ライフサイエンスコーパス: burnetii

1 r is a worldwide zoonosis caused by Coxiella burnetii.

2 rict the intracellular replication of the C. burnetii.

3 dying the human innate immune response to C. burnetii.

4 protective and effective vaccines against C. burnetii.

5 lar risk-factors and previous exposure to C. burnetii.

6 Q fever is an infection caused by Coxiella burnetii.

7 in mice before intranasal infection with C. burnetii.

8 restrict the intracellular replication of C. burnetii.

9 ophila, Legionella longbeachae, and Coxiella burnetii.

10 on, SCID mice were exposed to aerosolized C. burnetii.

11 early immune response against aerosolized C. burnetii.

12 old contacts were traced and screened for C. burnetii.

13 se caused by the bacterial pathogen Coxiella burnetii.

14 ed to decreased cytokine production after C. burnetii 3262 stimulation but not after C. burnetii Nine

15 Nine Mile and the Dutch outbreak isolate C. burnetii 3262.

16 recognition of C. burnetii Nine Mile and C. burnetii 3262.

17 Q fever is caused by Coxiella burnetii, a bacterium that persists in M2-polarized macr

18 Q fever is a zoonosis caused by Coxiella burnetii, a unique bacterium that is widespread but infr

19 Together, these results demonstrate that C. burnetii actively directs PV-autophagosome interactions

20 tion increased during infection; however, C. burnetii actively prevented CHOP nuclear translocation a

21 Recent reports suggest that C. burnetii actively recruits autophagosomes to the PV to d

22 nting progesterone-mediated inhibition of C. burnetii activity.

23 We have developed a safe and reproducible C. burnetii aerosol challenge in three different animal mod

24 We evaluated our top candidates in a live C. burnetii aerosol challenge model in C56BL/6 mice and fou

25 er of 1E4 would protect SCID mice against C. burnetii aerosol infection.

26 l as designing vaccine countermeasures to C. burnetii aerosol transmission.

27 al Gram-negative species, including Coxiella burnetii, Agrobacterium tumefaciens and Legionella pneum

28 urnetii To accomplish this, we formulated C. burnetii Ags with a novel TLR triagonist adjuvant platfo

29 cs the intracellular replicative niche of C. burnetii and allows axenic growth of the bacteria.

30 , suggesting that neutrophils cannot kill C. burnetii and C. burnetii may be using infection of neutr

31 role in early vaccine protection against C. burnetii and contribute to antibody isotype switching.

32 stance, mammalian pathogens such as Coxiella burnetii and Francisella tularensis, as well as Coxiella

33 nses by direct ELISpot to both whole-cell C. burnetii and individual peptides in chronic patients tha

34 on understanding the interaction between C. burnetii and innate immune cells in vitro and in vivo.

35 , we investigated the interaction between C. burnetii and other pulmonary cell types apart from the l

36 ollectively demonstrate interplay between C. burnetii and specific components of the eIF2alpha signal

37 erial cell mass spectrometry of wild-type C. burnetii and the DeltapmrA mutant uncovered new componen

38 Studying the interaction between C. burnetii and the innate immune system can provide a mode

39 (IL-8), neutrophil-attracting response to C. burnetii and ultimately shifted to an M2-polarized pheno

40 pothesize that inefficient recognition of C. burnetii and/or activation of host-defense in individual

41 eria such as Enterococcus faecalis, Coxiella burnetii, and Clostridium difficile.

42 anthracis; Francisella tularensis; Coxiella burnetii; and Ebola, Marburg, and Lassa fever viruses us

43 Various formats using different C. burnetii antigens were tested.

44 in vitro stimulation of whole blood with C. burnetii antigens.

45 The effector proteins delivered by C. burnetii are predicted to have important functions durin

46 d significant protection against virulent C. burnetii as early as 7 days postvaccination, which sugge

47 ne Mile phase II (NMII) clone 4 strain of C. burnetii, as a model to investigate host and bacterial c

48 the obligate intracellular pathogen Coxiella burnetii, as it allows the completion of the lengthy bac

49 B cells were able to phagocytose virulent C. burnetii bacteria and form Coxiella-containing vacuoles

50 Despite Coxiella burnetii being an obligate intracellular bacterial patho

51 During infection with C. burnetii, both TFEB and TFE3 were activated, as demonstr

52 r kinase), a protein kinase identified in C. burnetii by in silico analysis.

