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1 ei rhodesiense and falcipain-2 of Plasmodium falciparum.
2 irst genome-wide nascent RNA profiling in P. falciparum.
3 activity against liver and blood stages of P falciparum.
4 cking vaccine (TBV) candidate for Plasmodium falciparum.
5 lication throughout schizogony in Plasmodium falciparum.
6 rs of the human malaria parasite, Plasmodium falciparum.
7 difference in the Fulani susceptibility to P.falciparum.
8 ys with proteasomes isolated from Plasmodium falciparum.
9 lled Human Malaria Infection with Plasmodium falciparum.
10 virulent human malaria parasite, Plasmodium falciparum.
11 of malaria in humans is caused by Plasmodium falciparum.
12 he human malaria-causing parasite Plasmodium falciparum.
13 ation, affecting most laboratory lines of P. falciparum.
14 r severe malaria in adults diagnosed with P. falciparum.
15 nt role in asexual development of Plasmodium falciparum.
16 s a potential target for vaccines against P. falciparum.
17 R0 and R2), and AMA1 antigens of Plasmodium falciparum.
18 quito bite: a major challenge for Plasmodium falciparum.
22 ctron microscopy structure of the Plasmodium falciparum 80S ribosome with the (+)-mefloquine enantiom
23 lts to the species level revealed Plasmodium falciparum (92.0%), Plasmodium ovale (5.6%), and Plasmod
24 active pericentromeric heterochromatin in P. falciparum, a region devoid of the characteristic H3K9me
27 esent study antibody responses to Plasmodium falciparum AMA-1, MSP-119 and CSP were measured with the
29 ecreased 5-fold from 2006 to 2010; 72% of P. falciparum and 87% of P. vivax infections were submicros
30 y against a multidrug resistant strain of P. falciparum and arrest parasites at the ring phase of the
33 tory activity against multiple strains of P. falciparum and P. vivax in vitro, is efficacious against
34 strongly inhibited oocyst development of P. falciparum and Plasmodium berghei expressing PfCelTOS in
36 pecies causing malaria in humans, Plasmodium falciparum and Plasmodium vivax, rely on two distinct ho
38 hat the unexpected target of actinonin in P. falciparum and Toxoplasma gondii is FtsH1, a homolog of
40 ples from Cambodian patients infected with P falciparum and treated with dihydroartemisinin-piperaqui
41 used by the Apicomplexan parasite Plasmodium falciparum, and results in significant global morbidity
43 ning chimeric rodent parasites expressing P. falciparum antigens and a flow cytometric readout of inf
45 ch may influence the emergence of Plasmodium falciparum artemisinin-resistant phenotypes and genotype
46 re identified: (1) children infected with P. falciparum as detected by rapid diagnostic testing (RDT)
48 0 pM in a PfPKG kinase assay and inhibits P. falciparum blood stage proliferation in vitro with an EC
49 itical for asexual development of Plasmodium falciparum, but its precise function and substrates rema
50 sinin-resistant and -sensitive strains of P. falciparum by combining liquid chromatography-mass spect
51 t least one P. vivax parasitaemia and 10% P. falciparum, by qPCR, both of which were predominantly su
52 st that the dominant artemisinin-resistant P falciparum C580Y lineage probably arose in western Cambo
53 suggest that protective immunity against P. falciparum can be achieved via multiple mechanisms and h
54 er various environmental perturbations in P. falciparum can yield quantitative insights into fundamen
55 exposure to the malaria parasite Plasmodium falciparum cause an accumulation of specific responses a
60 lysophosphatidylcholine (LysoPC) controls P. falciparum cell fate by repressing parasite sexual diffe
62 vel mutation within the gene encoding the P. falciparum chloroquine resistance transporter, PfCRT.
63 didate of malaria is based on the Plasmodium falciparum circumsporozoite protein (CSP), a major surfa
64 reported to be safe and protective against P falciparum controlled human malaria infection in malaria
65 ers of malaria incidence for P. vivax and P. falciparum corresponded to the pre- and first two years
66 xplore antibody binding in the context of P. falciparum CSP, we used negative-stain electron microsco
68 dazopyridine series targeting the Plasmodium falciparum cyclic GMP-dependent protein kinase (PfPKG).
