ライフサイエンスコーパス: T. gondii

1 T. gondii circulates in the bloodstream within infected

2 T. gondii Deltagra12 mutants were more vulnerable to be

3 T. gondii differs substantially in its broad distributio

4 T. gondii has evolved mechanisms to timely counteract th

5 T. gondii induces EGFR signaling in vitro during invasio

6 T. gondii infection of resistant and sensitive mouse str

7 T. gondii tachyzoites are capable of extracting l-Phe(D8

8 We identify 195 T. gondii encoded ligands originating from both secreted

9 We also identify and characterize a T. gondii homologue of Tom7 (TgTom7) that is important f

10 A CRISPR/Cas9 strategy was used to create a T. gondii strain that exhibits defective fertilisation,

11 translation initiation site preference for a T. gondii protein.

12 We demonstrate that a T. gondii homologue of Tom22 (TgTom22), a central compon

13 tly abundant (P <= 0.001 each), during acute T. gondii in immunocompetent mice, compared to controls.

14 After T. gondii infection, mice that expressed CD40 restricted

15 oIL-18) in intestinal epithelial cells after T. gondii or Citrobacter rodentium infection, but also m

16 -intrinsic memory-like characteristics after T. gondii vaccination.

17 taining to peptides that are presented after T. gondii infection.

18 histopathology in the brain and retina after T. gondii infection.

19 any people develop ocular disease soon after T. gondii infection.

20 shows strong antiparasitic activity against T. gondii The same compound inhibits invasion of the mos

21 of immunoglobulin G (IgG) antibodies against T. gondii embryogenesis-related protein (TgERP).

22 tion of IgG, IgM, and IgA antibodies against T. gondii in an approximately 1-mul serum or whole-blood

23 ing more effective, less toxic drugs against T. gondii.

24 the immune status of animals/humans against T. gondii.

25 sine (NECA) protected CD73(-/-) mice against T. gondii-induced immunopathology, suggesting that the a

26 tion in promoting sterile protection against T. gondii and provide strong evidence for rhoptry-regula

27 is involved in host immune responses against T. gondii infection.

28 ion of their diet with linoleic acid allowed T. gondii sexual development in mice.

29 f different isoforms of these enzymes allows T. gondii to rapidly adapt to diverse metabolic requirem

30 ipulation of the host immune response allows T. gondii to not only dampen the ability of the host to

31 se innate immune responses to N. caninum and T. gondii and found marked differences in cytokine level

32 protected against infection by T. cruzi and T. gondii, and survive infections that are lethal to wil

33 of ill children reflecting brain damage and T. gondii infection.

34 ticosteroid administration, aqueous GWC, and T. gondii PCR did not influence recurrences (P = .12, P

35 q) to profile the transcriptomes of mice and T. gondii during acute and chronic stages of infection.

36 und that seroprevalence of Brucella spp. and T. gondii antibodies likely increased through time, and

37 ophagy in CD40(+) endothelial cells and anti-T. gondii activity dependent on ULK1 and beclin 1.

38 th higher number of intense bands on aqueous T. gondii immunoblot (P = .006), and increased when veno

39 ruitment of the autophagy protein LC3 around T. gondii and spontaneous parasite killing dependent on

40 As T. gondii chronic infection and profilin (PRF) confer re

41 eal that systemic infectious agents, such as T. gondii, can induce long-term immune alterations assoc

42 Although an association between T. gondii exposure and prey specialization on marine sna

43 Phe operative during the interaction between T. gondii and its host cell.

44 g imaging flow cytometry, we found that both T. gondii and IL-10 inhibited virus-induced nuclear tran

45 site burdens at secondary sites colonized by T. gondii and succumb to infection.

46 similar functions in host cell engagement by T. gondii.

47 criptional downregulation of MHC-II genes by T. gondii was previously established, but the precise me

48 tion was inhibited only in cells infected by T. gondii, which inhibited neither uptake of GFP-HSV nor

49 Among the 81 women who were positive by T. gondii IgA antibody ELISA testing, 61 (75.3%) were ac

50 mechanism of inhibition of TLR signaling by T. gondii and IL-10 and suggest potential negative conse

51 ogenic functions during ileitis triggered by T. gondii, it was required for host defense against C. r

52 so the disrupted gene and protein are called T. gondii Brain Colonization Protein 1 (TgBCP1).

