ライフサイエンスコーパス: tachyzoite

1 dyzoite to a fast-replicating, highly motile tachyzoite.

2 surface antigens not previously observed in tachyzoites.

3 nt(s) that normally suppresses expression in tachyzoites.

4 all of lower magnitude than those induced by tachyzoites.

5 blood within leukocytes or as extracellular tachyzoites.

6 cal movements exhibited by Toxoplasma gondii tachyzoites.

7 es and dendritic cells) and as extracellular tachyzoites.

8 s within secretory compartments of T. gondii tachyzoites.

9 , which showed the same rates of motility as tachyzoites.

10 ily detected on the surface of newly invaded tachyzoites.

11 C1), a component of the membrane skeleton in tachyzoites.

12 imary ocular infection and challenge with RH tachyzoites.

13 re of surface proteins partially shared with tachyzoites.

14 roteinase inhibitors interrupted invasion by tachyzoites.

15 ve oxygen species (ROS) levels in N. caninum tachyzoites.

16 ns dominate the surface of Toxoplasma gondii tachyzoites.

17 washed, fibroblast-derived Toxoplasma gondii tachyzoites.

18 ng the host cell monolayer as effectively as tachyzoites.

19 ce to a challenge infection with virulent RH tachyzoites.

20 isin-type serine protease found in T. gondii tachyzoites.

21 g, as we show is also the case in Toxoplasma tachyzoites.

22 their survival after challenge with virulent tachyzoites.

23 ion of host cells by extracellular T. gondii tachyzoites.

24 were partially resistant to lethal doses of tachyzoites.

25 vivo by blocking infection of host cells by tachyzoites.

26 ere measured in host cells and extracellular tachyzoites.

27 er incubation of T cells with DC plus killed tachyzoites.

28 hallenged with the highly virulent RH strain tachyzoites.

29 in new macrophages, giving rise to dividing tachyzoites.

30 abelled Phe into proteins in individual live tachyzoites.

31 mmatory cytokines when exposed to toxoplasma tachyzoites.

32 gondii, we mapped the ubiquitin proteome of tachyzoites.

33 age the parasitic process driven by AMA1(KO) tachyzoites.

34 and sections were immunostained to identify tachyzoites.

35 ers of actively dividing, tissue-destructive tachyzoites.

36 and retinal cell lines, with YFP-expressing tachyzoites.

37 5 after intraperitoneal inoculation with 500 tachyzoites.

38 tly expressed protease inhibitor in parasite tachyzoites.

39 o laboratory or natural strains of T. gondii tachyzoites.

40 cation validating these molecular targets in tachyzoites.

41 were incubated with either Toxoplasma gondii tachyzoites (10:1, parasites per cell) or Escherichia co

42 mammalian cells, is active against T. gondii tachyzoites (50% effective concentration, 0.2 nM).

43 ation assays, retinas contained 110-250 live tachyzoites; 64.5-95.2% (mean =79.6%) were localized to

44 mpletely replaces the l-Phe within T. gondii tachyzoites 7-9 hours after infection.

45 Amounts of tachyzoite (acute stage form of T. gondii)-specific SAG1

46 s ability to switch between fast-replicating tachyzoite (acute) and quiescent bradyzoite (chronic) st

47 ve IL-12 responses to T. gondii Ags (soluble tachyzoite Ag (STAg)) were observed in MyD88(-/-) perito

48 Soluble tachyzoite Ag fractionation demonstrated that CCL2- and

49 hes between two forms: a rapidly replicating tachyzoite and an encysted bradyzoite.

50 ing (scRNA-seq) on >5,400 Toxoplasma in both tachyzoite and bradyzoite stages using three widely stud

51 were used to compare mRNA levels during the tachyzoite and bradyzoite stages.

52 cycle of this parasite: the rapidly dividing tachyzoite and the more slowly dividing, encysted bradyz

53 on occurs during stage conversion, such that tachyzoites and bradyzoites express closely related but

54 n) gave efficient expression of FLUC in both tachyzoites and bradyzoites, indicating that the bradyzo

55 in two interconverting developmental stages: tachyzoites and bradyzoites.

56 ltrastructural features intermediate between tachyzoites and bradyzoites.

57 TgCDPK1 protein was expressed in Toxoplasma tachyzoites and cofractionated precisely with the peak o

58 ligomers of arginine enter Toxoplasma gondii tachyzoites and encysted bradyzoites.

59 ss multiple membranes to enter intracellular tachyzoites and encysted bradyzoites.