53 ith cardiac valve disease, infection with C. burnetii can cause a life-threatening infective endocard

54 iella-containing vacuoles (CCVs) and that C. burnetii can infect and replicate in peritoneal B1a subs

55 ates were lower than 29%, suggesting that C. burnetii can infect neutrophils, but infection is limite

56 Infection with Coxiella burnetii can lead to acute and chronic Q fever.

57 Coxiella burnetii causes human Q fever, a zoonotic disease that p

58 ver is a flu-like illness caused by Coxiella burnetii (Cb), a highly infectious intracellular bacteri

59 severity of disease following intranasal C. burnetii challenge, suggesting that keratinocyte-derived

60 volved in protecting vaccinated mice from C. burnetii challenge-induced disease.

61 to confer significant protection against C. burnetii challenge.

62 Monocytes migrated toward C. burnetii-coated beads independently of the presence of T

63 required for endocytic trafficking of the C. burnetii-containing vacuole to the lysosome.

64 ing genes were recently discovered on the C. burnetii cryptic QpH1 plasmid, three of which are conser

65 To determine if C. burnetii cultured in ACCM-2 retains immunogenicity, we c

66 During intracellular growth, C. burnetii delivers bacterial proteins directly into the h

67 A C. burnetii DeltacvpA mutant exhibited significant defects

68 and PV generation, whereas the growth of C. burnetii DeltacvpB and DeltacvpC was rescued upon cohabi

69 C. burnetii DeltacvpB, DeltacvpC, DeltacvpD, and DeltacvpE

70 Compared to wild-type bacteria, C. burnetii DeltapmrA exhibited severe intracellular growth

71 drates, and proteins; thus, it is assumed C. burnetii derives nutrients for growth from these degrada

72 he intracellular bacterial pathogen Coxiella burnetii directs biogenesis of a parasitophorous vacuole

73 The obligate intracellular pathogen Coxiella burnetii displays antiapoptotic activity which depends o

74 The data show that C. burnetii does not grow in axenic media at pH 6.0 or high

75 nd viability are not impaired, indicating C. burnetii does not require by-products of hydrolase degra

76 critical virulence factor that regulates C. burnetii Dot/Icm secretion.

77 Over 100 C. burnetii Dot/Icm substrates have been identified, but th

78 translocation of effector proteins by the C. burnetii Dot/Icm system occurs after acidification of th

79 ecreted in a Dot/Icm-dependent fashion by C. burnetii during infection of human THP-1 macrophages.

80 Our data reveal IcaA as a novel C. burnetii effector protein that is secreted by the Dot/Ic

81 By investigating C. burnetii effector proteins containing eukaryotic-like do

82 e a beta-lactamase enzyme (BlaM) fused to C. burnetii effector proteins to study protein translocatio

83 We predict additional C. burnetii effectors localize to the PV membrane and regul

84 ed a machine-learning approach to predict C. burnetii effectors, and examination of 20 such proteins

85 To identify novel C. burnetii effectors, we applied a machine-learning approa

86 Collectively, these results indicate that C. burnetii encodes a large repertoire of T4SS substrates t

87 The human pathogen Coxiella burnetii encodes a type IV secretion system called Dot/I

88 Collectively, these data indicate C. burnetii encodes multiple effector proteins that target

89 Coxiella burnetii endocarditis is considered to be a late complic

90 edictors of progression toward persistent C. burnetii endocarditis.

91 onvalescents) to promiscuous HLA class II C. burnetii epitopes, providing the basis for a novel T-cel

92 However, we do not understand how C. burnetii evades the intracellular immune surveillance th

93 increased interleukin 10 production with C. burnetii exposure.

94 ized MAb as emergency prophylaxis against C. burnetii exposure.

95 vely accumulated around beads coated with C. burnetii extracts, and complete granulomas were generate

96 Moreover, icaA(-) mutants of C. burnetii failed to suppress the caspase-11-mediated infl

97 esicular trafficking pathways co-opted by C. burnetii for PV development are poorly defined; however,

98 C. burnetii formed a prototypical PV and replicated efficie

99 s Brucella spp., Toxoplasma gondii, Coxiella burnetii, Francisella tularensis, and Neospora caninum,

100 L-1 may be important for the clearance of C. burnetii from the lungs following intranasal infection.

101 hila as a surrogate host, reveals a novel C. burnetii gene (IcaA) involved in the inhibition of caspa

102 In human cells, C. burnetii generates a replication niche termed the parasi

103 However, significantly higher C. burnetii genome copy numbers were detected in the lungs

104 as set up to evaluate the impact of pH on C. burnetii growth and survival in the presence and absence

105 Unexpectedly, examination of C. burnetii growth in GNPTAB(-/-) HeLa cells revealed repli

106 vity, no p62 turnover was observed during C. burnetii growth in macrophages, suggesting that the path

107 The low rate of phase I and II Nine Mile C. burnetii growth in murine lungs may be a direct result o

108 Further assessment of the C. burnetii growth niche showed that macrophages mounted a

109 tion factor alpha, which was required for C. burnetii growth.