53 innate immune responses to restrict cerebral T. gondii growth.

54 T cell responses in the brain during chronic T. gondii infection.

55 propagate inflammation, and that in chronic T. gondii infection, microglia can release the alarmin I

56 oliferate to prevent reactivation of chronic T. gondii infection.

57 cytes that infiltrate the brain upon chronic T. gondii infection, plays a decisive role in host defen

58 Circulating T. gondii-infected leukocytes (dendritic cells used as a

59 human malaria parasite, using a conditional T. gondii ADF-knockout line complemented with ADF varian

60 antigenic recall in infants with congenital T. gondii infection.

61 udy we show that IL-1R(-/-) mice can control T. gondii burden throughout infection.

62 we determined that ZBP1 functions to control T. gondii growth.

63 nflammation and are critical for controlling T. gondii However, the dynamic and regional relationship

64 ology could be a useful tool for delineating T. gondii transmission routes in human populations.

65 Thirteen mussels (1.4%) had detectable T. gondii DNA and the presence of T. gondii in mussels w

66 during gestation is made mostly by detecting T. gondii-specific antibodies, including IgG and IgM, in

67 istic insight into the function of different T. gondii aldolases, we first determined the crystal str

68 pared the genomes of 62 globally distributed T. gondii isolates to several closely related coccidian

69 ations regulates their local behavior during T. gondii infection.

70 ocalization of monocytes in the brain during T. gondii CNS infection.

71 )) monocytes into the blood and brain during T. gondii infection of C57BL/6J and CCR2(RFP/+)CX3CR1(GF

72 Similarly, Tregs in the CNS during T. gondii infection are Th1 polarized, as exemplified by

73 tent pattern of monocyte infiltration during T. gondii infection to the olfactory tubercle, in contra

74 es and was not induced in macrophages during T. gondii infection.

75 n the metabolic profile of mouse sera during T. gondii infection.

76 Here we report that during T. gondii infection a strong NF-kappaB and inflammatory

77 lar factors directing robust and rapid early T. gondii-killing mechanisms in the LEW rat.

78 report a novel function of the endolysosomal T. gondii sortilin-like receptor (TgSORTLR), which media

79 Natural and engineered T. gondii antigens have led the way to understanding the

80 here demonstrated that N. caninum expressing T. gondii's GRA15 and ROP16 kinase are biologically acti

81 dispensable in T. gondii tachyzoites and for T. gondii infectivity.

82 ents that create a conducive environment for T. gondii sexual reproduction will allow for development

83 hat identify cats as the definitive host for T. gondii are unknown.

84 ban snails are competent transport hosts for T. gondii.

85 family, is a secreted protein important for T. gondii motility, host cell attachment, invasion, and

86 protein is also thought to be important for T. gondii-host interaction, pathogenesis, and immune eva

87 Physicians who ordered testing only for T. gondii IgG and IgM should also request additional tes

88 identify NLRP3 as an inflammasome sensor for T. gondii in primary human peripheral blood cells and to

89 n MHC class II tetramer reagent specific for T. gondii did not recognize Tregs isolated from the CNS.

90 ned the mechanism of species specificity for T. gondii sexual development and break the species barri

91 Here we summarize the major strategies for T. gondii genetic manipulation including genetic crosses

92 Our experiments reveal a sensing system for T. gondii by human cells that is based on the detection

93 Paternal serum samples were tested for T. gondii antibodies with immunoglobulin (Ig) G dye test

94 o (i) validate sensitive molecular tools for T. gondii detection in mussels and (ii) apply optimized

95 cular characterization revealed alleles from T. gondii types I, II/III, X at the B1 locus, and a nove

96 mically characterized cDNA encoding CBS from T. gondii (TgCBS), which represents a first example of p

97 Herein we purify HLA-A*02:01 complexes from T. gondii infected cells and characterize the peptide li

98 that whereas neutrophils and monocytes from T. gondii-infected infants display a combination of proi

99 d elevated levels of anti-Toxoplasma gondii (T. gondii) antibodies in patients with major mental illn

100 Witmer coefficient (GWC), Toxoplasma gondii (T. gondii) immunoblot, or T. gondii-specific polymerase

101 Toxoplasma gondii (T. gondii) is a protozoan parasite that uses conserved m

102 plexan protozoan parasite Toxoplasma gondii (T. gondii).

