ライフサイエンスコーパス: gametocyte

1 luding targeting the parasite sexual stages (gametocytes).

2 laria is mediated by sexual precursor cells (gametocytes).

3 d for transmission, the sexually reproducing gametocyte.

4 tive against asexual blood stages and mature gametocytes.

5 g gametocytes, then decrease in mature-stage gametocytes.

6 specific and 69 as proteins not expressed by gametocytes.

7 culocytes and mature into both schizonts and gametocytes.

8 ess reporter genes in mature male and female gametocytes.

9 mmitment to the production and maturation of gametocytes.

10 lood cells into non-dividing male and female gametocytes.

11 47; Pfs48/45), and mature (PF10_0303; Pfs25) gametocytes.

12 gametocytes; heterochromatic PTMs mark early gametocytes.

13 ito transmission, that is, the P. falciparum gametocytes.

14 -deficient mutants) that fail to form mature gametocytes.

15 cially available drug that eliminates mature gametocytes.

16 ces gametocytemia, but may not affect mature gametocytes.

17 e development of efficient molecules against gametocytes.

18 aquine showed activity only against immature gametocytes.

19 g the straight side of the D-shaped stage II gametocytes.

20 ties of asexual parasites and the absence of gametocytes.

21 on into non-replicating sexual stages called gametocytes.

22 asexual replication or differentiation into gametocytes.

23 m parasites (IC50 1-5 nM) as well as against gametocytes.

24 veloped into metabolically quiescent stage V gametocytes.

25 he previously developed P. falciparum female gametocyte activation assay (Pf FGAA), which assesses st

26 so affect parasite fitness, protect immature gametocytes against chloroquine action, and alter P. fal

27 tages of development, as well as in the male gametocyte and locates both at the apical and basal ends

28 This work has implications for monitoring gametocyte and transmission dynamics and responses to dr

29 say (SMFA) using cultured P. falciparum NF54 gametocytes and Anopheles stephensi mosquitoes.

30 weekly for 42 days to assess the presence of gametocytes and asexual parasites by microscopy.

31 we compared the gene expression profiles of gametocytes and asynchronous blood-stage P. falciparum p

32 ixing antibodies with cultured P. falciparum gametocytes and feeding them to mosquitoes through an ar

33 bodian clone NF135.C10 consistently produced gametocytes and generated substantial numbers of sporozo

34 lled studies are needed in participants with gametocytes and higher parasite densities.

35 imalarials on intraerythrocytic sexual stage gametocytes and identify transmission-blocking agents ha

36 lained by the preferential clearance of male gametocytes and may be due to an effect on gametocyte fi

37 s seem to arrest before formation of stage I gametocytes and may represent genes involved in commitme

38 7 is expressed on the surface of both female gametocytes and ookinetes where it serves distinct funct

39 we showed that FBG interacts with Plasmodium gametocytes and ookinetes, revealing the molecular mecha

40 EP1 can directly bind Plasmodia sexual stage gametocytes and ookinetes.

41 asion in mosquitoes through interacting with gametocytes and ookinetes.

42 biology of asexual blood-stage parasites and gametocytes and the ability to culture them in vitro len

43 ly after activation of the intraerythrocytic gametocyte, and during sporozoite migration.

44 ent, are incapable of producing mature-stage gametocytes, and are not transmitted to mosquitoes.

45 protein in sporozoites, asexual blood forms, gametocytes, and in the oocysts developing inside mosqui

46 ective treatment of infectious P. falciparum gametocytes, and may interrupt transmission and help con

47 red blood cell (RBC)-derived microvesicles, gametocytes, and uninfected RBCs.

48 ethods to detect P. falciparum, we show that gametocytes-and not their noninfectious asexual progenit

49 al profiling and detection of an early stage gametocyte antigen determined that a subset of these mut

50 recrudescent asexual parasitemia, and these gametocytes are again refractory to piperaquine treatmen

51 On the other hand, female gametocytes are enriched in proteins required for zygote

52 Although gametocytes are essential for malaria transmission, in A

53 Plasmodium falciparum gametocytes are essential for malaria transmission.

54 Gametocytes are essential for Plasmodium transmission, b

55 Plasmodium falciparum immature gametocytes are not observed in peripheral blood.

56 Committed gametocytes are refractory to the commonly used drug pip

57 Plasmodium falciparum stage V gametocytes are responsible for parasite transmission, a

58 is process, as only sexual parasites, called gametocytes, are infective to the mosquito vector.