72 2-2.30]; I(2)=26.1%; 34 estimates), as did P falciparum detected in placental samples (OR 1.95 [1.48-
76 y against asexual blood stages of Plasmodium falciparum, excellent parasite selectivity, and nanomola
78 This unexpected response of human mDCs to P. falciparum exhibited a transcriptional program distinct
79 fected controls, women with early Plasmodium falciparum exposure had retarded intrauterine growth bet
80 term decline in the prevalence of Plasmodium falciparum from 40% prevalence in the period 1900-1929 t
81 oth P. berghei and clinically circulating P. falciparum from malaria endemic areas in Kenya, but not
83 Even submicroscopic levels of Plasmodium falciparum gametocytes can infect mosquitoes and promote
84 ially, also blocks transmission of mature P. falciparum gametocytes to Anopheles stephensi mosquitoes
86 haracterize the regulatory regions of the P. falciparum gene PF3D7_1234700, encoding a CPW-WPC protei
88 reasons that remain unknown, the Plasmodium falciparum genome has an exceptionally high AT content c
89 ingle nucleotide polymorphisms within the P. falciparum genome were identified and only marginal diff
91 this article, we demonstrate that Plasmodium falciparum genomic DNA delivered to the cytosol of human
92 Plasmodium gallinaceum (>80%) and Plasmodium falciparum (>40%) models, an activity that was equivalen
94 he plasmepsin II/III genes within Plasmodium falciparum has been associated with decreased sensitivit
96 Proteases of the malaria parasite Plasmodium falciparum have long been investigated as drug targets.
97 but a higher proportion were positive for P. falciparum histidine rich protein 2 (192/246 [78.0%]) vs
98 t, this sensor was used to detect Plasmodium falciparum histidine-rich protein 2 (PfHRP2), an importa
99 Rapid diagnostic tests based on Plasmodium falciparum histidine-rich protein II (PfHRP-II) and P. f
100 ral flow malaria RDT that targets Plasmodium falciparum histidine-rich protein-II (HRPII) and Plasmod
104 P. vivax in vitro, is efficacious against P. falciparum in in vivo rodent models, produces parasite r
107 e findings in the Xenopus model extend to P. falciparum in vivo, our data suggest that PfCRT might pl
108 lassical LPS response, pointing to unique P. falciparum-induced activation pathways that may explain
110 immune effector mechanism against Plasmodium falciparum-infected erythrocytes (IE); however, current
111 y cytokine secretion, mDCs incubated with P. falciparum-infected erythrocytes activated antigen-speci
116 th a fever within the previous 14 days and P falciparum infection assessed by RDT who received an ACT
117 asymptomatic individuals with or without P. falciparum infection at the end of the 6-month dry seaso
118 oratory efficacy endpoint of time to first P falciparum infection beginning 28 days after the fifth v
120 are fast-acting compounds that can cure a P. falciparum infection in a humanized NOD/SCID mouse model
122 identified to be associated with Plasmodium falciparum infection in natural Anopheles gambiae popula
124 dren younger than 5 years with a fever and P falciparum infection increased across sub-Saharan Africa
127 icant protection in African adults against P falciparum infection throughout an entire malaria season
130 during the early immune response against P. falciparum infection, we investigated whether they could
131 red with women with no detected antenatal P. falciparum infection, women with positive RDT findings d
139 gens are widely deployed for detection of P. falciparum infection; however, these tests often miss ca
140 s that support liver stage human malaria (P. falciparum) infection in vitro, and also after implantat
141 vo IC50 64 nM), and murine P. berghei and P. falciparum infections (day 4 ED90 0.34 and 0.57 mg kg(-1
143 e studied spatial distribution of Plasmodium falciparum infections to compare simulated effects of th
144 (2) RDT-negative children whose untreated P. falciparum infections were detected retrospectively by P
146 e the first line of treatment for Plasmodium falciparum infections worldwide, but artemisinin resista
150 low-dose primaquine (PQ) reduces Plasmodium falciparum infectivity before it impacts gametocyte dens
153 d with the human malaria parasite Plasmodium falciparum (iRBCs) adhere to the vascular endothelium th
156 ity of pepstatin against cultured Plasmodium falciparum is highly variable depending on the commercia
158 ever, the human malaria parasite, Plasmodium falciparum, is incapable of pyrimidine salvage for mRNA
159 ssociated with drug resistance in Plasmodium falciparum isolated from subjects receiving DP or SP.