103 ondii IgG antibody test results who also had T. gondii IgA and IgM antibody tests performed.

104 Phe/Phe genotype was associated with higher T. gondii antibody levels in sera.

105 ggest potential negative consequences of HIV/T. gondii coinfection.

106 We discuss how T. gondii infection suppresses noradrenergic signaling a

107 ons, this study brings novel evidence on how T. gondii has devised a molecular weapon of choice to ta

108 However, T. gondii inhibited IFN-alpha and TNF-alpha produced in

109 the homologous type I or a distinct type II T. gondii genotypes.

110 role of CD73 and extracellular adenosine in T. gondii pathogenesis, we infected wild-type (WT) and C

111 However, the role of the IL-1 axis in T. gondii infection is unclear.

112 apicoplast has a key role in heme biology in T. gondii and is important for both mitochondrial and ge

113 nzyme in regulation of glucose catabolism in T. gondii.

114 ow a remarkable low level of conservation in T. gondii.

115 t classic cell-cycle regulators conserved in T. gondii were not detected in the ubiquitinome.

116 ic manipulation tools have been developed in T. gondii over the past 20 years.

117 findings in another study, is dispensable in T. gondii tachyzoites and for T. gondii infectivity.

118 lling invasion, egress, and cell division in T. gondii, the roles of most of these genes are unexplor

119 al B1 allele that was recently documented in T. gondii-infected carnivores from California.

120 ome sensor NLRP3 and for potassium efflux in T. gondii-induced IL-1beta production.

121 een PKA and PKG pathways to govern egress in T. gondii.

122 est alternative roles for the AHH enzymes in T. gondii, since AAH1 is essential for growth in nondopa

123 hese factors were involved in mRNA export in T. gondii.

124 ded to reveal the functions of many genes in T. gondii.

125 (ATP, nucleic acid, proteins, and lipids) in T. gondii, and either of them is sufficient to ensure th

126 nctional reverse transsulfuration pathway in T. gondii and demonstrates the crucial role of TgCBS in

127 ectopic expression of N. caninum profilin in T. gondii had no impact on early IFN-gamma production or

128 11 previously undescribed apical proteins in T. gondii and identify an essential component named cono

129 ensive analysis of palmitoylated proteins in T. gondii, identifying a total of 282 proteins, includin

130 ortant target of inhibition of resistance in T. gondii.

131 skeletal structures differs substantially in T. gondii, the molecular motor dependence of DG traffick

132 apicomplexan parasites, loss of TgPOFUT2 in T. gondii had only a modest impact on MIC2 levels and th

133 MS analysis, we found that the four TSRs in T. gondii MIC2 with protein O-fucosyltransferase 2 (POFU

134 prevalence and function of ubiquitination in T. gondii, we mapped the ubiquitin proteome of tachyzoit

135 a was significantly lower or undetectable in T. gondii-infected mice during the first 24 hpi.

136 s of modified CRISPR-Cas9 systems for use in T. gondii, such as regulation of gene expression, labeli

137 a cone-shaped assembly, the conoid, which in T. gondii comprises 14 spirally arranged fibers that are

138 Optical clearing of intact T. gondii-infected brains using iDISCO(+) and light-shee

139 Interestingly, T. gondii infection did not induce an IL-1beta response

140 s that contributes to resistance to invading T. gondii, and they thus unveil new avenues for developi

141 oxidative stress as a mechanism for killing T. gondii.

142 poietic compartments contributes to limiting T. gondii-induced immunopathology.

143 regions of increased sentinel marine mammal T. gondii infection.

144 solated from ZBP1 deletion (ZBP1(-/-)) mice, T. gondii has an increased rate of replication and a dec

145 Monoclonal T. gondii-specific CD8 T cells adoptively transferred in

146 laboratory aquaria, and to test for natural T. gondii contamination in field-collected snails.

147 evealed a high prevalence (29 of 81; 36%) of T. gondii infection in fathers, relative to the average

148 ctivated macrophages, even in the absence of T. gondii infection.

