ライフサイエンスコーパス: phagocytophilum

1 onserved and may be unique to the species A. phagocytophilum.

2 ourteen dogs (7.6%) were PCR positive for A. phagocytophilum.

3 N-gamma after in vitro restimulation with A. phagocytophilum.

4 d for IFN-gamma production in response to A. phagocytophilum.

5 r IFN-gamma secretion upon challenge with A. phagocytophilum.

6 e obligate intracellular bacterium Anaplasma phagocytophilum.

7 l role in the early eradication of Anaplasma phagocytophilum.

8 a variant strain, Ap-Variant 1, of Anaplasma phagocytophilum.

9 rtially protects mice from infection with A. phagocytophilum.

10 rane proteins and neutralizing targets of A. phagocytophilum.

11 es in both Anaplasma marginale and Anaplasma phagocytophilum.

12 e obligate intracellular bacterium Anaplasma phagocytophilum.

13 the model intracellular bacterium Anaplasma phagocytophilum.

14 ckettsia spp., Ehrlichia spp., and Anaplasma phagocytophilum.

15 mits the human anaplasmosis agent, Anaplasma phagocytophilum.

16 ulation with the rickettsial agent Anaplasma phagocytophilum.

17 ncluding human anaplasmosis agent, Anaplasma phagocytophilum.

18 is important during in vivo infection by A. phagocytophilum.

19 ometry identified the major protein as an A. phagocytophilum 12.5-kDa hypothetical protein, which was

20 ays for the detection of A. marginale and A. phagocytophilum 16S rRNA in plasma-free bovine periphera

21 The expression of the A. phagocytophilum 16S rRNA, sdhC, and sdhD genes was exami

22 Sequence variation between strains of A. phagocytophilum (90 to 100% identity at the nucleotide l

23 Infection with Anaplasma phagocytophilum, a gram-negative, lipopolysaccharide (LP

24 Anaplasma phagocytophilum, a member of the family Anaplasmataceae,

25 To identify the major surface proteins of A. phagocytophilum, a membrane-impermeable, cleavable bioti

26 Anaplasma phagocytophilum, a recently reclassified bacteria in the

27 of isoatp4056 expression had no effect on A. phagocytophilum acquisition from the murine host but aff

28 r presents the first direct evidence that A. phagocytophilum actively modifies its host cell-derived

29 This study identifies the first A. phagocytophilum adhesin-receptor pair and delineates the

30 The binding domains of A. phagocytophilum adhesins A. phagocytophilum invasion pro

31 A. phagocytophilum adhesion to and infection of neutrophils

32 f all seven dogs that were tested yielded A. phagocytophilum after a comparison to bacterial sequence

33 optosis than do components of heat-killed A. phagocytophilum alone.

34 Francisella tularensis and Anaplasma phagocytophilum alter host autophagy, Shigella flexneri

35 f human granulocytic anaplasmosis, Anaplasma phagocytophilum, among other pathogens.

36 The natural life cycle of Anaplasma phagocytophilum, an obligatory intracellular bacterium t

37 Anaplasma phagocytophilum, an obligatory intracellular bacterium t

38 dorferi and the rickettsial agents Anaplasma phagocytophilum and A. marginale.

39 lebrand factor immunofluorescence, Anaplasma phagocytophilum and Anaplasma marginale were successfull

40 Anaplasma phagocytophilum and Anaplasma ovis cause human infection

41 ted or infected with low- or high-passage A. phagocytophilum and assayed for hepatic histopathology a

42 etection of one genome equivalent copy of A. phagocytophilum and can reliably detect 125 bacteria/ml

43 and TH 17 immunity infection with Anaplasma phagocytophilum and Citrobacter rodentium respectively,

44 Caveolae-mediated endocytosis directs A. phagocytophilum and E. chaffeensis to an intracellular c

45 Clinical sensitivities for A. phagocytophilum and E. chaffeensis were 93% and 84%, res

46 , AnkA orthologues in the closely related A. phagocytophilum and Ehrlichia chaffeensis have been show

47 ugamushi, and infections caused by Anaplasma phagocytophilum and Ehrlichia chaffeensis with the ompA,

48 Anaplasma (formerly Ehrlichia) phagocytophilum and Ehrlichia chaffeensis, upon infectio

49 complexities of the interactions between A. phagocytophilum and host myeloid cells.

