ライフサイエンスコーパス: C. parvum

1 tes to initiate an innate immune response to C. parvum.

2 ons is caused by Cryptosporidium hominis and C. parvum.

3 to a subset of cells actively infected with C. parvum.

4 f successful and quantifiable infection with C. parvum.

5 ed apoptosis of epithelial cells infected by C. parvum.

6 ptosis is complex and crucial to the life of C. parvum.

7 ce with two genetically distinct isolates of C. parvum.

8 dium, and subtype families of C. hominis and C. parvum.

9 o enhanced the invasion of cultured cells by C. parvum.

10 ight provide new treatments for infection by C. parvum.

11 e examined in neonatal piglets infected with C. parvum.

12 involved in mediating initial resistance to C. parvum.

13 35 days and co-culturing was performed with C. parvum.

14 ssess nucleotide biosynthesis as a target in C. parvum.

15 ipts of very low protein-coding potential in C. parvum.

16 sts showed high selectivity for heat-shocked C. parvum.

17 ere produced to investigate the transport of C. parvum.

18 provide the same level of protection against C. parvum.

19 r infection with C. hominis protects against C. parvum.

20 ivators of transcription proteins induced by C. parvum.

21 e expression and characterization of TK from C. parvum.

22 Using C. parvum 18S rRNA gene fragment as a representative of

23 as apoptosis of infected cells and decreased C. parvum 18S rRNA levels.

24 They had C. hominis (141 persons), C. parvum (22 persons), C. meleagridis (17 persons), C.

25 itive samples to identify species, including C. parvum (41), C. andersoni (2), and C. hominis (2), an

26 93.5, 100, 100, and 95.5%, respectively; for C. parvum, 98.8, 100, 100, and 99.7%, respectively.

27 In a genetically divergent isolate of C. parvum, a majority of sequences was found to be recom

28 We previously demonstrated that C. parvum activates the Cdc42/neural Wiskott-Aldrich syn

29 ral antimicrobial peptides to carry out anti-C. parvum activity.

30 C. hominis is restricted to humans, whereas C. parvum also infects other mammals.

31 The C. parvum and C. hominis isolates were subgenotyped by s

32 eact with an approximately 30-kDa protein in C. parvum and C. hominis.

33 idium species most relevant to human health, C. parvum and C. hominis.

34 fferent risk factors for cases infected with C. parvum and C. hominis.

35 yptosporidium hominis, and one (1%) had both C. parvum and C. hominis.

36 The presence of C. hominis alleles in C. parvum and C. meleagridis isolates confirms earlier r

37 fies nucleotide excision repair genes in the C. parvum and Cryptosporidium hominis genomes and discus

38 This series of compounds inhibit CpKRS and C. parvum and Cryptosporidium hominis in culture, and ou

39 kDa Gal/GalNAc-specific lectin isolated from C. parvum and Cryptosporidium hominis sporozoites by Gal

40 deduced amino acid sequence of gp40/15 from C. parvum and from all Cryptosporidium hominis subtypes

41 reaction (qPCR) using probes for 18s rRNA of C. parvum and HCT-8 cells were performed.

42 review the evidence for such an organelle in C. parvum and its probable function.

43 w tools for elucidating the role of IMPDH in C. parvum and may serve as potential therapeutics for tr

44 sis of acyl transferases within PKS/FAS from C. parvum and other organisms clearly differentiates ace

45 Forty-four of 49 isolates were identified as C. parvum, and 1 was identified as C. hominis.

46 Three- to 4-week-old mice were infected with C. parvum, and infection was monitored by quantifying fe

47 Protein-binding specificity assays of C. parvum AP2 domains combined with motif conservation u

48 C. parvum AP2 domains display reduced binding diversity

49 C. hominis orthologs of putative C. parvum ApiAP2 proteins and target genes show greater

50 We recently reported that the C. parvum apical complex glycoprotein CSL contains a zoi

51 Here we show that the discharge of C. parvum apical organelles occurs in a temperature-depe

52 is but only partially against challenge with C. parvum, as compared with age-matched control animals

53 tion by dominant negative mutation inhibited C. parvum-associated actin remodeling, membrane protrusi

54 pClec is a novel C-type lectin that mediates C. parvum attachment and infection via Ca(2+)-dependent

55 Recombinant p30 inhibits C. parvum attachment to and infection of Caco-2A cells,

56 Like CpClec-Fc binding, C. parvum attachment to and infection of HCT-8 cells wer

57 and Caco-2 cells and competitively inhibited C. parvum attachment to and infection of HCT-8 cells.