110 nase pathways are most likely targeted by C. burnetii Icm/Dot effectors.

111 his study, we have expanded the subset of C. burnetii immunoreactive proteins validated by enzyme-lin

112 We report on evidence of infection with C. burnetii in a small group of regular consumers of raw (u

113 t the value of systematically testing for C. burnetii in antiphospholipid-associated cardiac valve di

114 for testing antibiotic susceptibility of C. burnetii in axenic media was set up to evaluate the impa

115 actericidal or bacteriostatic activity on C. burnetii in axenic media, suggesting that raising pH of

116 pin are effective at preventing growth of C. burnetii in axenic media, with moxifloxacin and doxycycl

117 re the aeration process, the transport of C. burnetii in bioaerosols via the air, the aerosolization

118 4SS are implicated in the pathogenesis of C. burnetii in flies.

119 wn about their role in the recognition of C. burnetii in humans.

120 e induction of cytokine responses against C. burnetii in humans.

121 R1, increased interleukin 10 responses to C. burnetii in individuals carrying the risk allele may con

122 PI-WVC stimulates protective immunity to C. burnetii in mice through stimulation of migratory behavi

123 rosols via the air, the aerosolization of C. burnetii in the shower, and the air filtration efficienc

124 loroquine is thought to inhibit growth of C. burnetii in vivo by raising the pH of typically acidic i

125 in TLRs and Nod-like receptors (NLRs) on C. burnetii-induced cytokine production was assessed.

126 nts of an LPS-specific MAb can neutralize C. burnetii infection and appears to be a promising step to

127 of clathrin-coated vesicle trafficking in C. burnetii infection and define a role for CvpA in subvert

128 sults suggest a versatile role for PKA in C. burnetii infection and indicate virulent organisms usurp

129 is a novel diagnostic assay for previous C. burnetii infection and shows similar performance and pra

130 st Rho GTPases for establishment of Coxiella burnetii infection and virulence in mammalian cell cultu

131 tical role in vaccine-induced immunity to C. burnetii infection by producing protective antibodies.

132 Fv1E4, and huscFv1E4 were able to inhibit C. burnetii infection in mice but that their ability to inh

133 ntibody (MAb) 1E4 significantly inhibited C. burnetii infection in mice, suggesting that 1E4 is a pro

134 an important role in host defense against C. burnetii infection in mice.

135 of interleukin-10 (IL-10) in response to C. burnetii infection in vitro suggest that B1a cells may p

136 inated WT mouse sera were able to inhibit C. burnetii infection in vivo, but only IgM from PIV-vaccin

137 lts indicate that 1E4 was able to inhibit C. burnetii infection in vivo, suggesting that 1E4 is a pro

138 20-KLH-immunized mice was able to inhibit C. burnetii infection in vivo, suggesting that m1E41920 may

139 eritoneal B cells in host defense against C. burnetii infection in vivo.

140 In contrast, our finding that C. burnetii infection induced more-severe splenomegaly and

141 Protective immunity against Coxiella burnetii infection is conferred by vaccination with viru

142 responses in the lung following pulmonary C. burnetii infection is lacking.

143 Fab1E4, muscFv1E4, or huscFv1E4 can block C. burnetii infection of macrophages.

144 d probed the role of PKA signaling during C. burnetii infection of macrophages.

145 this study, we investigated the impact of C. burnetii infection on activation of the three arms of th

146 f neutrophils in the host defense against C. burnetii infection remains unclear.

147 f B cells in host defense against primary C. burnetii infection remains unclear.

148 in mice but that their ability to inhibit C. burnetii infection was lower than that of 1E4.

149 t-pathogen interactions that occur during C. burnetii infection, stable-isotope labeling by amino aci

150 were differentially phosphorylated during C. burnetii infection, suggesting the pathogen uses PKA sig

151 eutrophils in protective immunity against C. burnetii infection, the RB6-8C5 antibody was used to dep

152 ibility of using humanized 1E4 to prevent C. burnetii infection, we examined whether the Fab fragment

153 not significantly affect the severity of C. burnetii infection-induced diseases in both severe combi

154 play an important role in inhibiting the C. burnetii infection-induced inflammatory response.

155 uired for PIV-mediated protection against C. burnetii infection.

156 ogenesis, were examined in the context of C. burnetii infection.

157 t play essential roles in the response to C. burnetii infection.