160 did a genome-wide association study of 297 P falciparum isolates from Cambodia to investigate the rel
161 rospectively sequenced the genomes of 194 P. falciparum isolates from five sites in Northwest Thailan
162 is observational study, we tested Plasmodium falciparum isolates from Myanmar, northeastern Thailand,
163 re performed by sequential cloning of six P. falciparum isolates growing in human erythrocytes in vit
164 on in malaria parasites, clinical Plasmodium falciparum isolates were sampled from patients and cultu
165 the benzoxaborole AN3661 against Plasmodium falciparum laboratory-adapted strains (mean IC50 32 nM),
167 histidine-rich protein II (PfHRP-II) and P. falciparum lactate dehydrogenase (PfLDH) antigens are wi
168 icans to fatal pathogens, such as Plasmodium falciparum, Lassa Virus and Trypanosoma brucei rhodesien
174 as first-line agents to treat uncomplicated falciparum malaria due to their activity against multidr
177 ations that confer artemisinin resistance in falciparum malaria have multiple independent origins acr
178 arative analysis of treatment regimen for P. falciparum malaria in adults in Stockholm during 2000-20
180 reasing, creating a problem for diagnosis of falciparum malaria in locations without quality-assured
183 demic sub-Saharan Africa are attributed to P falciparum malaria in pregnancy; the population attribut
185 administration for elimination of Plasmodium falciparum malaria is recommended by WHO in some setting
186 5a and 5c showed activity against Plasmodium falciparum malaria parasites (IC50 approximately 1 muM).
187 a-regression analysis of cure rates from all falciparum malaria treatment trials (n = 40) with monoth
189 pre-erythrocytic) prophylaxis of Plasmodium falciparum malaria with prolonged activity would substan
191 ria, severe (n = 21) and nonsevere (n = 109) falciparum malaria, and healthy controls (n = 50), we me
193 relatively better protection from Plasmodium falciparum malaria, as reflected by fewer symptomatic ca
194 urrent treatment of uncomplicated Plasmodium falciparum malaria, but ACT resistance is spreading acro
195 eved to confer protection against Plasmodium falciparum malaria, but the precise nature of the protec
196 ia correlates with the development of severe falciparum malaria, suggesting that platelets either con
207 n on maintenance of antibodies to Plasmodium falciparum merozoite antigens and infected erythrocytes
210 In this article, we show that Plasmodium falciparum merozoites, the invasive form of blood stage
213 cking robust adaptive immunity to Plasmodium falciparum Nevertheless, the host may partly control blo
214 he mitochondria of Plasmodium falciparum (P. falciparum) NF54-attB blood-stage parasites and evaluate
215 a deadly outcome of infection by Plasmodium falciparum, occurring when parasite-infected erythrocyte
216 e cytosol and the mitochondria of Plasmodium falciparum (P. falciparum) NF54-attB blood-stage parasit
217 ce and spread of fit artemisinin-resistant P falciparum parasite lineages, which then acquire partner
218 approach to detect hotspots using Plasmodium falciparum parasite prevalence and serological evidence
222 sess potent antimalarial activity against P. falciparum parasites comparable to the known antimalaria
223 hallenged with double chimeric P. berghei-P. falciparum parasites expressing both PfUIS3 and PfTRAP,
224 e recalled in human volunteers exposed to P. falciparum parasites in a controlled human malaria infec
225 PfHRP2-only RDTs is sufficient to select P. falciparum parasites lacking this protein, thus posing a
227 g whether successful sporogony of Plasmodium falciparum parasites through to human-infectious transmi
230 ne knockouts were not viable in the human P. falciparum pathogen, we used conditional knockdowns to d
231 observational cohort study, we evaluated P. falciparum pathogenesis in vitro in RBCs from pregnant w
