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 ulation with the rickettsial agent Anaplasma phagocytophilum.

8 l role in the early eradication of Anaplasma phagocytophilum.

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

10 rtially protects mice from infection with A. phagocytophilum.

11 rane proteins and neutralizing targets of A. phagocytophilum.

12 es in both Anaplasma marginale and Anaplasma phagocytophilum.

13 e obligate intracellular bacterium Anaplasma phagocytophilum.

14 ssue of C3H mice previously infected with A. phagocytophilum.

15 ion, we developed a novel method to clone A. phagocytophilum.

16 gene expression following infection with A. phagocytophilum.

17 mits the 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 A. phagocytophilum adhesion to and infection of neutrophils

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

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

33 Our Affymetrix data revealed that A. phagocytophilum altered the expression of transcription

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

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

36 Anaplasma phagocytophilum, an obligatory intracellular bacterium t

37 Anaplasma phagocytophilum, an unusual obligate intracellular patho

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 ese results suggest that coinfection with A. phagocytophilum and B. burgdorferi modulates pathogen bu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 Anaplasma phagocytophilum (Ap) is an obligate intracellular bacter

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

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

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

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

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

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

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

67 The addition of A. phagocytophilum, as well as Escherichia coli and serum-o

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

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

70 e suspected of being infected with Anaplasma phagocytophilum because of the finding of morulae in per

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

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

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

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

75 The A. phagocytophilum burden increases in salivary glands and

76 Antibody response to A. phagocytophilum, but not B. burgdorferi, was decreased i

77 Heat-killed A. phagocytophilum caused some similar initial alterations

78 A. phagocytophilum causes macrophage activation and hemopha

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

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

81 A. phagocytophilum combats neutrophil oxidative killing by

82 ect was initially mediated by exposure to A. phagocytophilum components in heat-killed bacteria.

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

84 vation of the p38 MAPK pathway leading to A. phagocytophilum-delayed neutrophil apoptosis is bypassed

85 1387 is not detectable on the surfaces of A. phagocytophilum dense core organisms bound at the HL-60

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

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

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

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

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

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

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

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

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

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

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

97 A. phagocytophilum evades neutrophil oxidative killing by p

98 Importantly, ingestion of A. phagocytophilum failed to trigger the neutrophil apoptos

99 promote bacterial survival: 1) uptake of A. phagocytophilum fails to trigger the apoptosis different

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

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

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

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

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

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

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

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

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

109 The promoters in both A. marginale and A. phagocytophilum have similar structure and activity, sup

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

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

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

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

114 A. phagocytophilum in blood and serologic response to both

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

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

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

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

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

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

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

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

123 A. phagocytophilum-induced actin phosphorylation resulted i

124 A. phagocytophilum-induced actin phosphorylation was depend

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

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

127 A. phagocytophilum induces ticks to express Ixodes scapular

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

129 60 cells cultured at 37 degrees C than in A. phagocytophilum-infected HL-60 cells cultured at 28 degr

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

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

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

133 tion of procaspase-3 processing occurs in A. phagocytophilum-infected human neutrophils.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 A. phagocytophilum infection also altered the apoptotic pro

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

150 tered, suggesting a possible link between A. phagocytophilum infection and iron metabolism.

151 2-deficient mice were more susceptible to A. phagocytophilum infection and showed splenomegaly, throm

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

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

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

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

156 We assessed the impact of A. phagocytophilum infection in NB4 promyelocytic leukemic

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

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

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

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

161 A. phagocytophilum infection induced a significant elevatio

162 Anaplasma phagocytophilum infection induces functional neutrophil

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

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

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

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

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

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

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

170 5-205) bind to, and competitively inhibit A. phagocytophilum infection of, host cells.

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

172 A. phagocytophilum infection resulted in elevated cathepsin

173 A. phagocytophilum infection resulted in the up- and down-r

174 in western Washington State suggests that A. phagocytophilum infection should be considered in differ

175 A. phagocytophilum infection significantly decreased phagoc

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

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

178 totic interleukin 8 (IL-8) expressed with A. phagocytophilum infection was excluded by the use of IL-

179 A. phagocytophilum infection was not detected in the sample

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

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

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

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

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

185 velopment of histopathologic lesions with A. phagocytophilum infection.

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

187 iptional response of human neutrophils to 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 ression site is present in all strains of A. phagocytophilum investigated.

194 Anaplasma phagocytophilum is a bacterium that is transmitted by Ix

195 Anaplasma phagocytophilum is a gram-negative obligate intracellula

196 Anaplasma phagocytophilum is a tick-borne rickettsial pathogen tha

197 Anaplasma phagocytophilum is an intragranulocytic bacterium that u

198 Anaplasma phagocytophilum is an obligate intracellular bacterium t

199 Anaplasma phagocytophilum is an obligate intracellular bacterium t

200 Anaplasma phagocytophilum is an obligate intracellular pathogen th

201 Anaplasma phagocytophilum is an obligate intracellular tick-transm

202 Anaplasma phagocytophilum is an obligate vacuolar bacterium that i

203 Anaplasma phagocytophilum is an obligatory intracellular bacterium

204 Anaplasma phagocytophilum is an obligatory intracellular bacterium

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

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

207 Anaplasma phagocytophilum is the agent of human anaplasmosis, the

208 Anaplasma phagocytophilum is the etiologic agent of human granuloc

209 Anaplasma phagocytophilum is the etiologic agent of human granuloc

210 Anaplasma phagocytophilum is the tick-transmitted obligate intrace

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

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

213 A. phagocytophilum lacking lpda1 revealed enlargement of th

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

215 , Italy, and Switzerland and 4 samples of A. phagocytophilum-like organisms obtained from white-taile

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

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

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

219 These data suggest that A. phagocytophilum may alter selected host pathways in orde

220 A. phagocytophilum migrated normally from A. phagocytophilu

221 Thus, A. phagocytophilum mitigates mast cell activation.

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

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

224 uence analysis of the recently discovered A. phagocytophilum msp2 gene corroborated these results.

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 ormation but did differentiate strains of A. phagocytophilum obtained from ruminants from those obtai

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

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

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

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

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

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

250 The zoonotic importance of A. phagocytophilum should support an increase in surveillan

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

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

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

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

264 To investigate the molecular basis of A. phagocytophilum survival within neutrophils, we used Aff

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 ri, the agent of Lyme disease, and Anaplasma phagocytophilum, the agent of human anaplasmosis, are bo

268 Anaplasma phagocytophilum, the agent of human anaplasmosis, persis

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

270 Anaplasma phagocytophilum, the agent of human granulocytic anaplas

271 Anaplasma phagocytophilum, the agent of human granulocytic anaplas

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

273 Anaplasma phagocytophilum, the causative agent of human granulocyt

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

275 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 garding the strategies employed by Anaplasma phagocytophilum to evade or subvert neutrophil killing m

286 This may be explained by the ability of A. phagocytophilum to functionally impair neutrophils, impo

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

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 Notably, A. phagocytophilum uptake induced fewer perturbations in ho

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

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 major membrane proteins, P44s, of Anaplasma phagocytophilum were hypothesized to be garnered by reco

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