158 tant role in host defense against primary C. burnetii infection.

159 fector that influences ER function during C. burnetii infection.

160 B cells alone may not be able to control C. burnetii infection.

161 tant role in host defense against primary C. burnetii infection.

162 eutrophils in protective immunity against C. burnetii infection.

163 4) retained the ability of 1E4 to inhibit C. burnetii infection.

164 mechanisms of pulmonary immunity against C. burnetii infection.

165 (+) T cell-deficient mouse sera inhibited C. burnetii infection.

166 ity of PIV to confer protection against a C. burnetii infection.

167 al role in PIV-induced protection against C. burnetii infection.

168 lactic measure that is protective against C. burnetii infections but is not U.S.

169 lactic measure that is protective against C. burnetii infections but is not U.S. Food and Drug Admini

170 i with huscFv1E4 can significantly reduce C. burnetii infectivity in human macrophages.

171 In humans, C. burnetii infects alveolar macrophages and promotes phago

172 Here, we show that C. burnetii inhibits caspase-1 activation in primary mouse

173 ne that the infection of macrophages with C. burnetii inhibits the caspase-11-mediated non-canonical

174 Interestingly, C. burnetii inside neutrophils can infect and replicate wit

175 ng a valuable approach for characterizing C. burnetii interactions with a human host.

176 ffector protein CvpA was found to promote C. burnetii intracellular growth and PV expansion.

177 Several effectors crucial for C. burnetii intracellular replication have been identified,

178 aintenance of the organelle that supports C. burnetii intracellular replication.

179 Coxiella burnetii is a Gram-negative bacterium that causes acute

180 C. burnetii is a Gram-negative intracellular bacterium that

181 Coxiella burnetii is a highly infectious bacterium that promotes

182 Coxiella burnetii is a zoonotic bacterial obligate intracellular

183 Coxiella burnetii is an intracellular bacterial pathogen that cau

184 Coxiella burnetii is an intracellular bacterium that causes query

185 Coxiella burnetii is an intracellular Gram-negative bacterium tha

186 Coxiella burnetii is an intracellular pathogen that replicates in

187 Coxiella burnetii is an obligate intracellular bacterial pathogen

188 Coxiella burnetii is an obligate intracellular bacterium and the

189 Coxiella burnetii is an obligate intracellular bacterium that cau

190 Coxiella burnetii is an obligate intracellular Gram-negative bact

191 Coxiella burnetii is an obligate intracellular Gram-negative bact

192 C. burnetii is considered a potential bioterrorism agent be

193 After human inhalation, C. burnetii is engulfed by alveolar macrophages and transit

194 The initial target of C. burnetii is the alveolar macrophage.

195 Coxiella burnetii is the causative agent of human Q fever, elicit

196 Coxiella burnetii is the causative agent of Q fever, a zoonotic d

197 he intracellular bacterial pathogen Coxiella burnetii is the etiological agent of the emerging zoonos

198 difference between virulent and avirulent C. burnetii is they have smooth and rough lipopolysaccharid

199 As Q fever, caused by Coxiella burnetii, is a major health challenge due to its cardiov

200 er, an infectious disease caused by Coxiella burnetii, is associated with granuloma formation.

201 we compared the sequences of ankG from 37 C. burnetii isolates and classified them in three groups ba

202 lso required for PV formation by virulent C. burnetii isolates during infection of primary human alve

203 n reading frame (CbuD1884) present in all C. burnetii isolates except the Nine Mile reference isolate

204 d, three of which are conserved among all C. burnetii isolates, suggesting that they are critical for

205 ia (Bartonella spp., Brucella spp., Coxiella burnetii, Leptospira spp., Rickettsia spp., Salmonella e

206 Recent studies have indicated that C. burnetii likely originated from a tick-associated ancest

207 hogens like Legionella pneumophila, Coxiella burnetii, Listeria monocytogenes, and Chlamydia trachoma

208 Coxiella burnetii load was high on-farm (2009), and lower off-far

209 dy provides further clarity on the unique C. burnetii-lung dynamic during early stages of human acute

210 t neutrophils cannot kill C. burnetii and C. burnetii may be using infection of neutrophils as an eva

211 es of both phase I and phase II Nine Mile C. burnetii multiply and are less readily cleared from the

212 st evidence of exposure of polar bears to C. burnetii, N. caninum, and F. tularensis.

213 chanisms of the innate immune response to C. burnetii natural infection, SCID mice were exposed to ae

214 dies (Abs) can provide protection against C. burnetii natural infection, we examined if passive trans

215 ing that 1E4 may be useful for preventing C. burnetii natural infection.