233 s, children acquired equal numbers of new P. falciparum (Pf) and Pv blood-stage infections/year (Pf-m
234 phoribosyltransferase (HGPRT) and Plasmodium falciparum (Pf) hypoxanthine-guanine-xanthine phosphorib
235 man malaria infection (CHMI) with Plasmodium falciparum (Pf) parasites homologous to the vaccine stra
236 ization with radiation-attenuated Plasmodium falciparum (Pf) sporozoites (PfSPZ) inoculated by mosqui
237 SP), the major surface antigen of Plasmodium falciparum (Pf) sporozoites, can protect from malaria in
238 ter of the human malaria parasite Plasmodium falciparum, PfCRT, is an important determinant of resist
241 Bicyclic azetidines targeting Plasmodium falciparum phenylalanyl-tRNA synthetase comprise one pro
242 pyridine that selectively targets Plasmodium falciparum PKG, inhibits blood stage parasite growth in
244 esistance in the malaria parasite Plasmodium falciparum poses a major threat to the control and elimi
246 to serve a different function in Plasmodium falciparum, protecting ookinetes from the mosquito immun
247 Placental accumulation is mediated by P. falciparum protein VAR2CSA, a leading PAM-specific vacci
248 eened proteomic data for highly expressed P. falciparum proteins and compared their features to those
249 asmodium yoelii orthologs of four Plasmodium falciparum proteins identified by an antibody-based geno
251 have almost entirely focussed on Plasmodium falciparum, providing a highly informative means to inve
252 th the homologous Brd PfGCN5 from Plasmodium falciparum rationalizes the high selectivity for PCAF an
260 any genes of the malaria parasite Plasmodium falciparum show clonally variant expression regulated at
264 nsgenic P. berghei parasites that express P. falciparum sporozoite antigens, we have been able to use
265 t the prevalence and intensity of Plasmodium falciparum sporozoite infection is significantly lower i
266 live-attenuated malaria vaccine, Plasmodium falciparum sporozoite vaccine (PfSPZ Vaccine), confers s
267 ) of 3200 aseptic, purified, cryopreserved P falciparum sporozoites (PfSPZ Challenge; Sanaria Inc, Ro
272 itive (NF54) and -resistant (Dd2 and 7G8) P. falciparum strains with 5/6 having IC50 < 100 nM against
273 d stages of drug-sensitive and -resistant P. falciparum strains, inhibits development of P. berghei i
274 The earliest transcriptomics studies in P. falciparum suggested a cascade of transcriptional activi
276 ent or replication of blood-stage Plasmodium falciparum The percentage of Plasmodium-infected (iRBCs)
277 und that the activation of DCs by Plasmodium falciparum, the main causative agent of human malaria, i
280 tro activity against different strains of P. falciparum, the toxicity, and the metabolic stability is
281 in malaria effector proteins from Plasmodium falciparum These findings imply a role for the RxLR moti
282 coadministered with the vaccine candidate P. falciparum thrombospondin-related adhesion protein (PfTR
283 ave characterised replication dynamics in P. falciparum throughout schizogony, using DNA fibre labell
285 established mathematical model of Plasmodium falciparum transmission dynamics with epidemiological, i
288 efforts to model the changing patterns of P. falciparum transmission intensity in Africa have been li
289 gent-based stochastic simulation model of P. falciparum transmission was used to investigate the sele
290 ested at each antenatal visit for Plasmodium falciparum, using an RDT and polymerase chain reaction a
291 enotypes and Abs specific for the Plasmodium falciparum vaccine candidate apical membrane Ag-1 (AMA1)
296 r in the human malarial parasite, Plasmodium falciparum, we have quantified cytosolic labile heme lev
297 tage-specific molecular methods to detect P. falciparum, we show that gametocytes-and not their nonin
298 The study suggests that early exposure to P. falciparum, which is not targeted for prevention by curr
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