei-infected B10.D2 mice correlated with increased r

149 In addition, IFN-beta-treated P. berghei-infected mice also had fewer brain T-cell infilt

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

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

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

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

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

155 Plasmodium berghei-infected mice treated with IFN-beta died later a

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

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

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

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

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

161 sential for high antimalarial efficacy in P. berghei-infected mice.

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

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

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

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

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

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

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

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

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

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

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

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

174 P. berghei infection resulted in increased expression of ch

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

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

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

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

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

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

181 Infection with Plasmodium berghei is lethal to mice, causing high levels of parasi

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

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

184 ration and phenotypic analysis of Plasmodium berghei knockout (KO) lines, characterizing 20 genes enc

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

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

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

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

189 than primaquine in vitro against Plasmodium berghei liver stage.

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

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

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

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

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

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

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

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

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

199 itoring liver stage burden in the Plasmodium berghei model.

200 ppresses parasites in vivo in the Plasmodium berghei model.

201 In a Plasmodium berghei mouse infection model, one lead compound lowered

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

203 35 exhibited 98% activity in the in vivo P. berghei mouse model (4-day test by Peters) at 4 x 50 mg/

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 in vivo by evolution of resistant Plasmodium berghei mutants.

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

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

221 reticulocyte-restricted parasite Plasmodium berghei NK65 1556Cl1.

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

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

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

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

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

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

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

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

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

231 CD8 T cells in the BALB/c mouse model of P. berghei or P. yoelii sporozoite infection to examine the

232 ction of mice with sporozoites of Plasmodium berghei or Plasmodium yoelii has been used extensively t

233 Immunization of mice with Plasmodium berghei or Plasmodium yoelii synthetic linear peptide ch

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

235 y, the transcripts coding for the Plasmodium berghei orthologues of those genes are stored and transl

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

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

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

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

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

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

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

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

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

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

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

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

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

249 fection strategy, we generated transgenic P. berghei parasites expressing a PbHT-GFP fusion protein s

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

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

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

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

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

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

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

257 on the surface of midgut-invading Plasmodium berghei parasites, targeting them for destruction.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 The Plasmodium berghei scavenger receptor-like protein PbSR is essentia

273 We identified a Plasmodium berghei secreted protein (PBANKA_131270) that plays dist

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

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

276 ite challenge than for protection against P. berghei sporozoite challenge.

277 emory CD8 T cells and reduced immunity to P. berghei sporozoite challenge.

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

279 ation that protects mice against multiple P. berghei sporozoite challenges for at least 19 months.

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

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

282 on, we also demonstrate that arg- Plasmodium berghei sporozoites show significantly decreased liver i

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

284 m infection with PfCSP transgenic Plasmodium berghei sporozoites.

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

286 ia by infecting C57BL/6 mice with 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 We genetically modified Plasmodium berghei to express Pfs25 and demonstrated that the trans

292 alciparum and the rodent parasite Plasmodium berghei using gene targeting strategies.

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 parasite Plasmodium berghei, we screened a panel of HIV PIs in vitro for eff

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

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

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

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