ライフサイエンスコーパス: gametocyte

1 iate into male or female sexual forms called gametocytes.

2 esponse may reduce the burden of circulating gametocytes.

3 ess reporter genes in mature male and female gametocytes.

4 gametocytes; heterochromatic PTMs mark early gametocytes.

5 ties of asexual parasites and the absence of gametocytes.

6 on into non-replicating sexual stages called gametocytes.

7 with GCalpha, a cGMP synthesizing enzyme in gametocytes.

8 asexual replication or differentiation into gametocytes.

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

10 veloped into metabolically quiescent stage V gametocytes.

11 tive against asexual blood stages and mature gametocytes.

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

13 specific and 69 as proteins not expressed by gametocytes.

14 culocytes and mature into both schizonts and gametocytes.

15 mmitment to the production and maturation of gametocytes.

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

17 bosomal protein genes in all stages but male gametocytes.

18 n cytoplasmic puncta of both male and female gametocytes.

19 ansmission of sexual stage parasites, called gametocytes.

20 laques containing both asexual parasites and gametocytes.

21 ert into non-replicating sexual forms called gametocytes.

22 nificant skin sequestration of P. falciparum gametocytes.

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

24 ges that cause disease, and activity against gametocyte activation that is required for transmission.

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

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

27 H(2)O(2) accumulation in bone marrow, where gametocytes and asexual parasites are therefore killed.

28 We directly quantified male and female gametocytes and asexual parasites in: i) finger prick bl

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

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

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

32 7 is expressed on the surface of both female gametocytes and ookinetes where it serves distinct funct

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

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

35 asion in mosquitoes through interacting with gametocytes and ookinetes.

36 we found that infection of erythroblasts by gametocytes and parasite-derived extracellular vesicles

37 Accurate quantification of female and male gametocytes and sex ratios in asymptomatic low-density m

38 Notably though, the interactions between gametocytes and this hematopoietic niche have not been i

39 from asexual blood stages to male and female gametocytes and to ookinetes in the rodent malaria paras

40 arabiensis tested negative for P. falciparum gametocytes and, on experimental infection with P. falci

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

42 at are specific to the elusive P. vivax male gametocytes, and will be useful for analyzing gene expre

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

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

45 Just like their asexual counterparts, gametocytes are contained within the infected host's ery

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

47 Although gametocytes are essential for malaria transmission, in A

48 Plasmodium falciparum gametocytes are essential for malaria transmission.

49 lated genes, suggesting that male and female gametocytes are independently regulated.

50 Although gametocytes are intra-erythrocytic when present in infec

51 Committed gametocytes are refractory to the commonly used drug pip

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

53 Gametocytes are the only Plasmodium life stage infectiou

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

55 plement factor H levels, lower expression of gametocyte-associated genes but higher expression of tra

56 rtion of asexual parasites that convert into gametocytes at each multiplication cycle, is variable an

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

58 ause primaquine and methylene blue sterilize gametocytes before affecting their density and sex ratio

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

60 ays 9 to 16 did not increase the quantity of gametocytes but did increase quality, as measured by ooc

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

62 he in vivo dynamics of Plasmodium falciparum gametocytes by establishing a framework which incorporat

63 ex process that starts with the ingestion of gametocytes by female Anopheles mosquitoes during a bloo

64 The sex of Plasmodium falciparum gametocytes can be determined microscopically but recent

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

66 for P falciparum sexual stages and show that gametocytes can fully develop inside these nucleated cel

67 Plasmodium gametocytes can induce an immune response in humans that

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

69 However, with Plasmodium falciparum, gametocytes can only be detected in peripheral blood whe

70 Only sexually differentiated parasites (gametocytes) can be successfully transmitted to complete

71 he gametocyte surface, when co-ingested with gametocytes, can influence transmission to mosquitoes.

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

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

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

75 ession was used to quantify PQ effect on (i) gametocyte carriage in the first two weeks post-treatmen

76 fourteen studies, PQ reduced PCR-determined gametocyte carriage on days 7 and 14, most apparently in

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

78 The rate of decline in gametocyte carriage was faster when PQ was combined with

79 emoglobin concentration, adverse events, and gametocyte carriage.

80 Primaquine substantially reduced gametocyte carriage.

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

82 Microscopic gametocyte carriers attracted almost 2 times more mosqui

83 In naturally infected gametocyte carriers from Burkina Faso, we assessed infec

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

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

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

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

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

89 preceding pfap2-g transcripts, indicative of gametocyte commitment (rho = 0.62; P = 0.002).