59 We hereby report on a dual-luciferase gametocyte assay with immature and mature P. falciparum

60 assay times are commonly reported in current gametocyte assays measuring gametocyte-expressed fluores

61 rasite free, harbored asexual stages, or had gametocytes at submicroscopic densities.

62 on, harbor a third of infections with patent gametocytes between May and August, when transmission tr

63 el approaches and provided new insights into gametocyte biology.

64 lears asexual malaria parasites and immature gametocytes but does not prevent posttreatment malaria t

65 Deltapyhmgb2 parasites develop into gametocytes but have drastic impairment of oocyst format

66 In addition, we show how functionally viable gametocytes can be used to evaluate transmission-blockin

67 bmicroscopic levels of Plasmodium falciparum gametocytes can infect mosquitoes and promote onward tra

68 associated with a 2-fold longer duration of gametocyte carriage (P = .0007), a higher likelihood of

69 iated with a 73% (95% CI 24-90) reduction in gametocyte carriage (P = .013).

70 directly linked to disease severity such as gametocyte carriage and infection chronicity is less wel

71 a longer prophylactic time after treatment, gametocyte carriage and malaria transmission to mosquito

72 d for multiplicity of infections by nPCR and gametocyte carriage by nucleic acid sequence-based ampli

73 the non-inferiority of the mean duration of gametocyte carriage in the test doses compared with the

74 P. vivax gametocyte carriage mirrors asexual-stage infection.

75 The mean duration of gametocyte carriage was 5.5 days (95% CI, 3.6-8.5) for A

76 The mean duration of gametocyte carriage was 6.6 days (95% CI 5.3-7.8) in the

77 Gametocyte carriage was determined by molecular methods

78 Gametocyte carriage was determined by Pfs25 quantitative

79 emoglobin concentration, adverse events, and gametocyte carriage.

80 Primaquine substantially reduced gametocyte carriage.

81 ts resuspended with autologous plasma of the gametocyte carrier, and iii) blood pellets resuspended w

82 n potential, but an increasing proportion of gametocyte carriers are asymptomatic and submicroscopic

83 Microscopic gametocyte carriers attracted almost 2 times more mosqui

84 transmission potential of naturally infected gametocyte carriers highlighted considerable variation i

85 Abundant low-density gametocyte carriers impede clone detectability, which ma

86 Most efforts to identify gametocyte carriers use polymerase chain reaction amplif

87 = 72), primaquine was associated with faster gametocyte clearance (hazard ratio = 2.42 [95% confidenc

88 se association of single-dose primaquine for gametocyte clearance and for safety in P falciparum mala

89 r-lumefantrine (AL), relative to non-ACTs on gametocyte clearance and transmission interruption.

90 In a pilot study in the third cohort, gametocyte clearance following administration of 15 mg,

91 volumes and detecting initially sequestered gametocyte clones in follow-up samples.

92 on the portfolio of the most promising anti-gametocytes compounds is also presented.

93 rials comparing AL to non-ACTs that reported gametocyte counts or results of mosquito-feeding assays.

94 sis of male and female Plasmodium falciparum gametocytes coupled with a comprehensive proteome analys

95 rticular emphasis is placed upon operating a gametocyte culture facility on a continuous cycle.

96 Current protocols for P. falciparum gametocyte culture usually require complex parasite sync

97 ly infected with P. falciparum (NF54 strain) gametocyte cultures slightly enhanced oocyst infection.

98 d to the isolation of 29 clones (insertional gametocyte-deficient mutants) that fail to form mature g

99 We also measured mRNA dynamics in F12 gametocyte-deficient parasites and demonstrate that the

100 interval, 1.39-4.19], P = .002) and reduced gametocyte densities (P = .018).

101 the probability of generating transmissible gametocyte densities without causing illness.