50 e used to identify patients infected with A. phagocytophilum and is the microbiologic gold standard,

51 d tick hosts for more complete control of A. phagocytophilum and its associated diseases.

52 fections, with two of Babesia microti and A. phagocytophilum and one of B. microti and E. chaffeensis

53 OmpA for protecting against infection by A. phagocytophilum and other Anaplasmataceae pathogens.

54 ce were more refractory to infection with A. phagocytophilum and produced increased levels of IFN-gam

55 As therapeutic options for A. phagocytophilum and related organisms are limited, these

56 ate understanding the interaction between A. phagocytophilum and the host.

57 he obligatory intracellular parasitism of A. phagocytophilum and their biochemical activities were un

58 hift assays provide further evidence that A. phagocytophilum and XA influences isoatp4056 expression.

59 Borrelia miyamotoi, Anaplasma phagocytophilum, and Babesia spp. were not detected in a

60 ty-four (40%) were seroreactive to Anaplasma phagocytophilum, and five (2.7%) were seropositive for Y

61 ates, an ankyrin repeat protein of Anaplasma phagocytophilum, AnkA, is delivered into the host cytopl

62 e of clinical signs were seropositive for A. phagocytophilum antibodies but negative for Ehrlichia ca

63 Anaplasma phagocytophilum (Ap) is an obligate intracellular bacter

64 Anaplasma phagocytophilum (Ap), the agent of the tick-borne diseas

65 Anaplasma phagocytophilum (Ap), the etiologic agent of the tick-bo

66 predicted structural homology to OmpA of A. phagocytophilum (ApOmpA), an adhesin that uses key lysin

67 c 44-kDa major outer membrane proteins of A. phagocytophilum are dominant antigens recognized by pati

68 protein family, the surface components of A. phagocytophilum are largely unknown.

69 trophils and promyelocytic HL-60 cells to A. phagocytophilum are linked to bacterial usage of P-selec

70 anisms used by the tick to control Anaplasma phagocytophilum are not known.

71 lar bacteria such as Ehrlichia and Anaplasma phagocytophilum, as well as obligate intracellular bacte

72 A was recovered from the Ap-ha variant of A. phagocytophilum, associated exclusively with human infec

73 ime PCR assays for Ehrlichia spp., Anaplasma phagocytophilum, Babesia spp., or Lyme Borrelia spp.

74 A. phagocytophilum binding to and invasion of BMMCs do not

75 A. phagocytophilum binding to sialyl Lewis x (sLe(x)) and o

76 We demonstrate that A. phagocytophilum binds and/or infects murine bone marrow-

77 sitivity for the identification of Anaplasma phagocytophilum, Borrelia miyamotoi, Borrelia mayonii, a

78 n of XA induces isoatp4056 expression and A. phagocytophilum burden in both tick salivary glands and

79 The A. phagocytophilum burden increases in salivary glands and

80 le to detect 100% of previously diagnosed A. phagocytophilum cases.

81 Anaplasma phagocytophilum causes granulocytic anaplasmosis, a debi

82 A. phagocytophilum causes macrophage activation and hemopha

83 tion enzymes, suggesting that most of the A. phagocytophilum cells were no longer dividing.

84 llenge and elicit antibodies that inhibit A. phagocytophilum cellular infection in vitro These data d

85 xpression was upregulated the most during A. phagocytophilum cellular invasion.