60 n another study, is dispensable in T. gondii tachyzoites and for T. gondii infectivity.

61 no acid hydroxylases were negligible both in tachyzoites and in bradyzoites.

62 early bradyzoite nucleus and is repressed in tachyzoites and in mature bradyzoites from 30-d infected

63 nses was found during extended incubation of tachyzoites and Mphi in that 24 h of incubation of infec

64 although the roles differ between Toxoplasma tachyzoites and Plasmodium erythrocytic stages.

65 inoculated intraperitoneally with T. gondii tachyzoites and sacrificed from 6 to 72 h later.

66 rvive an otherwise lethal dose of Toxoplasma tachyzoites and that complementation of the mutant with

67 imately 8 h in response to injection of live tachyzoites and that this is correlated with increased t

68 is known to block the motility of Toxoplasma tachyzoites and their attachment to host cells.

69 which encompass examples of constitutive and tachyzoite- and bradyzoite-specific genes, are able to r

70 eomic analysis of T. gondii extract (soluble tachyzoite antigen [STAg]), which preserves the immunosu

71 Neither soluble tachyzoite antigen nor secreted products were suppressiv

72 Vaccination of BALB/c mice with a soluble tachyzoite antigen preparation, STAg, in combination wit

73 In whole tachyzoite antigen-expanded bovine T-lymphocyte lines, r

74 using immunoblotting following separation of tachyzoite antigens by two-dimensional gel electrophores

75 cyst antigen CST1, failure to down-regulate tachyzoite antigens, such as tachyzoite surface antigens

76 least, the observed physiology of T. gondii tachyzoites appears to phenocopy cancer cells, which hol

77 T. gondii tachyzoites are capable of extracting l-Phe(D8) from hos

78 ikely necessitates host cell modulation, and tachyzoites are known to modify a number of signaling ca

79 ediate hosts such as humans: rapidly growing tachyzoites are responsible for acute illness, whereas s

80 The tachyzoites arising in the subinoculated animals were ge

81 ive mutant of TPK2 (TPK2-HA-dn) in T. gondii tachyzoites arrested replication.

82 1 does not affect the invasion and growth of tachyzoites as TgCPC2 is then up-regulated and may subst

83 orporation into the nuclear DNA of T. gondii tachyzoites as the surrogate endpoint for growth, the IC

84 ons show that these mutants behave more like tachyzoites at a global level, even under bradyzoite dif

85 umerous punctate structures in the nuclei of tachyzoites, bradyzoites, and sporozoites but not oocyst

86 Da, designated TgPI-1(43) and TgPI-1(41), in tachyzoites, bradyzoites, and sporozoites.

87 DeltaTgPI1 parasites replicate normally as tachyzoites but exhibit increased bradyzoite gene transc

88 the new test is based on complement lysis of tachyzoites, but it is much easier to perform and the re

89 DPK2 was only expressed at the mRNA level in tachyzoites, but no protein was detected.

90 an index of T. gondii proliferation, because tachyzoites, but not human cells, incorporate uracil dir

91 munized mice showed recognition of T. gondii tachyzoites by immunofluorescence and exhibited high tit

92 We found that the administration of tachyzoites by this route induced a rapid tissue recruit

93 the most highly expressed cathepsin mRNA in tachyzoites (by real-time PCR), but three cathepsins, Tg

94 was used to identify four cDNA clones from a tachyzoite cDNA library.

95 w ESTs from the 5' ends of randomly selected tachyzoite cDNAs.

96 ose factors is tightly controlled during the tachyzoite cell cycle to permit their correct packaging

97 two distinct control points in the T. gondii tachyzoite cell cycle.

98 sts before the middle of the G1 stage of the tachyzoite cell cycle.

99 We used tachyzoite clonal lines expressing genetically encoded c

100 Expression of SporoSAG in tachyzoites conferred enhanced invasion on transgenic pa

101 lence in mice of Toxoplasma gondii RH strain tachyzoites containing various copies of the chloramphen

102 In N. caninum tachyzoite culture supernatant, three NcCyP bands of 19,

103 hyzoite lysate antigen (NcAg) and N. caninum tachyzoite culture supernatant.

104 antly greater radioactivity was measured for tachyzoites cultured with retinal versus other cell subt

105 th soluble T. gondii extracts or heat-killed tachyzoites, demonstrating a requirement for live parasi

106 We show here that T. gondii tachyzoites depleted of TgAMA1 are severely compromised

107 s-competent but also in glycolysis-deficient tachyzoites despite a mitochondrial localization.