102 transmission efficiency caused by a rise in gametocyte densities, although the uneven distribution o

103 The reliability of pathogen (e.g. gametocyte) densities, and the accompanying diagnostic s

104 s though the non-linear relationship between gametocyte density and mosquito infection means that (pe

105 Gametocyte density and positivity correlated closely wit

106 model parameters suggests that reducing the gametocyte density in the blood meal most significantly

107 Interventions reducing gametocyte density need to be highly effective in order

108 Seven days after treatment, gametocyte density was significantly reduced in the DP-P

109 ium falciparum infectivity before it impacts gametocyte density.

110 The analytical sensitivity for gametocyte detection was evaluated for 25 genes with the

111 ertoire of biomarkers available for superior gametocyte detection, we compared the gene expression pr

112 tify methylene blue as a potent inhibitor of gametocyte development across all stages.

113 l replication are also capable of inhibiting gametocyte development and blocking malaria transmission

114 proposed to play a key role in P falciparum gametocyte development in the host and to represent nove

115 ual replication, sexual conversion and early gametocyte development in the major human malaria parasi

116 nes that are necessary for the initiation of gametocyte development in the subsequent cell cycle.

117 nship between hematological disturbances and gametocyte development in this tissue.

118 owth, but surprisingly also had no effect on gametocyte development or exflagellation, suggesting tha

119 tep in this pathway, are severely altered in gametocyte development, are incapable of producing matur

120 mmitment or at any subsequent stage of early gametocyte development.

121 xhibited changes in abundance during ABS and gametocyte development.

122 molar activity against the earliest forms of gametocyte development.

123 te intraerythrocytic asexual replication and gametocyte differentiation in the low micromolar range.

124 t the overall transcriptional program during gametocyte differentiation is surprisingly similar to th

125 Replacing the plasma of the gametocyte donor with malaria naive control serum result

126 sessing infectiousness of pregnant women and gametocyte dynamics during different trimesters of pregn

127 laria requires knowledge of Plasmodium vivax gametocyte dynamics.

128 eporters, endogenous ATP levels, activity of gametocyte enzymes, or redox-dependent dye fluorescence.

129 Mature gametocytes exhibit increased deformability and reappear

130 We introduce Plasmodium falciparum gametocyte exported protein-5 (PfGEXP5) transcript analy

131 he development of serologic tools to monitor gametocyte exposure in populations targeted for malaria

132 ese proteins may be a sensitive indicator of gametocyte exposure, although further studies are needed

133 g vaccines (TBV) would be boosted by natural gametocyte exposure, and also inform the development of

134 ed immunity would be boosted through natural gametocyte exposure, and that antibody responses to part

135 to particular antigens may reliably indicate gametocyte exposure.

136 orted in current gametocyte assays measuring gametocyte-expressed fluorescent or luciferase reporters

137 e gametocytes and may be due to an effect on gametocyte fitness.

138 slational repression in P. falciparum female gametocytes for the first time.

139 lecular mechanisms involved in commitment to gametocyte formation is extremely limited, and disruptin

140 in PfAP2-G correlate strongly with levels of gametocyte formation.

141 n of sexual-stage-specific transcription and gametocyte formation.

142 ges of malaria parasites, including ring and gametocyte forms, using attenuated total reflectance Fou

143 parum asexual blood stages and transmissible gametocyte forms.

144 block transmission of Plasmodium falciparum gametocytes from humans to mosquitoes.

145 m do not prevent transmission of circulating gametocytes from infected humans to mosquitoes.

146 resence of this drug, by protecting immature gametocytes from its lethal action.

147 Here we produce gametocytes from parasite clinical isolates that display

148 upting the FC gene also caused no defects in gametocyte generation or maturation but resulted in a gr

149 ing from PfAP2-G ablation, we identify early gametocyte genes as probable targets of PfAP2-G and show

150 ased differentiation of 6 length-polymorphic gametocyte genes.

151 Stage V gametocytes harboring Cas9-introduced pfmdr1 mutations a

152 were first identified (over a century ago), gametocytes have remained elusive, and basic questions r

153 PTMs are abundant during schizogony and late gametocytes; heterochromatic PTMs mark early gametocytes

154 ity against stage IV-V Plasmodium falciparum gametocytes (IC50 = 1.16 +/- 0.37 muM).