149 n 2 (MIC2), a motility-associated adhesin of T. gondii, has highly glycosylated thrombospondin repeat

150 ther, structural and biochemical analyses of T. gondii aldolase and aldolase-like proteins reveal div

151 e potential to revolutionize the analysis of T. gondii biology and help us to better develop new drug

152 progress toward understanding the biology of T. gondii infection using rodent models, human cell expe

153 ylated H4K31 is enriched in the core body of T. gondii active genes but inversely correlates with tra

154 to contribute most to the disease burden of T. gondii, ocular disease from acquired infection was re

155 Clusters of T. gondii and individual monocytes across the brain were

156 a role for ZBP1 in assisting host control of T. gondii infection.

157 Control of T. gondii replication by mGBP2 requires GTP hydrolysis a

158 amine scaffold interrupts the lytic cycle of T. gondii at submicromolar concentration by targeting AS

159 al to the intracellular replicative cycle of T. gondii including secretion of adhesins, motility, inv

160 of the signals governing the lytic cycle of T. gondii, with particular focus on egress from infected

161 o lack of sensitive methods for detection of T. gondii in water, this study utilized an alternative s

162 leting the mitochondrion-associated DHODH of T. gondii (TgDHODH) failed.

163 y platforms, as the serological diagnosis of T. gondii infection does not rely on the detection of a

164 ecal pellets, snails may facilitate entry of T. gondii into the nearshore marine food web.

165 Amounts of tachyzoite (acute stage form of T. gondii)-specific SAG1 mRNA and numbers of foci associ

166 529 qPCR does not depend on the genotype of T. gondii isolates and that, in fact, it is superior to

167 The growth of T. gondii aldolase crystals in acidic conditions enabled

168 t contributes to the virulence and growth of T. gondii in mice.

169 sease associated with emerging haplotypes of T. gondii and our lack of effective treatments to steril

170 The importance of T. gondii in human health was made clear with the first

171 clin 1 to stimulate autophagy and killing of T. gondii.

172 proteins along the cortical microtubules of T. gondii, established during daughter biogenesis and re

173 ses using a vaccine-challenge mouse model of T. gondii infection.

174 ffective in acute and latent mouse models of T. gondii infection, significantly reducing the amount o

175 apeutics, we screened insertional mutants of T. gondii for a reduced ability to form cysts in the bra

176 ns of GRA12 to the molecular pathogenesis of T. gondii infection were examined in vitro and in vivo.

177 st but not least, the observed physiology of T. gondii tachyzoites appears to phenocopy cancer cells,

178 Resistant populations of T. gondii were selected by culture in increasing concent

179 detectable T. gondii DNA and the presence of T. gondii in mussels was significantly associated with p

180 t human monocytes recognized the presence of T. gondii infection by detecting the alarmin S100A11 pro

181 Altogether, EGFR is a novel regulator of T. gondii invasion of neural tissue, enhancing invasion

182 However, sexual reproduction of T. gondii occurs only in felids, wherein fertilisation o

183 as to measure concentration and retention of T. gondii by marine snails in laboratory aquaria, and to

184 e relative importance of different routes of T. gondii transmission.

185 determine the prevalence and genotype(s) of T. gondii in mussels.

186 n ESI + mode and 74 in ESI - mode in sera of T. gondii-infected mice compared to the control mice.

187 ent of therapeutics that prevent shedding of T. gondii parasites.

188 to be significantly correlated with sites of T. gondii clusters.

189 Remarkably, at least 350 host species of T. gondii have been described to date, and it is estimat

190 strated that the acute (tachyzoite) stage of T. gondii depends on cooperativity of glucose and glutam

191 ely hardy free-living environmental stage of T. gondii shed in faeces of domestic and wild felids, ar

192 RNA-Seq analysis of cat enteric stages of T. gondii uncovered genes expressed uniquely in microgam

193 Strains of T. gondii are globally diverse, with more than 16 distin

194 Nevertheless, atypical strains of T. gondii in endemic locations cause severe pathology in

195 inflammation generated by certain strains of T. gondii infection can be neuroprotective in the contex

196 e infection by type I and type II strains of T. gondii, and this vaccination also severely reduced or

197 how that the unusual population structure of T. gondii is characterized by clade-specific inheritance

198 ich may underlie the promiscuous survival of T. gondii tachyzoites in diverse host cells.

199 rogress of anhedonia and despair symptoms of T. gondii-infected subjects.