108 Acute-stage tachyzoites differentiate into chronic-stage bradyzoites

109 endritic cells were more permissive to rapid tachyzoite division than neutrophils or lymphocytes.

110 e major mediator to prevent proliferation of tachyzoites during acute infection, but does require per

111 Equivalent studies of the tachyzoites during host cell invasion, by contrast, disc

112 is definitively not an essential protein for tachyzoite entry and multiplication in host cells, it cl

113 Tachyzoites express invasion and virulence factors that

114 nt method using transgenic Toxoplasma gondii tachyzoites expressing beta-galactosidase was developed

115 d gp15 reacted with the surface membranes of tachyzoites expressing the Cpgp40/15 construct, and this

116 FACS analysis of tachyzoites expressing TPK2-HA-dn revealed an increase i

117 generated against recombinant C-18 inhibited tachyzoite extract-induced synthesis of IL-12.

118 man myeloid cells fail to respond to soluble tachyzoite extracts and instead require contact with liv

119 in Plasmodium liver stages and in Toxoplasma tachyzoites fatty acid synthesis is an essential role of

120 proteins modified by O-Fuc are important for tachyzoite fitness, O-fucosylation by TgSPY is not essen

121 ion consisting of live, avirulent N. caninum tachyzoites followed by virulent challenge during subseq

122 Interestingly, infectivity of tachyzoites for human foreskin fibroblasts, cells that a

123 To determine the preference of tachyzoites for human retinal neuronal versus glial popu

124 a gondii converts from a rapidly replicating tachyzoite form during acute infection to a quiescent en

125 Confirming this, T. gondii tachyzoites formed fewer cysts following alkaline pH str

126 gene encoding this protein was identified in tachyzoites genetically complemented with a sporozoite c

127 feron knockout mice inoculated with emergent tachyzoites grew at a slow rate and expressed BAG1, conf

128 oups of CBA/J mice, which display continuous tachyzoite growth in their brains during the later stage

129 stly by the antibodies of mice with cerebral tachyzoite growth include MIC6, the rhoptry protein ROP1

130 The spontaneous change in tachyzoite growth rate preceded the expression of the br

131 mulation of CD3(+) T cells into the areas of tachyzoite growth was significantly less frequent in the

132 on of chronic T. gondii infection to control tachyzoite growth.

133 oup of mice, either with or without cerebral tachyzoite growth.

134 ntibodies of infected hosts that do not have tachyzoite growth.

135 Viable and killed tachyzoites had contrasting effects on cytokine producti

136 2 h, whereas purified and extensively washed tachyzoites had no effect.

137 contrast, only the group immunized with live tachyzoites had strong cellular and gamma interferon res

138 tition studies between mixtures of T. gondii tachyzoites harbouring wild-type or mutant DHFR-TS allel

139 t of infection in the human eye by T. gondii tachyzoites have not been investigated.

140 d to arginine oligomers enters extracellular tachyzoites, host cells, tachyzoites inside parasitophor

141 actin filaments at the anterior end of each tachyzoite in association with the conoid, where they fo

142 nds (5a,h,k,l) were tested against T. gondii tachyzoites in culture and were found to have a potency

143 derlie the promiscuous survival of T. gondii tachyzoites in diverse host cells.

144 Growth of Deltaspy tachyzoites in fibroblasts is modestly affected, despite

145 Dissemination of tachyzoites in human foreskin fibroblasts was reduced fo

146 st challenge infections with highly virulent tachyzoites in immunized mice via their role as helper c

147 bits ENR activity, tachyzoites in vitro, and tachyzoites in mice.

148 r vaccination-induced resistance to virulent tachyzoites in order to produce antibodies and that anti

149 arly mortality and pathology associated with tachyzoites in the brain in the infected muMT mice.

150 emical staining demonstrated a low number of tachyzoites in the liver.

151 ells were incubated with RH-strain T. gondii tachyzoites in the presence of [(3)H]-uracil.

152 Human monocytes were infected with tachyzoites in the presence of antiparasite antibodies,

153 lyzable ester linkage inhibits ENR activity, tachyzoites in vitro, and tachyzoites in mice.

154 vely inhibits the infection of host cells by tachyzoites in vitro.

155 ult in attenuation of virulence of Deltaasp5 tachyzoites in vivo.