58 Altogether, 13 subtypes of C. parvum (belonging to four subtype allele families) an

59 on Cryptosporidium parvum and the removal of C. parvum by physical filtration in porous ceramic filte

60 tissues derived from macaques infected with C. parvum by the Ussing chamber technique.

61 aper describes the effective inactivation of C. parvum by UV light, identifies nucleotide excision re

62 oridiosis are associated with C. hominis and C. parvum; C. canis and C. felis are responsible for onl

63 myosin IIB significantly inhibits (P < 0.05) C. parvum cellular invasion (by 60 to 80%).

64 s involved in the membrane protrusion during C. parvum cellular invasion, phenomena that may also be

65 t cell-parasite interface, thus facilitating C. parvum cellular invasion.

66 vum-induced actin accumulation and inhibited C. parvum cellular invasion.

67 or asymptomatic infection after experimental C. parvum challenge.

68 C. parvum-challenged mice showed prolonged weight loss (

69 We identified C. parvum Clec (CpClec), a novel mucin-like glycoprotein

70 ulated with Mphi from SCIDbg mice exposed to C. parvum (CP-Mphi) or resident Mphi previously cultured

71 sL) system is involved in paracrine-mediated C. parvum cytopathicity in cholangiocytes, we also teste

72 Tat affects TLR expression and, hence, anti-C. parvum defense responses.

73 tellite-2 region (ML-2) where C. hominis and C. parvum differ by one nucleotide substitution.

74 hat apical organelles play a central role in C. parvum entry into host cells.

75 The mechanism of the C. parvum enzyme involves the random addition of substra

76 C. hominis and C. parvum exhibit very similar gene complements, and phe

77 C. parvum exhibits a high rate of recombination commensu

78 PKS1 protein resembles a previously reported C. parvum fatty acid synthase (CpFAS1), which is encoded

79 e further show that the purine metabolism in C. parvum follows a highly streamlined pathway.

80 sinfection likely contribute to treatment of C. parvum for silver impregnated ceramic water filters,

81 nomic DNA was generated, and we identified a C. parvum gene coding for inosine 5-monophosphate-dehydr

82 eviously, a large-scale random survey of the C. parvum genome conducted in our laboratory revealed th

83 dy, exhaustive BLAST screening of a complete C. parvum genome sequence database resulted in identific

84 resent study, TBLASTN screening of available C. parvum genomic sequences by using TSP1 domains as que

85 e isolate selected to sequence the genome of C. parvum genotype 1 and is currently used in several re

86 ort for the hypothesis that human and bovine C. parvum genotypes may be separate species.

87 atterns similar to those found on the native C. parvum glycoproteins would greatly facilitate the mol

88 nt in a C. parvum lysate cleaved recombinant C. parvum gp40/15 protein into 2 peptides, identified as

89 Triacsin C was highly effective against C. parvum growth in vitro (median inhibitory concentrati

90 ecule was a 121-nucleotide sequence from the C. parvum heat shock protein 70 (hsp70 mRNA from U71181

91 hominis (2), and the predominant subtype was C. parvum IIa A17G2R1.

92 including the higher nucleotide diversity of C. parvum IId GP60 sequences in Western Asia, as well as

93 A clonal population structure was seen in C. parvum IId isolates from China and Sweden.

94 of cattle, sheep, and goats, indicated that C. parvum IId subtypes were probably dispersed from West

95 e report a selective urea-based inhibitor of C. parvum IMPDH (CpIMPDH) identified by high-throughput

96 iously identified several parasite-selective C. parvum IMPDH (CpIMPDH) inhibitors by high-throughput

97 ynamic properties of the NAD binding site of C. parvum IMPDH can be exploited to develop parasite-spe

98 re we describe the expression of recombinant C. parvum IMPDH in an Escherichia coli strain lacking th

99 Because C. parvum IMPDH is highly divergent from the host counte

100 The pronounced resistance of C. parvum IMPDH to mycophenolic acid inhibition is in st

101 assay that can differentiate C. hominis from C. parvum in a rapid and cost-effective manner.