155 ng the addition of pharmacological agents to gametocytes implicated cGMP in exflagellation--the emerg

156 DHP prevented development of gametocytes in 277 patients without gametocytes on day 3

157 ssociated with a higher prevalence of mature gametocytes in bone marrow.

158 rug that clears mature Plasmodium falciparum gametocytes in infected human hosts, thereby preventing

159 evaluating the earliest (ring) stage sexual gametocytes in the blood of infected individuals.

160 The formation of Plasmodium falciparum gametocytes in the human host takes several days during

161 ignals that mediate activation of P. berghei gametocytes in the mosquito and egress of Plasmodium fal

162 al differentiation of malaria parasites into gametocytes in the vertebrate host and subsequent gamete

163 2, a top lead compound (IC50 = 8 nM against gametocytes in vitro), completely blocked oocyst formati

164 ty of producing mature Plasmodium falciparum gametocytes in vitro-the parasite stage responsible for

165 Deformability of Plasmodium falciparum gametocyte-infected erythrocytes (GIEs) allows them to p

166 ost takes several days during which immature gametocyte-infected erythrocytes (GIEs) sequester in hos

167 The gametocyte infectiousness to mosquitoes was determined b

168 lear how the density of transmission stages (gametocytes) influences infection (proportion of mosquit

169 Mendelian inheritance via gametocyte integration results in HHV-6 in every nucleat

170 res the successful development of Plasmodium gametocytes into flagellated microgametes upon mosquito

171 ceived PQ were less likely to carry P. vivax gametocytes (IRR = 0.27 [95% CI 0.19, 0.38], p < 0.001).

172 ty in the transition from immature to mature gametocytes is accompanied by the deassociation of paras

173 a 230-kDa sexual stage protein expressed in gametocytes is an alternative vaccine candidate.

174 Es and that regained deformability of mature gametocytes is associated with their release in the bloo

175 by the asexual blood stages, the presence of gametocytes is directly responsible for the infection of

176 amete formation from the terminally arrested gametocytes is exceptionally rapid, completing three mit

177 low-dose primaquine to eliminate circulating gametocytes is needed in areas where artemisinin and ACT

178 uman erythrocytes to produce male and female gametocytes, is a critical step in malaria transmission

179 nally repressed in female Plasmodium berghei gametocytes, is activated translationally during ookinet

180 PPKL is produced in schizonts and female gametocytes, is maternally inherited where its absence l

181 Specific HIV treatments have gametocyte killing and transmission-blocking effects.

182 asite from human to mosquito, yet developing gametocytes lack expression of surface proteins required

183 much less likely to occur at submicroscopic gametocyte levels.

184 development at stage I or in early stage II gametocytes, likely representing genes involved in gamet

185 Transcribed in gametocytes, LIMP is translated in the ookinete from mat

186 epresent genes involved in commitment to the gametocyte lineage.

187 g artemisinin-based combination therapies on gametocyte load are thus reviewed herein, making the dif

188 t of dose- and time-dependent drug action on gametocyte maturation and transmission.

189 cytes, likely representing genes involved in gametocyte maturation.

190 ssessed to determine the effects of drugs on gametocyte maturation.

191 l phase IIa trials, are strong inhibitors of gametocyte maturation/gamete formation and impact sporog

192 5% CI 1.68-2.19) while the infectiousness of gametocytes may be reduced during the replacement proced

193 /mL; in comparison, Pfs25 detected only 25.3 gametocytes/mL.

194 gametocyte-spiked whole blood, detecting 10 gametocytes/mL; in comparison, Pfs25 detected only 25.3

195 ith AC genotype carried parasites, including gametocytes, more often than their AA counterparts (OR 3

196 d derivatives were active against stage IV/V gametocytes of P. falciparum in vitro.

197 s been confirmed to be effective against the gametocytes of P. falciparum.

198 pment of gametocytes in 277 patients without gametocytes on day 3.

199 l analysis was stratified by the presence of gametocytes on day 3.

200 product that prevents FREP1 from binding to gametocytes or ookinetes was isolated and identified as

201 hibition of the development of P. falciparum gametocytes or ookinetes.

202 y very potent activity against the liver and gametocyte parasite life-cycle stages.