156 s the parasite's interconversion between the tachyzoite (in acute infection) and bradyzoite (in chron

157 al macrophages stimulated with IFN-gamma and tachyzoites indicated that under limiting concentrations

158 Inoculation of 5,000 T. gondii tachyzoites induced significant intraocular inflammation

159 IL-12 and TNF-alpha production, a result of tachyzoite-induced blockade of NF-kappaB nuclear translo

160 nthetic p38 catalytic-site inhibitor blocked tachyzoite-induced p38alpha MAPK phosphorylation.

161 Toxoplasma gondii tachyzoites infect host cells by an active invasion proc

162 radyzoite infection and compared to those of tachyzoite-infected and uninfected hosts cells 2 days po

163 Tachyzoite infection and replication were accelerated in

164 ielded only about half the changes seen with tachyzoite infection, and those changes that did occur w

165 group of genes were specifically induced by tachyzoite infection, including granulocyte-macrophage c

166 fic Abs, in resistance to persistent active (tachyzoite) infection with T. gondii in mice, especially

167 nters extracellular tachyzoites, host cells, tachyzoites inside parasitophorous vacuoles within host

168 Cytochalasin D, a drug blocking tachyzoite invasion of, but not adherence to, Mphi, seve

169 sistent with this, both plaque formation and tachyzoite invasion were broadly similar in the presence

170 r antibody-and-complement-dependent lysis of tachyzoites is a crucial mechanism of resistance.

171 n of intracellular Ca2+ in Toxoplasma gondii tachyzoites is stored within acidocalcisomes.

172 Tachyzoite isolates containing >/=five copies of the fus

173 tion of infected leukocytes or extracellular tachyzoites led to reduced parasite loads in mice with D

174 The lytic cycle, driven by the tachyzoite life stage, is responsible for acute toxoplas

175 The distinctive T. gondii tachyzoite lipid profile may be particularly suited to t

176 Vbeta8(-) population after stimulation with tachyzoite lysate Ags in vitro.

177 NcCyP was detected in whole-cell N. caninum tachyzoite lysate antigen (NcAg) and N. caninum tachyzoi

178 etal death, whereas immunization using whole-tachyzoite lysate in different adjuvants fails to protec

179 nd lysis were required for this response, as tachyzoite lysates alone had no effect on IL-8 secretion

180 is known that whilst inside a host cell the tachyzoite maintains its single mitochondrion at its per

181 development against bovine neosporosis, the tachyzoite major surface proteins NcSAG1 and NcSRS2 were

182 represent a novel means by which Toxoplasma tachyzoites manipulate the host.

183 scular endothelium to infection by T. gondii tachyzoites may explain, at least in part, preferential

184 tudies indicate that, after entering retina, tachyzoites may navigate multiple tissue layers.

185 ignificantly higher (p </= 0.005) numbers of tachyzoites measured in glial verus neuronal cell lines.

186 and release of MIC2 by ionophore-stimulated tachyzoites mimics the redistribution of MIC2 that occur

187 ritic cell as a potential taxi for T. gondii tachyzoites moving across the human retinal endothelium,

188 If vaccinated with attenuated T. gondii tachyzoites, muMT mice are susceptible to a challenge in

189 tified a microbial protein in the N. caninum tachyzoite N. caninum cyclophilin (NcCyP) as a major com

190 These results indicate that the N. caninum tachyzoite naturally produces a potent IFN-gamma-inducin

191 or-dependent phagocytosis of antibody-coated tachyzoites nor antibody-dependent cellular cytotoxicity

192 of TgAMA1 from the surface of extracellular tachyzoites occurs exclusively via cleavage within the l

193 Deltaspy tachyzoites of a luciferase-expressing type II strain ex

194 Tachyzoites of both strains induced p38 MAPK-dependent m

195 Tachyzoites of each of the three major parasite strain t

196 We demonstrate that viable, but not killed, tachyzoites of T. gondii altered the phenotype of immatu

197 covered a sugar-binding activity (lectin) in tachyzoites of T. gondii that plays a role in vitro in e

198 tochondrial membrane potential (DeltaPsi) of tachyzoites of the apicomplexan parasite Toxoplasma gond

199 l pigment epithelial cell line (ARPE-19) and tachyzoites of the apicomplexan protozoan parasite Toxop

200 Macrophages (Mphi) infected with tachyzoites of the opportunistic protozoan Toxoplasma go

201 In contrast to L3, live tachyzoites of Toxoplasma gondii, an intracellular paras

202 ions about the outcome associated with these tachyzoites once inoculated in the peritoneal cavity of

203 ysaccharide but not to either live T. gondii tachyzoites or soluble antigen.