86 gdorferi and the rickettsial agent Anaplasma phagocytophilum Collectively, we highlight the importanc

87 demonstrate that the respective roles of A. phagocytophilum DCs and RCs are consistent with analogou

88 1387 is not detectable on the surfaces of A. phagocytophilum dense core organisms bound at the HL-60

89 Here we identified APH_1387 as the first A. phagocytophilum-derived protein that associates with the

90 During A. phagocytophilum development in human promyelocytic HL-60

91 he tick-borne rickettsial pathogen Anaplasma phagocytophilum develops within membrane-bound inclusion

92 Although ingestion of A. phagocytophilum did not elicit significant PMN ROS, proi

93 at a single transposon insertion into the A. phagocytophilum dihydrolipoamide dehydrogenase 1 gene (l

94 The PCR also detected A. phagocytophilum DNA in blood samples obtained from 53 pa

95 Previous results demonstrated that A. phagocytophilum does not induce the production of ROS as

96 of msp2(p44) transcripts is expressed by A. phagocytophilum during in vitro cultivation.

97 lement of Msp2(P44) paralogs expressed by A. phagocytophilum during infection of sLe(x)-competent HL-

98 larifying essential proteins expressed by A. phagocytophilum during transmission from ticks to mammal

99 the order Rickettsiales, including Anaplasma phagocytophilum, Ehrlichia canis, E. chaffeensis, E. ewi

100 erved with orthologous proteins in Anaplasma phagocytophilum, Ehrlichia chaffeensis, and Ehrlichia ca

101 RNA gene-based genetic variants of Anaplasma phagocytophilum from dogs in the western United States d

102 Transstadial transmission of A. phagocytophilum from larvae to nymphal stage was also ev

103 ition, larval ticks successfully acquired A. phagocytophilum from mice that were previously infected

104 IFN-gamma release and protected mice from A. phagocytophilum, further demonstrating the inhibitory ef

105 Interestingly, transcription of the A. phagocytophilum gene encoding the DNA binding protein Ap

106 Thus, characterizing A. phagocytophilum genes that affect the inflammatory proce

107 The recently completed sequence of the A. phagocytophilum genome confirmed our findings and indica

108 ys, of recombination were detected in the A. phagocytophilum genome.

109 of the open reading frames (ORFs) in the A. phagocytophilum genome.

110 hwestern Wisconsin, local transmission of A. phagocytophilum has not to date been documented.

111 trate that the isolated outer membrane of A. phagocytophilum has porin activity, as measured by a lip

112 By using an A. phagocytophilum Himar1 transposon mutant library, we sho

113 a plays a critical role in the control of A. phagocytophilum; however, the mechanisms that regulate I

114 The illness caused by A. phagocytophilum, human granulocytic anaplasmosis, occurs

115 gulator, tr1, and a homolog of the Anaplasma phagocytophilum, identified here as A. platys omp-1X.

116 major improvement for early diagnosis of A. phagocytophilum in human patients and suggest a role for

117 We now show that the presence of A. phagocytophilum in I. scapularis ticks increases their a

118 ions for the maintenance and detection of A. phagocytophilum in its vector and early pathogen interac

119 pies of 16S rRNA of both A. marginale and A. phagocytophilum in the same reaction.

120 to Bartonella and the exposure of dogs to A. phagocytophilum in this study.

121 a marginale and the human pathogen Anaplasma phagocytophilum, in order to examine the ability of phi2

122 To explore the mechanism by which A. phagocytophilum increases CDP activity, we assessed the

123 A. phagocytophilum increases the binding of a repressor, CC

124 Remarkably, A. phagocytophilum induced the expression of iafgp, thereby

125 A. phagocytophilum-induced actin phosphorylation resulted i

126 A. phagocytophilum-induced actin phosphorylation was depend

127 We now show that A. phagocytophilum induces expression of the Ixodes scapula

128 We show that A. phagocytophilum induces the phosphorylation of actin in

129 A. phagocytophilum induces ticks to express Ixodes scapular

130 Moreover, A. phagocytophilum-infected cells are inhibited in the rele

131 60 cells cultured at 37 degrees C than in A. phagocytophilum-infected HL-60 cells cultured at 28 degr