102 parasites, we analyzed the transcriptome of C. parvum in oocysts, sporozoites and infected cell mono

103 oxoplasma gondii, Plasmodium falciparum, and C. parvum In the present study, BKIs were screened for e

104 er elucidate the origin and dissemination of C. parvum in the world.

105 fe cycle development and long-term growth of C. parvum in vitro using "air-liquid interface" (ALI) cu

106 ion, and consequently, infection dynamics of C. parvum in vitro.

107 easure inhibitory activities of BKIs against C. parvum in vitro.

108 gamma-mediated innate immune pathway against C. parvum in which IL-18 and macrophages play prominent

109 impact of multiple concentrations of CYA on C. parvum inactivation (at 20 and 40 mg/L free chlorine;

110 were increased in HCT-8 cells infected with C. parvum, including calreticulin, a major calcium-bindi

111 ferent isolates (MD, GCH1, UCP, and IOWA) of C. parvum, indicating that both Cp900 and Cp40 are immun

112 ion of host cell c-Src significantly blocked C. parvum -induced accumulation and tyrosine phosphoryla

113 ebbistatin significantly decrease (P < 0.02) C. parvum-induced accumulation of SGLT1 at infection sit

114 us functionally deficient mutants, decreased C. parvum-induced actin accumulation and inhibited C. pa

115 ifferentiation protein 88 (MyD88), inhibited C. parvum-induced activation of IL-1R-associated kinase,

116 Tat significantly (P < 0.05) increased C. parvum-induced apoptosis in bystander cells in a dose

117 nscription (Tat)-mediated FasL regulation on C. parvum-induced apoptosis in cholangiocytes by semiqua

118 caspase-8 inhibitor Z-IETD-fmk both blocked C. parvum-induced apoptosis in cholangiocytes.

119 We found that C. parvum-induced apoptosis was associated with transloc

120 transfection of miR-513 precursor inhibited C. parvum-induced B7-H1 protein expression.

121 s, accompanied by significant suppression of C. parvum-induced caspase 3 activity and expression of P

122 onally deficient mutants of frabin inhibited C. parvum-induced Cdc42 accumulation at the host cell-pa

123 Moreover, LY294002 abolished C. parvum-induced Cdc42 activation in infected cells.

124 intensify) cryptosporidiosis by suppressing C. parvum-induced cell turnover and caspase-dependent ap

125 he data demonstrated that HIV-1 Tat enhances C. parvum-induced cholangiocyte apoptosis via a paracrin

126 Moreover, Tat enhanced both C. parvum-induced FasL membrane translocation and releas

127 ion were each associated with a reduction of C. parvum-induced human beta-defensin-2 expression.

128 C. parvum-induced inflammation and increased NO(*) synth

129 ng RNA to TLR2, TLR4, and MyD88 also blocked C. parvum-induced NF-kappaB activation.

130 n of let-7i causes reciprocal alterations in C. parvum-induced TLR4 protein expression, and consequen

131 decreased TLR4 protein levels and suppressed C. parvum-induced TLR4 protein expression.

132 ecreased let-7 expression is associated with C. parvum-induced up-regulation of TLR4 in infected cell

133 However, the molecular mechanisms by which C. parvum induces membrane translocation/insertion of SG

134 We found that C. parvum infected and developed in this tissue model fo

135 ted and uninfected cells were recovered from C. parvum-infected cell monolayers.

136 TLR4 mRNA expression in both uninfected and C. parvum-infected cholangiocytes.

137 activated human T cells after coculture with C. parvum-infected cholangiocytes.

138 Intracellular polyamine levels of C. parvum-infected human epithelial cells were determine

139 were detected in the exosomes released from C. parvum-infected intestinal epithelial cells.

140 ynitrite formation or peroxidative injury of C. parvum-infected mucosa and had no impact on the sever

141 The presence of neutrophils in C. parvum-infected mucosa was associated with enhanced b

142 ident Mphi previously cultured with PMN from C. parvum-infected SCIDbg mice (CP-PMN).

143 were increased in jejunal samples following C. parvum infection and were accompanied by increased ba

144 leased from intestinal epithelial cells upon C. parvum infection can activate immune cells by shuttli

145 d from intestinal epithelial cells following C. parvum infection could activate the nuclear factor ka

146 LPS stimulation or C. parvum infection decreased cholangiocyte expression o

147 C. parvum infection has been associated with induction o

148 nd interferon gamma knockout mouse models of C. parvum infection identified BKIs with in vivo activit

149 udy, BKIs were screened for efficacy against C. parvum infection in the neonatal mouse model.