204 trophils were incubated either with purified tachyzoites or with conditioned medium derived from T. g

205 The number of tachyzoites per 100 macrophages at 20 h postinfection wa

206 Importantly, we found that tachyzoite phagocytosis, but not host cell invasion, is

207 plasma gondii RH-AMA1 knockout (RH-AMA1(KO)) tachyzoite population, in vitro, raised key questions ab

208 We demonstrate that T. gondii tachyzoites possess regulatory volume decrease capabilit

209 Tachyzoites preferentially infect glial cells, which exi

210 mulation of the T cells into the areas where tachyzoites proliferate to prevent reactivation of chron

211 tigens increase in association with cerebral tachyzoite proliferation (reactivation of infection) in

212 eived treatment with sulfadiazine to prevent tachyzoite proliferation during the chronic stage of inf

213 We examined whether tachyzoite proliferation in the brains of immunocompeten

214 cells may play an important role in limiting tachyzoite proliferation in the eyes.

215 feration and differentiation steps, of which tachyzoite proliferation is the most relevant to pathoge

216 ransductive peptide conjugated PMO (PPMO) on tachyzoite protein expression and replication in vitro a

217 ltaTgPL1 bradyzoites did not convert back to tachyzoites readily in tissue culture.

218 MA1 protein is produced during intracellular tachyzoite replication and initially localizes to the mi

219 f T. gondii infection, allowing uncontrolled tachyzoite replication and severe organ damage.

220 id not appear to be a result of uncontrolled tachyzoite replication, because both parasite-specific R

221 Expression of TPK2-HA-wt did not arrest tachyzoite replication.

222 character of the immune response and control tachyzoite replication.

223 zyme necessary for folate synthesis, limited tachyzoite replication.

224 ging of mice intraperitoneally infected with tachyzoites revealed that during an acute infection, wil

225 In contrast, tachyzoite SAG2A and B were completely absent whereas a

226 Finally, Toxoplasma tachyzoites showed a reduced ability to infect epithelia

227 Tachyzoites showed higher [(3)H]-uracil incorporation af

228 ess the bradyzoite antigen BAG-1 but not the tachyzoite-specific antigen SAG-2 but are different from

229 adyzoite-specific SRS9 (SRS9(c)) mutants and tachyzoite-specific SAG1 (SAG1(c)) mutants.

230 after sulfadiazine discontinuation, cerebral tachyzoite-specific SAG1 mRNA levels and numbers of infl

231 Despite the tachyzoite specificity of this protein, mice infected wi

232 Tachyzoites spread throughout the body through the blood

233 The rapidly dividing tachyzoite stage displays a different subset of family o

234 The tachyzoite stage lactate dehydrogenase (LDH1) from the p

235 essary for either a rapid replication of the tachyzoite stage or a quiescent lifestyle typical of the

236 M1, TgROM4, and TgROM5 were expressed in the tachyzoite stage responsible for the disease, whereas Tg

237 abolic model (iTgo) for the fast-replicating tachyzoite stage, harmonized with experimentally observe

238 ere, we show that in the rapidly replicating tachyzoite stage, TgPL1 is localized within vesicles ins

239 gainst an immune response raised against the tachyzoite stage.

240 ur earlier work demonstrated that the acute (tachyzoite) stage of T. gondii depends on cooperativity

241 The tachyzoite stages of T. gondii express thioredoxin (TgTr

242 hesins that are secreted onto the Toxoplasma tachyzoite surface and capped to its posterior pole are

243 n activated macrophages, colocalizing with a tachyzoite surface antigen, SAG1, and oriented with its

244 itopes of a conserved, immunodominant 65-kDa tachyzoite surface antigen.

245 o down-regulate tachyzoite antigens, such as tachyzoite surface antigens 1 and 2A, and decreased resi

246 The tachyzoite surface has been reported to comprise five ma

247 net, indicating their nonessential roles for tachyzoite survival.

248 ith [(13)C]glucose showed that intracellular tachyzoites synthesized a range of long and very long ch

249 AC]-fixed versus that of formalin [HS]-fixed tachyzoites) test (AC/HS test) has primarily been used i

250 Upon release of mature tachyzoites, TgAMA1 is found distributed predominantly o

251 hereas the other protein is not expressed in tachyzoites (TgPEPCKnet).