90 on gametocyte production, suggesting higher gametocyte commitment following IBSM.

91 Here, we quantify early gametocyte-committed ring (gc-ring) stage, P. falciparum

92 in patient blood samples with high levels of gametocyte-committed ring stage parasites.

93 osquito infection experiments, we found that gametocytes continuously exposed to 8.2 mM lactic acid s

94 to transmissible stage V gametocytes using a gametocyte conversion assay (GCA).

95 arious times were monitored using blood film gametocyte counts and RNA analysis throughout 2 weeks of

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

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

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

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

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

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

102 Gametocyte densities in peripheral blood are thus inform

103 Mean gametocyte densities were frequently below 1 female and

104 ven by molecular methods, therefore ultralow gametocyte densities were quantified in large blood volu

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

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

107 at allow sex-ratio assessments at much lower gametocyte densities.

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

109 Gametocyte density and positivity correlated closely wit

110 Gametocyte density and sex ratio can predict the proport

111 Peak gametocyte density correlated with preceding pfap2-g tra

112 Median peak gametocyte density was 1304 gametocytes/mL (interquartil

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

114 human isolate of P. vivax that reached high gametocyte density within weeks.

115 ium falciparum infectivity before it impacts gametocyte density.

116 ify differences in PfAP2-G occupancy between gametocytes derived via next-cycle and same-cycle conver

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

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

119 Immature gametocytes develop in the human bone marrow parenchyma,

120 t affect P. falciparum blood stage growth or gametocyte development but reduces efficiency of roundin

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

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

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

124 ounts and RNA analysis throughout 2 weeks of gametocyte development in vitro for a total of 5 biologi

125 nd blood-stage P. falciparum and blockade of gametocyte development, thereby preventing transmission,

126 molar activity against the earliest forms of gametocyte development.

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

128 xhibited changes in abundance during ABS and gametocyte development.

129 provides a niche for asexual replication and gametocyte development.

130 urrently unclear to what extent sex-specific gametocyte diagnostics obviate the need for mosquito fee

131 These sex-specific gametocyte diagnostics were recently used to examine gam

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

133 Gametocytes differentiation to gametes (gametogenesis) w

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

135 te diagnostics were recently used to examine gametocyte dynamics in controlled and natural infections

136 mproved measurements of parasitemia, a novel gametocyte dynamics model and model fitting using Bayesi

137 reached 97% following membrane feeding with gametocyte-enriched blood, and sporozoites developed int

138 Mature gametocytes exhibit increased deformability and reappear

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

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

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

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

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

144 to particular antigens may reliably indicate gametocyte exposure.

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

146 f rounding up, egress, and exflagellation of gametocytes following activation.

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

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

149 parum asexual blood stages and transmissible gametocyte forms.

150 ible, and efficient transmission of P. vivax gametocytes from humans to mosquitoes, and have establis

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

152 at establishes a system to transmit P. vivax gametocytes from humans to mosquitoes.

153 Here we produce gametocytes from parasite clinical isolates that display

154 highlight the ongoing search for additional gametocyte/gamete surface antigens, as well as antigens

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

156 Analyses of gametocyte genes reveal two distinct clusters of co-regu

157 P2-G is a transcriptional activator of early gametocyte genes, and identify differences in PfAP2-G oc

158 G not only as a transcriptional activator of gametocyte genes, but also as a potential regulator of g

159 Stage V gametocytes harboring Cas9-introduced pfmdr1 mutations a

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

161 odest antimalarial efficacy against parasite gametocytes; however, potency is enhanced ca.1000 fold i

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

163 mmarize evidence for naturally acquired anti-gametocyte immunity and the current state of transmissio

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

165 a multilayered mechanism operating in female gametocytes in preparation for fertilization and zygote

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

167 are pivotal for the maintenance of immature gametocytes in the bone marrow and provide further insig

168 ransmission is dependent on the formation of gametocytes in the human blood.

169 Activation of gametocytes in the mosquito midgut triggers "rounding up

170 I 1.21 - 3.33, p = 0.007), concentrations of gametocytes in the subdermal skin vasculature were not h

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

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

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

174 gens, as well as antigens on the surfaces of gametocyte-infected erythrocytes, which can potentially

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

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

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

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

179 ultiplication to sexual differentiation into gametocytes is essential for transmission to mosquitos.

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

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

182 osquito transmission - a process mediated by gametocyte kinetics in human hosts.