150 er, these findings suggest that p30 mediates C. parvum infection in vitro and raise the possibility t

151 CpClec expression during C. parvum infection in vitro is maximal at 48 h postinfe

152 Furthermore, C. parvum infection inhibited staurosporine-induced apop

153 at the resistance of SCIDbg mice early after C. parvum infection is displayed through the function of

154 N), suggesting that the severity early after C. parvum infection is strongly influenced by the functi

155 for Cdc42 in the activation of Cdc42 during C. parvum infection of biliary epithelial cells.

156 Here, we report that C. parvum infection of cholangiocytes recruits host-cell

157 C. parvum infection of cultured cholangiocytes induces t

158 Moreover, C. parvum infection of cultured cholangiocytes results i

159 e role of TLRs in host-cell responses during C. parvum infection of cultured human biliary epithelia

160 We found that C. parvum infection of cultured human biliary epithelial

161 The furin inhibitor Dec-RVKR-cmk decreased C. parvum infection of HCT-8 cells, suggesting that a fu

162 C. parvum infection resulted in a significant increase i

163 C. parvum infection resulted in low-level activation of

164 th associated production of Tat protein, and C. parvum infection synergistically increase cholangiocy

165 arrow-derived cells therefore suffices for a C. parvum infection to be cleared, while CD40 expression

166 used an established neonatal piglet model of C. parvum infection to examine the role of neutrophils i

167 In a C. parvum infection with 1 x 10(6) oocysts/mouse in SCID

168 ost cells was significantly upregulated upon C. parvum infection, and a higher level of ITGA2 protein

169 s treatment also affected the progression of C. parvum infection, as reinfection, normally seen late

170 eric protozoan and its downregulation during C. parvum infection, which is detrimental to parasite cl

171 of the SCIDbgMN mice died within 16 days of C. parvum infection, while 100% of the SCIDbg mice expos

172 angiocytes in response to LPS stimulation or C. parvum infection.

173 expression by cholangiocytes in response to C. parvum infection.

174 -PMN alone or resident Mphi alone died after C. parvum infection.

175 butes to epithelial immune responses against C. parvum infection.

176 targets of cellular immune responses during C. parvum infection.

177 pithelium and contributes to host defense in C. parvum infection.

178 dditive effect in conferring protection from C. parvum infection.

179 that contributes to the clearance of initial C. parvum infection.

180 ression profile detected in host cells after C. parvum infection.

181 receptor interactions in the pathogenesis of C. parvum infection.

182 o the nuclei of host epithelial cells during C. parvum infection.

183 ibit parasite growth in an in vitro model of C. parvum infection.

184 dinates epithelial expression of SOCS4 after C. parvum infection.

185 xpression in epithelial cells in response to C. parvum infection.

186 Cs thus outperform CD103- DCs in controlling C. parvum infections and represent a primary target of h

187 tory genes in the liver and spleen following C. parvum intestinal infection in neonatal mice.

188 leton-associated protein tyrosine kinase, in C. parvum invasion of biliary epithelia.

189 We previously demonstrated that efficient C. parvum invasion of biliary epithelial cells (cholangi

190 C. parvum invasion of biliary epithelial cells requires

191 at the attachment sites, thereby inhibiting C. parvum invasion of biliary epithelial cells.

192 hibition of host-cell AQP1 and SGLT1 hampers C. parvum invasion of cholangiocytes.

193 s detected; an antibody to CP2 decreased the C. parvum invasion of cholangiocytes.

194 These data suggest that C. parvum invasion of target epithelia results from the

195 mportant component of the complex process of C. parvum invasion of target epithelia results from the

196 nstitutively active mutant of Cdc42 promoted C. parvum invasion, overexpression of a dominant negativ

197 ering RNA-mediated gene silencing, inhibited C. parvum invasion.

198 ve mutants of RhoA and Rac1 had no effect on C. parvum invasion.

199 sociated actin polymerization also inhibited C. parvum invasion.

200 pression of the p85 subunit of PI3K promoted C. parvum invasion.

201 d to the parasite-host cell interface during C. parvum invasion.

202 also, inhibition of dynamin 2 did not block C. parvum invasion.