132 RNA was approximately threefold higher in A. phagocytophilum-infected HL-60 cells cultured at 37 degr

133 rly, the amount of p44 mRNA obtained from A. phagocytophilum-infected HL-60 cells per bacterium was s

134 in ApxR was also significantly greater in A. phagocytophilum-infected HL-60 cells than in infected IS

135 roughout RNA sequencing in uninfected and A. phagocytophilum-infected I. scapularis ISE6 tick cells,

136 e amount obtained from salivary glands of A. phagocytophilum-infected Ixodes scapularis nymphs.

137 Low-passage A. phagocytophilum-infected mice also showed significantly

138 Neutrophils from A. phagocytophilum-infected mice demonstrate elevated ferri

139 hagocytophilum-infected mice, low-passage A. phagocytophilum-infected mice had more severe hepatic le

140 ic histopathology severity in low-passage A. phagocytophilum-infected mice peaked on day 2 at the tim

141 A. phagocytophilum migrated normally from A. phagocytophilum-infected mice to the gut of engorging sa

142 Compared to high-passage A. phagocytophilum-infected mice, low-passage A. phagocytop

143 to the AVM in neutrophils recovered from A. phagocytophilum-infected mice.

144 phagocytophilum that entered ticks fed on A. phagocytophilum-infected mice.

145 ther gene expression profiling studies of A. phagocytophilum-infected neutrophils and promyelocytic c

146 optosis inhibition in live or heat-killed A. phagocytophilum-infected neutrophils.

147 ount of p44 mRNA obtained from spleens of A. phagocytophilum-infected SCID mice was approximately 10-

148 an efficient method not only to generate A. phagocytophilum-infected ticks but also provides a tool

149 ficient microinjection method to generate A. phagocytophilum-infected ticks in laboratory conditions.

150 ly induced during transmission feeding of A. phagocytophilum-infected ticks on mice and is upregulate

151 as induced during transmission feeding of A. phagocytophilum-infected ticks on mice and was upregulat

152 We now show that A. phagocytophilum infection also enhances the binding of C

153 2-deficient mice were more susceptible to A. phagocytophilum infection and showed splenomegaly, throm

154 en dietary and genetic factors facilitate A. phagocytophilum infection and up-regulate a proinflammat

155 However, differences in ROS response to A. phagocytophilum infection between human and tick cells m

156 more susceptible than control animals to A. phagocytophilum infection due to the absence of IL-18 se

157 t-butyldimethylsilyl)-c-di-GMP, inhibited A. phagocytophilum infection in HL-60 cells.

158 duced apolipoprotein E (apoE) activity on A. phagocytophilum infection in mice.

159 holesterol diet significantly facilitated A. phagocytophilum infection in the spleen, liver, and bloo

160 g pathway plays a key role in controlling A. phagocytophilum infection in ticks by regulating the exp

161 d ferritin mRNA and protein levels during A. phagocytophilum infection in vitro using HL-60 cells and

162 nderstand the role of host cholesterol in A. phagocytophilum infection in vivo, we analyzed the effec

163 A. phagocytophilum infection induced a significant elevatio

164 blocking APH_1235 with antibodies reduced A. phagocytophilum infection levels in mammalian cell cultu

165 A. phagocytophilum infection of BMMCs depends on alpha1,3-f

166 -Asp55 peptide sera partially neutralized A. phagocytophilum infection of HL-60 cells in vitro.

167 s, but not from control groups, inhibited A. phagocytophilum infection of HL-60 cells.

168 oteins have a critical role in inhibiting A. phagocytophilum infection of host cells.

169 Silencing of these genes increased A. phagocytophilum infection of tick salivary glands and tr

170 microbial peptides is highly induced upon A. phagocytophilum infection of tick salivary glands.