200 tility primarily facilitate the transport of T. gondii through tissues and promote systemic dissemina

201 re still major holes in our understanding of T. gondii biology, including the genes controlling paras

202 is context, IFN-gamma activates a variety of T. gondii-targeting activities in immune and nonimmune c

203 the blood-brain barrier (BBB) within 2 wk of T. gondii infection, exhibited distinct rolling and craw

204 rovide broad-based functional information on T. gondii genes and will facilitate future approaches to

205 or mechanism that functions against not only T. gondii cysts but also other large targets, including

206 Toxoplasma gondii (T. gondii) immunoblot, or T. gondii-specific polymerase chain reaction (PCR) in aq

207 manifestations were associated with paternal T. gondii infection status.

208 ther of two genetically distinct, persistent T. gondii strains (Prugniaud/type II/haplogroup 2 and CE

209 ost and parasite, that facilitate persistent T. gondii infection.

210 690 consecutive pregnant women with positive T. gondii IgG antibody test results who also had T. gond

211 n of JNK, CaMKKbeta, AMPK, or ULK1 prevented T. gondii killing in CD40-activated macrophages.

212 NK cell IFN-gamma production during primary T. gondii infection, in the absence of IL-12 using IL-12

213 However, prior T. gondii infection blocks IFN-gamma-dependent gene tran

214 ected role of phagocytic cells in processing T. gondii oocysts, in line with non-classical routes of

215 letion of GRA12 in type I RH and type II Pru T. gondii strains did not affect the parasite growth and

216 applied as a method for confirming putative T. gondii oocysts detected in snail faeces and tissues b

217 We have recently reported that the putative T. gondii CGL gene encodes a functional enzyme.

218 revalence of chronic and incidence of recent T. gondii infections in fathers of congenitally infected

219 , 8.2 chain have a potent activity to remove T. gondii cysts from the brain.

220 activate CD8(+) T cells capable of removing T. gondii cysts.

221 demonstrate higher than previously reported T. gondii contamination of California coastlines, and de

222 l cell-leukocyte interaction, CD40 restricts T. gondii invasion of neural tissue through a mechanism

223 for control of and survival after secondary T. gondii infection.

224 rotective role for NK cells during secondary T. gondii infection that is dependent on IL-12 and IL-23

225 We further demonstrated that the secreted T. gondii protein kinase ROP17 was required for enhanced

226 Upon stimulation, T. gondii-infected ZBP1(-/-) macrophages display increas

227 s to facilitate drug development: EGS strain T. gondii forms cysts in vitro that induce oocysts in ca

228 rrent reliance on companion animals to study T. gondii sexual development, this work will allow the T

229 Surprisingly, T. gondii ligands are significantly longer than uninfect

230 ic T cells to penetrate into a large target, T. gondii cysts, for their elimination.

231 We now have identified TgIST (T. gondii inhibitor of STAT1 transcriptional activity) a

232 fluorescence microscopy, we determined that T. gondii invaded but did not induce IFN-alpha or TNF-al

233 We determined that T. gondii sexual development occurs when cultured feline

234 In summary, our results indicate that T. gondii C-mannosyltransferase DPY19 is not essential f

235 Our data indicate that T. gondii is capable of evading host detection during th

236 Collectively, these data indicate that T. gondii may not cause a life-long CNS infection.

237 Taken together, our results indicate that T. gondii suppresses pDC activation by mimicking IL-10's

238 ongenitally infected children indicates that T. gondii infections cluster within families in North Am

239 It has long been known that T. gondii interferes with major histocompatibility compl

240 Recently, we showed that T. gondii harbors a novel AMA designated as TgAMA4 that

241 We have recently shown that T. gondii-induced muscle atrophy meets the clinical defi

242 sexual development, this work will allow the T. gondii field to use of alternative models in future s

243 ng and colleagues uncover a new role for the T. gondii protein GRA15 in inducing an anti-parasite res

244 ize the involvement of the apicoplast in the T. gondii heme biosynthesis pathway, we investigated the

245 ntify an intrinsic role for autophagy in the T. gondii parasite and its close relatives.

246 as partially reversed by a deficiency in the T. gondii-derived ROP16 kinase, known to directly phosph

247 Here, the longevity of the T. gondii-induced chronic cachexia model revealed that c

248 ate IFN-gamma was partially dependent on the T. gondii mouse profilin receptor Toll-like receptor 11

249 We further demonstrate that the T. gondii armadillo repeats-only protein (TgARO) mutant,

250 palmitoylation is ubiquitous throughout the T. gondii proteome and reveal insights into the biology

251 BALB/c mice experimentally infected with the T. gondii Pru strain (Genotype II).

252 To test if these T. gondii experienced NK cells were intrinsically differ

253 Thus, T. gondii PTMs are implicated as critical regulators of

254 efractoriness of LEW rat peritoneal cells to T. gondii infection, resulting in proliferation of paras

255 owever, a novel biomarker that correlated to T. gondii infection and associated behaviors is demanded

256 y to only those patients recently exposed to T. gondii.