203 f cortactin in the epithelia also diminished C. parvum invasion.

204 assay the role of c-Src signaling pathway in C. parvum invasion.

205 rc and cortactin and significantly decreased C. parvum invasion.

206 To obtain a 3-log inactivation of C. parvum Iowa oocysts, contact times of 105 and 128 min

207 The genome sequence of C. parvum is approaching completion, and we have used th

208 reliable way to differentiate C. hominis and C. parvum is based on DNA sequencing analysis of PCR amp

209 cation of transporters/channels initiated by C. parvum is essential for membrane extension and parasi

210 We propose that C. parvum is less reliant on ApiAP2 regulators in part b

211 s an anthroponotic transmission cycle, while C. parvum is zoonotic, infecting cattle and other rumina

212 ce polymorphism at the Cpgp40/15 locus of 20 C. parvum isolates from HIV-infected South African child

213 a in conferring resistance to infection with C. parvum, it suggests that MyD88-mediated pathways also

214 , supported by structures of both PfKRS1 and C. parvum KRS (CpKRS).

215 Infection with C. parvum led to upregulation of genes encoding inhibito

216 n furin and a protease activity present in a C. parvum lysate cleaved recombinant C. parvum gp40/15 p

217 40/15 and a synthetic furin substrate by the C. parvum lysate was inhibited by serine protease inhibi

218 ) and was also cleaved by both furin and the C. parvum lysate.

219 d in inhibition of cleavage by furin and the C. parvum lysate.

220 C. parvum may provide clues to the ancestral state of ap

221 Antiserum against C. parvum membrane proteins blocked accumulation of c-Sr

222 findings, along with the known functions of C. parvum mucin-like glycoproteins and of CTLD-containin

223 Furthermore, C. parvum obtained its IMPDH gene by lateral transfer fr

224 cal estimator for attachment efficiencies of C. parvum oocyst deposition in porous media for a variet

225 ed the transport of surface-treated, sterile C. parvum oocyst in porous media.

226 pecifically addressed the effects of ClO2 on C. parvum oocyst infectivity in chlorinated recreational

227 ognizing COWP8 specifically localized to the C. parvum oocyst wall, supporting the hypothesis that mu

228 method is described for cryopreservation of C. parvum oocysts by vitrification using custom high asp

229 Vitrification of C. parvum oocysts in larger volumes will expedite progre

230 and amplification of mRNA from as few as 30 C. parvum oocysts was demonstrated directly on-chip and

231 NA derived from as few as 5 x 10(3) purified C. parvum oocysts was successfully detected.

232 , MIC was used to identify live and inactive C. parvum oocysts with over 90% certainty, whilst also d

233 ng (APCR), as well as DFA (G. duodenalis and C. parvum or C. hominis) or trichrome stain (E. histolyt

234 99.5% for G. duodenalis, 95.5% and 99.6 for C. parvum or C. hominis, and 100% and 100% for E. histol

235 ucosa cultured as explants was infected with C. parvum or C. hominis, and gene expression was analyze

236 dding and the number of intestine-associated C. parvum organisms, accompanied by significant suppress

237 ntified in cells after exposure to infective C. parvum parasite or parasite lysate.

238 The C. hominis and C. parvum PCRs specifically detected only species/genoty

239 molecules have isoelectric points similar to C. parvum (pH approximately 2), and glycoprotein is a ma

240 non-methylated C2 units are incorporated by C. parvum polyketide and fatty acid synthases.

241 significantly longer for HuG1 than for BoG2 C. parvum (prepatent, 8.6 vs. 5.6 days; patent, 16.6 vs.

242 at investigated mammalian cell cytotoxicity, C. parvum proliferation inhibition in vitro, anti-human

243 nly a single pathway has been identified for C. parvum purine nucleotide salvage.