171 n (STAT) pathway plays a critical role in A. phagocytophilum infection of ticks.

172 5-205) bind to, and competitively inhibit A. phagocytophilum infection of, host cells.

173 ly demonstrates multifactorial effects of A. phagocytophilum infection on NB4 promyelocytic leukemic

174 A. phagocytophilum infection resulted in elevated cathepsin

175 regulates the IL-18/IFN-gamma axis during A. phagocytophilum infection through its effect on caspase-

176 the role of tick oxidative stress during A. phagocytophilum infection was characterized through the

177 The resistance of jnk2-null mice to A. phagocytophilum infection was due to elevated levels of

178 A. phagocytophilum infection was not detected in the sample

179 sed dramatically at the CYBB locus during A. phagocytophilum infection, particularly around AnkA bind

180 r Ixodes scapularis in response to Anaplasma phagocytophilum infection, the causative agent of human

181 ase mitochondrial ROS production to limit A. phagocytophilum infection, while pathogen inhibits alter

182 aused a marked reduction in the degree of A. phagocytophilum infection.

183 that may be targeted for the treatment of A. phagocytophilum infection.

184 r components in the early pathogenesis of A. phagocytophilum infection.

185 ritical for IFN-gamma-mediated control of A. phagocytophilum infection.

186 velopment of histopathologic lesions with A. phagocytophilum infection.

187 NK2) inhibits IFN-gamma production during A. phagocytophilum infection.

188 and precise detection of A. marginale and A. phagocytophilum infections in cattle.

189 hat a c-di-GMP-receptor complex regulates A. phagocytophilum intracellular infection.

190 We investigated the hypotheses that A. phagocytophilum invades mast cells and inhibits mast cel

191 p14 and outer membrane protein A, another A. phagocytophilum invasin, pronouncedly reduced infection

192 ays in neutrophils and macrophages during A. phagocytophilum invasion and highlight the importance of

193 ng domains of A. phagocytophilum adhesins A. phagocytophilum invasion protein A (AipA), A. phagocytop

194 ression site is present in all strains of A. phagocytophilum investigated.

195 Anaplasma phagocytophilum is a bacterium that is transmitted by Ix

196 Anaplasma phagocytophilum is a tick-borne rickettsial pathogen tha

197 Anaplasma phagocytophilum is an intracellular pathogen transmitted

198 Anaplasma phagocytophilum is an intragranulocytic bacterium that u

199 Anaplasma phagocytophilum is an obligate intracellular bacterium t

200 Anaplasma phagocytophilum is an obligate intracellular bacterium t

201 Because A. phagocytophilum is an obligate intracellular bacterium,

202 Anaplasma phagocytophilum is an obligate intracellular pathogen th

203 Anaplasma phagocytophilum is an obligate intracellular tick-transm

204 Anaplasma phagocytophilum is an obligate vacuolar bacterium that i

205 Anaplasma phagocytophilum is an obligatory intracellular bacterium

206 Anaplasma phagocytophilum is an obligatory intracellular bacterium

207 The life cycle of A. phagocytophilum is biphasic, transitioning between the n

208 The tricarboxylic acid (TCA) cycle of A. phagocytophilum is incomplete and requires the exogenous

209 Anaplasma phagocytophilum is the agent of human anaplasmosis, the

210 Anaplasma phagocytophilum is the etiologic agent of human granuloc

211 Anaplasma phagocytophilum is the etiologic agent of human granuloc

212 Anaplasma phagocytophilum is the tick-transmitted obligate intrace

213 Thus, multiple A. phagocytophilum isolates share the ability to use sLe(x)

214 Because it was unknown whether other A. phagocytophilum isolates share this ability, we extended

215 A. phagocytophilum lacking lpda1 revealed enlargement of th

216 sults reported here suggest that although A. phagocytophilum-like organisms from white-tailed deer ma