203 rtilization, and variable number of ingested gametocytes per strain on the optimal gametocyte sex rat

204 Although able to form gametocytes, PNP-deficient parasites did not form oocyst

205 40% more samples from asymptomatic adults as gametocyte positive.

206 first clinical episode, force of infection, gametocyte positivity, and time to first P. ovale infect

207 ted closely with parasitemia, and population gametocyte prevalence decreased 3-fold for P. falciparum

208 The primary end point was gametocyte prevalence during follow-up, as determined by

209 nopheles species, combined with their higher gametocyte prevalence in patients, may explain the rapid

210 The gametocyte prevalence of Plasmodium falciparum at baseli

211 Differentiation between gametocyte-producing Plasmodium falciparum clones depend

212 he steps required for reliable P. falciparum gametocyte production and highlights common factors that

213 theless, differences in invasion efficiency, gametocyte production and the length of the asexual cycl

214 xually replicating parasites are induced for gametocyte production by the addition of conditioned med

215 ng clone to transmission and the dynamics of gametocyte production in multiclone infections can be st

216 Gametocyte production rates vary depending on environmen

217 is used to measure asexual proliferation and gametocyte production via DNA dye staining and the gamet

218 plication throughout the erythrocytic cycle, gametocyte production, mosquito infections, and sporozoi

219 nts a simple mechanism for a low baseline of gametocyte production.

220 In addition, IgGs specific for the gametocyte proteins Pfmdv1, Pfs16, PF3D7_1346400, and PF

221 ade and proliferate or to differentiate into gametocytes ready for continuation of sexual development

222 e commonly used drug piperaquine, and mature gametocytes reappear in the bloodstream 10 days after th

223 le and female gametes from their precursors (gametocytes) remain sparse in P. falciparum.

224 lay an unsuspected yet vital role in stage V gametocytes, rendering these cells exquisitely sensitive

225 l drugs are not active against P. falciparum gametocytes, responsible for the spread of malaria.

226 r transcribed at low levels in blood stages (gametocyte/ring) of the parasite in the human host.

227 We show that gametocyte rings are detected in the peripheral blood im

228 ream 10 days after the initial appearance of gametocyte rings.

229 Overall, this TCAMS gametocyte screen provides 276 promising antimalarial mo

230 The ratio of male to female gametocytes seen in infections of Plasmodium and related

231 Here, we examined the effect of PQ on gametocyte sex ratio as a possible explanation for this

232 Twenty-four hours after treatment, gametocyte sex ratio became male-biased and was not sign

233 Gametocyte sex ratio was examined in relation to time si

234 (>0.125 mg/kg) 48 hours after treatment, and gametocyte sex ratio was not associated with mosquito in

235 varying fecundity and population size on the gametocyte sex ratio when strains maximize their individ

236 gested gametocytes per strain on the optimal gametocyte sex ratio.

237 ation of incomplete fertilization on optimal gametocyte sex ratio.

238 usible explanation for the high variation in gametocyte sex ratios of P. falciparum observed in natur

239 During maturation, midstage gametocytes show low deformability and sequester in the

240 proteomic data, we classified 91 proteins as gametocyte specific and 69 as proteins not expressed by

241 A clear understanding of gametocyte-specific antibody responses in exposed popula

242 For gametocyte-specific detection, the microscopy prevalence

243 cyte production via DNA dye staining and the gametocyte-specific expression of a fluorescent protein,

244 sing P. falciparum lines that stably express gametocyte-specific GFP-luciferase reporters, which enab

245 The overall breadth and magnitude of gametocyte-specific IgG responses increased during the m

246 P2-G transcriptional regulator and a lack of gametocyte-specific mRNA stabilization.

247 nic 3D7 strain expressing luciferase under a gametocyte-specific promoter revealed its activity again

248 Using the pfs16 gametocyte-specific promoter to express FCU-GFP in 3D7 p

249 lymerase chain reaction amplification of the gametocyte-specific transcript Pfs25.

250 or analytical sensitivity against a panel of gametocyte-spiked whole blood, detecting 10 gametocytes/

251 of 56 molecules abundantly expressed in the gametocyte stage of the parasite.

252 g the transcriptional dynamics of the sexual gametocyte stage transition, a process that is essential

253 tly prevented male gamete formation from the gametocyte stage with a 50% inhibition concentration of

254 genes show a peak of mRNA expression at the gametocyte stage.