252 and TgROM4 localized to the cell surface in tachyzoites, TgROM5 was primarily at the posterior of th

253 known suppressor of mitotic defects, and in tachyzoites, TgXPMC2-YFP localized to the parasite nucle

254 harbored a greater number of brain cysts and tachyzoites than did their wild-type counterparts.

255 p29 and Ncp35, respectively) from N. caninum tachyzoites that are the predominant antigens recognized

256 immune response during acute infection with tachyzoites that eliminates most of the parasites and to

257 traperitoneal infection with highly virulent tachyzoites that similarly vaccinated B-cell-sufficient

258 In addition, T. gondii tachyzoites (the rapidly multiplying and invasive stage

259 calize to constitutive secretory vesicles of tachyzoites, the dense granules.

260 ed only once every 15 h and, unlike emergent tachyzoites, they grew at this slower rate over several

261 rgoes transformation from a rapidly dividing tachyzoite to a long-lived, slow-dividing bradyzoite con

262 We have generated tachyzoite to bradyzoite differentiation (Tbd-) mutants

263 hing in Toxoplasma gondii, from the virulent tachyzoite to the relatively quiescent bradyzoite stage,

264 from parasites induced to differentiate from tachyzoites to bradyzoites in vitro.

265 Differentiation of tachyzoites to bradyzoites was measured in an immunofluo

266 a gene necessary for efficient conversion of tachyzoites to bradyzoites.

267 n the stress-induced conversion of T. gondii tachyzoites to bradyzoites.

268 The ability of Toxoplasma gondii tachyzoites to differentiate into latent bradyzoite form

269 To evaluate the ability of tachyzoites to navigate the human retina, we developed a

270 dergoes differentiation from rapidly growing tachyzoites to slowly growing bradyzoites during its lif

271 ent also reduced the replication of emergent tachyzoites to the rate of growth-shifted parasites, sup

272 bility may relate to preferential binding of tachyzoites to the retinal vascular endothelial surface,

273 s the transition from its replicative stage (tachyzoite) to the latent stage (bradyzoite) that persis

274 We have previously generated tachyzoite-to-bradyzoite differentiation (Tbd(-)) mutant

275 In rapidly replicating tachyzoites, translation initiates at the third methioni

276 with laboratory or natural strain T. gondii tachyzoites transmigrated in larger numbers across simul

277 opy of both free and intracellular T. gondii tachyzoites using purified universal V-PPase polyclonal

278 ocytes, but inhibition of growth and loss of tachyzoite vacuoles were evident in IFN-gamma-treated as

279 Growth of the tachyzoites was approximately 2.8-fold higher in retinal

280 to the parasitophorous vacuole of transgenic tachyzoites was completely inhibited by the cathepsin C

281 nfection, and near-normal histology with few tachyzoites was observed in the eyes of mice immunized i

282 Although tachyzoites were able to divide in each of these cell ty

283 st evident in their brains; small numbers of tachyzoites were also detectable in their lungs.

284 mice, as the initially fast-growing emergent tachyzoites were avirulent (100% lethal dose, >10(4) par

285 Toxoplasma gondii tachyzoites were fractionated by modification of an iodi

286 When tachyzoites were incubated with human peripheral blood l

287 numbers of inflammatory foci associated with tachyzoites were markedly greater in anti-alpha4 integri

288 On the other hand, extracellular tachyzoites were not able to consume l-Phe(D8) after 24

289 ts and areas of inflammation associated with tachyzoites were observed in brains of muMT than in cont

290 e areas of necrosis associated with numerous tachyzoites were observed only in brains of muMT mice.

291 AG1 mRNA and numbers of foci associated with tachyzoites were significantly greater in the former tha

292 The surviving tachyzoites were then induced for in vitro bradyzoite fo

293 osine transporter of the parasite, T. gondii tachyzoites were transfected with an insertional mutagen

294 Jasplakinolide-treated tachyzoites were unable to invade host cells, but once t

295 ssive, and heat-inactivated, antibody-coated tachyzoites, which efficiently entered the cell through

296 characterize a novel organelle in T. gondii tachyzoites, which is visible by light microscopy and po

297 zyme does not affect the growth of T. gondii tachyzoites, which suggests that the de novo pyrimidine

298 brary was screened against Toxoplasma gondii tachyzoites with activity discovered for N-(4-ethylbenzo

299 were associated with the presence of viable tachyzoites within the intestinal lumen.

300 ng of a number of tissue cysts but few or no tachyzoites within the placenta and fetal adrenal and he