217 UV cross-linking of A. phagocytophilum lysate with c-di-[(32)P]GMP detected an

218 fection with the rickettsial agent Anaplasma phagocytophilum Macrophages deficient in annexin A2 secr

219 A. phagocytophilum major surface protein 2 [Msp2(P44)] is e

220 A. phagocytophilum migrated normally from A. phagocytophilu

221 Thus, A. phagocytophilum mitigates mast cell activation.

222 uring pathogen infection, and showed that A. phagocytophilum modifies I. scapularis tick cell miRNA p

223 We now demonstrate that A. phagocytophilum modifies the I. scapularis microbiota to

224 asma marginale and Anaplasma ovis, Anaplasma phagocytophilum MSP2 (p44), Ehrlichia chaffeensis p28-OM

225 A. phagocytophilum MSP2(P44) orthologs expressed by other p

226 confirm differential modification of any A. phagocytophilum MSP2(P44) paralog and the first to provi

227 ferential expression and glycosylation of A. phagocytophilum Msp2(P44).

228 Thus, A. phagocytophilum needs to usurp and acquire various compo

229 All positive specimens were Anaplasma phagocytophilum; no Ehrlichia species were identified.

230 A. phagocytophilum not only fails to activate the normal ne

231 -derived protein that associates with the A. phagocytophilum-occupied vacuolar membrane (AVM).

232 the view that the p44 gene conversion in A. phagocytophilum occurs through the RecF pathway.

233 We have previously demonstrated that A. phagocytophilum organisms of the NCH-1 strain that utili

234 ction, we conducted proteomic analyses on A. phagocytophilum organisms purified from HL-60 cells.

235 Pretreatment of A. phagocytophilum organisms with OmpA antiserum reduces th

236 ogous copies of msp2 within the genome of A. phagocytophilum Our novel RPA assay targeting this seque

237 Here, we demonstrate the importance of A. phagocytophilum outer membrane protein A (OmpA) APH_0338

238 present study investigated regulation of A. phagocytophilum p44 genes, which encode the P44 major su

239 The surface of A. phagocytophilum plays a crucial role in subverting the h

240 t completely blocked the infection of the A. phagocytophilum population that predominantly expressed

241 The abilities of DC- and RC-enriched A. phagocytophilum populations to bind and/or infect HL-60

242 a but not with A. platys-negative sera or A. phagocytophilum-positive sera.

243 ity shift assays revealed the presence of A. phagocytophilum proteins that interact with the promoter

244 ptured by affinity purification were five A. phagocytophilum proteins, Omp85, hypothetical proteins A

245 work represents an extensive study of the A. phagocytophilum proteome, discerns the complement of pro

246 thereby verifying 23.7% of the predicted A. phagocytophilum proteome.

247 lation, replaced by alanine) or two other A. phagocytophilum recombinant response regulators.

248 a burgdorferi, Babesia microti and Anaplasma phagocytophilum rely almost exclusively on a single loop

249 gdorferi s.l., Borrelia miyamotoi, Anaplasma phagocytophilum, Rickettsia spp., Candidatus Neoehrlichi

250 While the conservation of the A. phagocytophilum Sdh proteins, including the residues req

251 monstrate that ticks infected with Anaplasma phagocytophilum show enhanced fitness against freezing i

252 2 proteins from A. platys with those from A. phagocytophilum showed sequence identities of 86.4% for

253 In this study, we show that A. phagocytophilum specifically up-regulates I. scapularis

254 A. phagocytophilum stimulated IPAK1 activity via the G prot

255 d into multiple 42- to 44-kDa isoforms by A. phagocytophilum strain HGE1 during infection of HL-60 ce

256 sue culture isolates of the unique Anaplasma phagocytophilum strain, Ap-Variant 1, were obtained in t

257 region directly downstream of the Anaplasma phagocytophilum (strain MRK) 16S rRNA gene identified ho