244 Our studies demonstrate that C. parvum relies on a conserved actin-myosin motor for m

245 C. parvum relies on inosine 5'-monophosphate dehydrogena

246 C. parvum removal efficiencies ranged from 1.5 log (96.4

247 Protection against C. parvum required additional signals provided by the gu

248 Incubation with C. parvum resulted in patchy disruption of the epitheliu

249 suggest that the invasion of HCT-8 cells by C. parvum results in an ER stress response by the host c

250 oridiosis, we report here that some of these C. parvum RNA transcripts were selectively delivered int

251 Site-directed mutagenesis of the C. parvum RSRR sequence to ASRR resulted in inhibition o

252 implicates a potential strategy to attenuate C. parvum's effects by modulating apoptosis and promotin

253 Salvage of adenosine provides C. parvum's sole source of purines.

254 Moreover, C. parvum selectively up-regulated human beta-defensin-2

255 Genes encoding UV repair proteins exist in C. parvum, so the parasite should be able to regain infe

256 rent subgenotypes were identified within the C. parvum species, and two of these were responsible for

257 vum, Cp900 and Cp40 but not Cp15, stimulated C. parvum-specific proliferative immune responses of mes

258 These data demonstrate that the discharge of C. parvum sporozoite apical organelle contents occurs an

259 gp40/15 gene, gp40 and gp15, are involved in C. parvum sporozoite attachment to and invasion of host

260 Lastly, CpClec-Fc binding and C. parvum sporozoite attachment were significantly decre

261 inhibition of apical organelle discharge by C. parvum sporozoites blocked parasite invasion of, but

262 We established and optimized transfection of C. parvum sporozoites in tissue culture.

263 C. parvum sporozoites moved more rapidly than T. gondii

264 Real-time video microscopy demonstrated that C. parvum sporozoites undergo circular and helical glidi

265 Motility by C. parvum sporozoites was prevented by latrunculin B and

266 lcium also decreased the gliding motility of C. parvum sporozoites.

267 ppression of CIS and contributed to LPS- and C. parvum-stimulated CIS protein expression.

268 Transfection of miR-98 precursor abolished C. parvum-stimulated SOCS4 up-regulation.

269 Seven C. hominis and C. parvum subtype families (including a new family, IIm)

270 genetic structure studies involving various C. parvum subtype families using high-resolution tools a

271 C. parvum subtype IIc-a also has an elevated level of in

272 N mice orally infected with a lethal dose of C. parvum survived after they were inoculated with Mphi

273 C. parvum synthesizes guanine nucleotides from host aden

274 o identified the RPA2 and RPA3 subunits from C. parvum, the latter of which had yet to be reported to

275 T cells may be important for elimination of C. parvum, these cells are dispensable for controlling t

276 ved for any other gene or protein studied in C. parvum to date.

277 Our data demonstrate that C. parvum transcripts of low protein-coding potential ar

278 show any difference in tumor latency between C. parvum-treated and control groups.

279 An increase in the FoxP3(+)T-reg cells in C. parvum-treated p53-/-NOS2+/+ mice indicates a role of

280 C. parvum-treated p53-/-NOS2+/+ mice showed an increase

281 In C. parvum-treated p53-/-NOS2+/+ mice, tumor development

282 R analysis of transcript levels reveals that C. parvum TSP genes were developmentally regulated with

283 We report the complete genome sequence of C. parvum, type II isolate.

284 dispar, G. lamblia assemblages A and B, and C. parvum types 1 and 2 in a single assay.

285 Many overrepresented motifs in C. parvum upstream regions are not AP2 binding motifs.

286 signed BKIs were tested for efficacy against C. parvum using in vitro and in vivo (mouse infection mo

287 4 mediate cholangiocyte defense responses to C. parvum via activation of NF-kappaB.

288 l epithelial cells is actively suppressed by C. parvum via upregulation of survivin, favoring parasit

289 associated with diarrhea, and infection with C. parvum was associated with chronic diarrhea and vomit

290 The one specimen false negative for C. parvum was confirmed to be positive by immunofluoresc

291 C. parvum was the predominant species in the first 2 stu

292 eaction), and the species (ie, C. hominis or C. parvum) was determined.

293 IFN-gamma) is known to mediate resistance to C. parvum, we also studied infection in MyD88(-/-) mice

294 res with size, density, and shape similar to C. parvum were coated with biotin (free and containing a

295 enced genomes, one motif is abundant only in C. parvum, whereas the other is shared with (but has pre

296 Two species, C. hominis and C. parvum, which differ in host range, genotype and path

297 -513) was reduced in cells after exposure to C. parvum, which resulted in a relief of 3' untranslated

298 tomatic volunteers after oral challenge with C. parvum, which suggests a role for IL-15 in the contro

299 nsferase and thymidine kinase, are unique to C. parvum within the phylum Apicomplexa.

300 gesting that this genotype originated from a C. parvum x C. hominis recombination event.