257 Additionally, the odds of exposure to T. gondii were greater for bears that used land than for

258 Following exposure to T. gondii-containing seawater, oocysts were detected by

259 the mechanisms of cell-intrinsic immunity to T. gondii in the brain and muscle, and the long-term eff

260 rd the hypothesis that sustained immunity to T. gondii requires repeated antigenic stimulations.

261 he Lewis (LEW) rat is extremely resistant to T. gondii infection.

262 ion of how human cells detect and respond to T. gondii.

263 od-producing innate cytokines in response to T. gondii and demonstrate an unappreciated requirement f

264 00A11 induced a potent chemokine response to T. gondii by engaging its receptor RAGE, and regulated m

265 understanding of the host immune response to T. gondii infection and summarize the key limitations fo

266 enes differentially expressed in response to T. gondii infection are similar between males and female

267 ls neither provided a protective response to T. gondii infection nor mediated autoimmune colitis.

268 IL-1beta cleavage and release in response to T. gondii infection, without affecting the release of TN

269 n both result in increased susceptibility to T. gondii, the basis for this phenotype reveals distinct

270 excretion following infection with wild-type T. gondii, demonstrating that this mutant is an attenuat

271 Here, we characterized a unique T. gondii homologue of mammalian lecithin:cholesterol ac

272 f IL-22 in innate lymphoid cells (ILCs) upon T. gondii infection.

273 TF4), modifies gene expression patterns upon T. gondii infection.

274 nantly proinflammatory profile upon in vitro T. gondii stimulation.

275 stitute the lytic cycle, as well as the ways T. gondii manipulates host cells to ensure its survival.

276 ial-agglutination and IgG avidity tests when T. gondii IgG and IgM results were positive and serum sa

277 granzyme B were detected in association with T. gondii bradyzoites.

278 investigated the impact of coinfection with T. gondii on the innate virus-directed responses of huma

279 ced immunological phenotypes consistent with T. gondii strains.

280 ined as acutely or chronically infected with T. gondii based on a panel of serologic tests performed

281 uman population is chronically infected with T. gondii cysts, the dormant form of the parasite.

282 Unexpectedly, T-bet(-/-) mice infected with T. gondii develop a strong NK cell IFN-gamma response th

283 umbers of DCs, Flt3L(-/-) mice infected with T. gondii displayed an expansion of CD8alpha(+) and CD11

284 vident in immunodeficient mice infected with T. gondii, as associated with high expression level (P <

285 sting, 61 (75.3%) were acutely infected with T. gondii, while of the 547 who were negative by IgA tes

286 ntervention to combat chronic infection with T. gondii by targeting the persistent cysts of the paras

287 dling cat litter, as maternal infection with T. gondii can be transmitted to the fetus with potential

288 um N-glycomics changes during infection with T. gondii in BALB/c mice, immunocompetent, or in severe

289 hypothesized that a prolonged infection with T. gondii may protect against age-associated decline in

290 hology during intraperitoneal infection with T. gondii than WT mice.

291 tibodies to have had a recent infection with T. gondii Toxoplasma IgA antibody testing can therefore

292 onic toxoplasmosis after oral infection with T. gondii.

293 nt to prevent reactivation of infection with T. gondii.

294 responses to control cerebral infection with T. gondii.

295 ected wild-type (WT) and CD73(-/-) mice with T. gondii cysts systemically by the intraperitoneal (i.p

296 2rx7 knockout mice were infected orally with T. gondii and their pathologic profiles were analyzed.

297 results demonstrate that pregnant women with T. gondii IgA antibodies are more likely than pregnant w

298 st cell completely replaces the l-Phe within T. gondii tachyzoites 7-9 hours after infection.

299 e LEW rat versus the BN rat, with or without T. gondii infection, in order to unravel molecular facto

300 are more likely than pregnant women without T. gondii IgA antibodies to have had a recent infection