258 These results suggest that A. phagocytophilum strains from ruminants could share some

259 Asp14 localized to the A. phagocytophilum surface and was expressed during in vivo

260 hagocytophilum invasion protein A (AipA), A. phagocytophilum surface protein (Asp14), and outer membr

261 These results identify Asp14 as an A. phagocytophilum surface protein that is critical for inf

262 d that aph_0248 (designated asp14 [14-kDa A. phagocytophilum surface protein]) expression was upregul

263 th isoatp4056 mRNA significantly affected A. phagocytophilum survival and isoatp4056 expression in ti

264 However, the mechanisms of A. phagocytophilum survival in neutrophils and the inhibiti

265 expression of salp16, a gene crucial for A. phagocytophilum survival.

266 xpression interfered with the survival of A. phagocytophilum that entered ticks fed on A. phagocytoph

267 omains in alum followed by challenge with A. phagocytophilum The bacterial peripheral blood burden wa

268 racellular Gram-negative bacterium Anaplasma phagocytophilum The disease often presents with nonspeci

269 Anaplasma phagocytophilum, the agent of human anaplasmosis, persis

270 cs and transcriptome sequencing to Anaplasma phagocytophilum, the agent of human granulocytic anaplas

271 Anaplasma phagocytophilum, the agent of human granulocytic anaplas

272 umerous human pathogens, including Anaplasma phagocytophilum, the agent of human granulocytic anaplas

273 Anaplasma phagocytophilum, the causative agent of human granulocyt

274 Anaplasma phagocytophilum, the causative agent of human granulocyt

275 tick colonization by the bacterium Anaplasma phagocytophilum, the causative agent of human granulocyt

276 des ticks, which can also transmit Anaplasma phagocytophilum, the cause of human granulocytic anaplas

277 aris tick, which can also transmit Anaplasma phagocytophilum, the cause of human granulocytic anaplas

278 Anaplasma phagocytophilum, the etiologic agent of human granulocyt

279 Anaplasma phagocytophilum, the etiologic agent of human granulocyt

280 Anaplasma phagocytophilum, the etiologic agent of human granulocyt

281 However, Anaplasma phagocytophilum, the obligatory intracellular bacterium

282 ite-tailed deer may be closely related to A. phagocytophilum, they could be more diverse.

283 athepsin L activity is a strategy used by A. phagocytophilum to alter CDP activity and thereby global

284 Instead, MAb 3E65 inhibited internalized A. phagocytophilum to develop into microcolonies called mor

285 rate that AipA and Asp14 are critical for A. phagocytophilum to productively infect mice, and immuniz

286 ck "antifreeze glycoprotein." This allows A. phagocytophilum to successfully propagate and survive to

287 These ticks successfully transmitted A. phagocytophilum to the murine host.

288 A. phagocytophilum undergoes a biphasic developmental cycle

289 A. phagocytophilum undergoes a biphasic developmental cycle

290 iosis was recently reclassified as Anaplasma phagocytophilum, unifying previously described bacteria

291 Sukumaran et al. recently showed that A. phagocytophilum uses a tick salivary protein, Salp16, to

292 hils and tick cells, thus supporting that A. phagocytophilum uses common mechanisms for infection of

293 These data define a mechanism that A. phagocytophilum uses to selectively alter arthropod gene

294 entially represent a novel means by which A. phagocytophilum usurps host defense mechanisms and shed

295 athogen coevolution by hypothesizing that A. phagocytophilum utilizes common molecular mechanisms for

296 ta suggest similar genetic mechanisms for A. phagocytophilum variation in all hosts but worldwide div

297 donor p44 and the p44 expression locus of A. phagocytophilum was detected in an HL-60 cell culture by

298 The dense-core (DC) form of A. phagocytophilum was isolated from in vitro cultures and

299 , we show that the AnkA protein of Anaplasma phagocytophilum, which is translocated into the host cel

300 cytoplasmic inclusions characteristic of A. phagocytophilum with pleomorphic bacteria in membrane-bo