255 assay with immature and mature P. falciparum gametocyte stages expressing red and green-emitting luci

256 However, gametocyte stages in organs such as bone marrow have nev

257 lumefantrine and pyronaridine against early gametocyte stages, along with moderate inhibition of mat

258 ditional activity against parasite liver and gametocyte stages, making them potential candidates for

259 to be very potent in the parasite liver and gametocyte stages, which makes them of high interest.

260 um-infected persons without smear-detectable gametocytes still infect mosquitoes.

261 rgeting Pfs25 messenger RNA [mRNA]) and male gametocytes (targeting Pf3D7_1469900 mRNA) in 2 randomiz

262 ion assays were developed to quantify female gametocytes (targeting Pfs25 messenger RNA [mRNA]) and m

263 s described for the first time as late-stage gametocyte-targeting molecules.

264 site in Burkina Faso, children harbour more gametocytes than adults though the non-linear relationsh

265 lopment and maturation of intra-erythrocytic gametocytes that are transmissible to Anopheles mosquito

266 y of daughter merozoites takes place, and in gametocytes that infect Anopheles mosquitoes.

267 lood stages and is active against developing gametocytes, the forms responsible for transmission.

268 In PfMOP-deficient gametocytes, the IMC formation defect causes maturation

269 the parasite gene pvs25 that is expressed in gametocytes, the life cycle stage infectious to mosquito

270 use they often persist for months and harbor gametocytes, the parasite stage infectious to mosquitoes

271 metabolic processes in the mature (stage V) gametocytes, the sexual stages circulating in the bloods

272 the skeletal meshwork increase in developing gametocytes, then decrease in mature-stage gametocytes.

273 In male gametocytes there is an enrichment of proteins involved

274 ew drugs that kill circulating P. falciparum gametocytes, thereby preventing transmission.

275 icipants were confirmed positive carriers of gametocytes through microscopy and had normal function o

276 intained below a threshold in the developing gametocyte to allow subsequent differentiation to procee

277 to interrogate malaria transmission from the gametocyte to the sporozoite stage: assays that augment

278 antibodies by feeding cultured P. falciparum gametocytes to Anopheles mosquitoes in the presence of t

279 blocks transmission of mature P. falciparum gametocytes to Anopheles stephensi mosquitoes.

280 e investigated the susceptibility of stage V gametocytes to compounds specifically affecting redox me

281 results reveal a high sensitivity of mature gametocytes to the glutathione reductase inhibitor and r

282 re it serves distinct functions in promoting gametocyte-to-ookinete development and protecting ookine

283 iable male gametes produced by a single male gametocyte, towards 1 to 1, which is demonstrated to be

284 g and stabilization of a subset of essential gametocyte transcripts.

285 es, along with moderate inhibition of mature gametocyte transmission to Anopheles mosquitoes.

286 C protein and named here Upregulated in Late Gametocytes (ULG8), which we have leveraged to express r

287 c force microscopy indicates that developing gametocytes undergo remarkable shifts in their erythrocy

288 say (Pf FGAA), which assesses stage V female gametocyte viability and functionality using Pfs25 expre

289 as used to determine the effects of drugs on gametocyte viability, and exflagellation was assessed to

290 In Kenya, the median proportion of male gametocytes was 0.33 at baseline.

291 heral blood (n = 25), prevalence of immature gametocytes was higher in bone marrow than peripheral bl

292 The 8.4% of patients with smear-detectable gametocytes were >20 times more likely to infect mosquit

293 Although gametocytes were first described in 1880, our understand

294 In contrast, mature gametocytes were more prevalent (100% vs 51%, P < .001)

295 Gametocytes were present at day 28 in 23.8% (10/42) of p

296 olymerase chain reaction (PCR) analysis, and gametocytes were quantified by reverse-transcription qPC

297 ferentiation initiates the production of the gametocyte, which is the malaria parasite stage required

298 ned for parasites that no longer form mature gametocytes, which led to the isolation of 29 clones (in

299 Treatment of midstage gametocytes with cytochalasin D decreases the vertical c

300 mpounds were active against three strains of gametocytes with different drug sensitivities and geogra