183 piperaquine treatment, asexual parasite and gametocytes kinetics were assessed and mosquito feeding

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

185 erythroid differentiation, thereby allowing gametocyte maturation to coincide with the release of th

186 ted humans, developing Plasmodium falciparum gametocytes may express proteins on the surface of red b

187 Median peak gametocyte density was 1304 gametocytes/mL (interquartile range (IQR) 308-1607) foll

188 IQR) 308-1607) following IBSM compared to 14 gametocytes/mL (IQR 10-64) following MB (P < 0.001), des

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

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

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

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

193 ing of 59 membrane proteins expressed in the gametocytes of Plasmodium yoelii and identify that GEP1

194 Gametocytes often escape detection even by molecular met

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

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

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

198 most all infections with >=1 female and male gametocyte per 2.5 uL mosquito bloodmeal, and thus with

199 nsmit, assuming at least 1 female and 1 male gametocyte per 2.5 uL mosquito bloodmeal.

200 Based on model estimates of female and male gametocytes per 2.5 uL blood, P. falciparum-positive ind

201 Gametocyte persistence and infectivity are lower when PQ

202 40% more samples from asymptomatic adults as gametocyte positive.

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

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

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

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

207 The gametocyte prevalence of Plasmodium falciparum at baseli

208 Differentiation between gametocyte-producing Plasmodium falciparum clones depend

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

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

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

212 markers are also sensitive enough to monitor gametocyte production in asymptomatic P. falciparum carr

213 lines and develop an algorithm that predicts gametocyte production in ex vivo samples and volunteer i

214 Gametocyte production rates vary depending on environmen

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

216 d a striking effect of inoculation method on gametocyte production, suggesting higher gametocyte comm

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

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

219 Here, we found that lactic acid increases gametocyte quantity and quality in P. falciparum culture

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

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

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

223 We developed a robust assay using gametocyte-reporter parasite lines to accurately measure

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

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

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

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

228 We estimated the sexual commitment rate and gametocyte sequestration time to be 0.54% (95% credible

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

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

231 we review recent and historic assessments of gametocyte sex ratio in relation to host and parasite ch

232 Gametocyte sex ratio was examined in relation to time si

233 (>0.125 mg/kg) 48 hours after treatment, and gametocyte sex ratio was not associated with mosquito in

234 Gametocyte sex ratios from qRT-PCR were compared with th

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

236 Although gametocyte skin sequestration has long been hypothesized

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

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

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

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

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

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

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

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

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

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

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

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

249 the parasite but little activity against the gametocyte stage.

250 dent upon mosquito ingestion of the parasite gametocyte stage.

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

252 tion of PfISN1 and expression in asexual and gametocyte stages of the parasite.

253 vities against the asexual blood, liver, and gametocyte stages of the Plasmodium parasite with no cro

254 ocytic asexual cycle and between asexual and gametocyte stages was observed suggesting that cis-polyi

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

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

257 hepatic metabolism to exert activity against gametocyte stages.

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

259 ranscript abundance in all stages but female gametocytes suggesting that transcription in this stage

260 ogether with known mRNA repression in female gametocytes suggests a multilayered mechanism operating

261 The Plasmodium falciparum gametocyte surface protein, Pfs48/45, is a potential tar

262 t antibodies against antigens present on the gametocyte surface, when co-ingested with gametocytes, c

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

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

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

266 um falciparum transmission depends on mature gametocytes that can be ingested by mosquitoes taking a

267 tive host, felines, Toxoplasma converts into gametocytes that produce infectious oocysts (sporozoites

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

269 Plasmodium falciparum gametocytes, the sexual stage responsible for malaria pa

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

271 lier evidence on isn1 upregulation in female gametocytes, the structures reported in this study may c

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

275 the samples have gc-rings, but the ratio of gametocyte to asexual-committed rings (GCR) varies widel

276 s to ingest at least one male and one female gametocyte to become infected with malaria.

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

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

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

280 select three genes, not expressed in mature gametocytes, to develop as biomarkers.

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

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

283 es were frequently below 1 female and 1 male gametocyte/uL by qRT-PCR.

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

285 le as committed forms before converting into gametocytes upon re-invasion, or a direct route with con

286 s before maturation to transmissible stage V gametocytes using a gametocyte conversion assay (GCA).

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

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

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

290 Gametocytes were identified in 58% (93/161) P. falciparu

291 red to other blood compartments; only sparse gametocytes were observed in skin tissue.

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

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

294 Female and male gametocytes were quantified in 161 PCR-positive Plasmodi

295 Gametocytes were visualized in skin tissue by confocal m

296 velopmental switch into the sexual stage (or gametocyte), which is essential for transmission.

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

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

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

300 ro and in vivo, leading to infectious mature gametocytes within reticulocytes.