ライフサイエンスコーパス: tachyzoite

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

2 all of lower magnitude than those induced by tachyzoites.

3 cal movements exhibited by Toxoplasma gondii tachyzoites.

4 s within secretory compartments of T. gondii tachyzoites.

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

6 in new macrophages, giving rise to dividing tachyzoites.

7 ily detected on the surface of newly invaded tachyzoites.

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

9 imary ocular infection and challenge with RH tachyzoites.

10 abelled Phe into proteins in individual live tachyzoites.

11 re of surface proteins partially shared with tachyzoites.

12 mmatory cytokines when exposed to toxoplasma tachyzoites.

13 roteinase inhibitors interrupted invasion by tachyzoites.

14 ns dominate the surface of Toxoplasma gondii tachyzoites.

15 washed, fibroblast-derived Toxoplasma gondii tachyzoites.

16 ng the host cell monolayer as effectively as tachyzoites.

17 ce to a challenge infection with virulent RH tachyzoites.

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

19 their survival after challenge with virulent tachyzoites.

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

21 vivo by blocking infection of host cells by tachyzoites.

22 ere measured in host cells and extracellular tachyzoites.

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

24 hallenged with the highly virulent RH strain tachyzoites.

25 gondii, we mapped the ubiquitin proteome of tachyzoites.

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

27 d release LTB4; this interaction damages the tachyzoites.

28 tained data on approximately 7,400 ESTs from tachyzoites.

29 and sections were immunostained to identify tachyzoites.

30 ers of actively dividing, tissue-destructive tachyzoites.

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

32 5 after intraperitoneal inoculation with 500 tachyzoites.

33 tly expressed protease inhibitor in parasite tachyzoites.

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

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

36 cation validating these molecular targets in tachyzoites.

37 were partially resistant to lethal doses of tachyzoites.

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

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

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

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

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

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

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

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

46 Soluble tachyzoite Ag fractionation demonstrated that CCL2- and

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

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

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

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

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

52 in two interconverting developmental stages: tachyzoites and bradyzoites.

53 ltrastructural features intermediate between tachyzoites and bradyzoites.

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Neither soluble tachyzoite antigen nor secreted products were suppressiv

68 J macrophages with soluble Toxoplasma gondii tachyzoite antigen or the synthetic flavone analog 5, 6-

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

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

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

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

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

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

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

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

77 The tachyzoites arising in the subinoculated animals were ge

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

79 1 does not affect the invasion and growth of tachyzoites as TgCPC2 is then up-regulated and may subst

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

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

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

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

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

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

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

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

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

89 to be expressed on the surface of Toxoplasma tachyzoites by immunofluorescence.

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

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

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

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

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

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

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

97 We used tachyzoite clonal lines expressing genetically encoded c

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

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

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

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

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

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

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

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

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

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

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

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

110 Tachyzoites express invasion and virulence factors that

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

112 with 6-thioxanthine to inhibit the growth of tachyzoites expressing HXGPRT.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 Fast tachyzoite growth was not persistent, and following appr

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

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

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

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

133 Viable and killed tachyzoites had contrasting effects on cytokine producti

134 2 h, whereas purified and extensively washed tachyzoites had no effect.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 f ADP could not be obtained in permeabilized tachyzoites in the presence of either pyruvate, 3-oxo-gl

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

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

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

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

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

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

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

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

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

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

160 Tachyzoite infection and replication were accelerated in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 Tachyzoites of both strains induced p38 MAPK-dependent m

189 Tachyzoites of each of the three major parasite strain t

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

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

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

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

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

195 eas infection of human monocytes with viable tachyzoites of Toxoplasma gondii resulted in rapid induc

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

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

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

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

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

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

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

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

204 Tachyzoites preferentially infect glial cells, which exi

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

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

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

208 We examined whether tachyzoite proliferation in the brains of immunocompeten

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

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

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

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

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

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

215 gher cyst burdens and exhibited uncontrolled tachyzoite replication in the brain.

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

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

218 character of the immune response and control tachyzoite replication.

219 host cell type appears to influence emergent tachyzoite replication.

220 zyme necessary for folate synthesis, limited tachyzoite replication.

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

222 arison of the data sets from bradyzoites and tachyzoites reveals many previously uncharacterized sequ

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

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

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

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

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

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

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

230 Tachyzoites spread throughout the body through the blood

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

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

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

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

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

236 gainst an immune response raised against the tachyzoite stage.

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

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

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

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

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

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

243 The tachyzoite surface has been reported to comprise five ma

244 net, indicating their nonessential roles for tachyzoite survival.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 Differentiation of tachyzoites to bradyzoites was measured in an immunofluo

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

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

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

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

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

268 The factors affecting the transition of tachyzoites to the latent bradyzoite stage remain to be

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

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

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

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

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

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

275 nge of mice immunized with a live attenuated tachyzoite vaccine which confers total protection agains

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

277 Tachyzoites (VEG strain) that emerge from host cells inf

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

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

280 This mast cell activity against the tachyzoites was inhibited by the 5-LO inhibitor A-63162

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