216 finding was the divergent recognition of C. burnetii Nine Mile and C. burnetii 3262.

217 uclear cells (PBMCs) were stimulated with C. burnetii Nine Mile and the Dutch outbreak isolate C. bur

218 Both virulent C. burnetii Nine Mile phase I (NMI) and avirulent Nine Mile

219 a pigs were infected intratracheally with C. burnetii Nine Mile phase I (NMI) and demonstrated suscep

220 nt study demonstrated that virulent Coxiella burnetii Nine Mile phase I (NMI) is capable of infecting

221 ective efficacies of formalin-inactivated C. burnetii Nine Mile phase I (PIV) and phase II (PIIV) vac

222 ective efficacy of a formalin-inactivated C. burnetii Nine Mile phase I vaccine (PIV) in beta(2)-micr

223 Whole blood incubated for 24 hours with C. burnetii Nine Mile showed optimal performance.

224 . burnetii 3262 stimulation but not after C. burnetii Nine Mile stimulation.

225 for TNF produced upon immune detection of C. burnetii NMII by TLRs, rather than cytosolic PRRs, in en

226 adult Drosophila flies are susceptible to C. burnetii NMII infection and that this bacterial strain,

227 The C. burnetii NMII T4SS translocates bacterial products into

228 factor (TNF) produced upon TLR sensing of C. burnetii NMII was required to control bacterial replicat

229 cytokines shows that cells exposed to the C. burnetii nopA::Tn or a Dot/Icm-defective dotA::Tn mutant

230 ile raising the important question of how C. burnetii obtains essential nutrients from its host.

231 as opposed to cells exposed to wild-type C. burnetii or the corresponding nopA complemented strain.

232 has further enhanced our understanding of C. burnetii pathogenesis, the host-pathogen interactions th

233 cal role for extrachromosomal elements in C. burnetii pathogenesis.

234 mechanisms of formalin-inactivated Coxiella burnetii phase I (PI) vaccine (PIV)-induced protection,

235 Here, we constructed a C. burnetii pmrA deletion mutant to directly probe PmrA-med

236 Indeed, the C. burnetii PmrA/B regulon, responsible for transcriptional

237 that particular amino acids activate the C. burnetii PmrA/B two-component system.

238 Within whole lung tissue, C. burnetii preferentially replicated in hAMs.

239 present the first published case of Coxiella burnetii prosthetic joint infection.

240 ociated with the production of additional C. burnetii proteins involved in host cell parasitism.

241 Thirty-three C. burnetii proteins, previously identified as immunoreacti

242 an important role in host defense against C. burnetii pulmonary infection.

243 he intracellular bacterial pathogen Coxiella burnetii Q fever presents with acute flu-like and pulmon

244 e T4SS effector repertoire encoded by the C. burnetii QpH1, QpRS, and QpDG plasmids that were origina

245 aused by the intracellular pathogen Coxiella burnetii, relies mainly on serology and, in prevaccinati

246 Designing new vaccines against C. burnetii remains a challenge and requires the use of cli

247 Previous studies showed that C. burnetii replicates efficiently in primary human alveola

248 Although C. burnetii replicates in most cell types in vitro, the pat

249 The Q fever bacterium Coxiella burnetii replicates inside host cells within a large Cox

250 ation of the specialized vacuole in which C. burnetii replicates represents a two-stage process media

251 Coxiella burnetii replicates within permissive host cells by empl

252 Formation of a PV that supports C. burnetii replication requires a Dot/Icm type 4B secretio

253 ned to have a direct inhibitory effect on C. burnetii replication.

254 n of HeLa cells, which are permissive for C. burnetii replication.

255 y siRNA treatment significantly inhibited C. burnetii replication.

256 To establish this unique niche, C. burnetii requires the Dot/Icm type IV secretion system (

257 C. burnetii requires this lysosomal environment for replica

258 lonization by the Q fever pathogen, Coxiella burnetii, requires translocation of effector proteins in

259 Here we show that the C. burnetii secreted effector Coxiella vacuolar protein B (

260 These results suggest that C burnetii should be added to the list of bacteria that pr

261 nfection of placenta-derived JEG-3 cells, C. burnetii showed sensitivity to progesterone but not the

262 ring natural infection of female animals, C. burnetii shows tropism for the placenta and is associate

263 In all assay formats, C. burnetii-specific IFN-gamma production was higher (P < .

264 In this study, C. burnetii-specific interferon gamma (IFN-gamma) productio

265 RK led to decreased cytokine responses in C. burnetii-stimulated human PBMCs.

266 Moreover, a CstK-overexpressing C. burnetii strain displayed a severe CCV development pheno

267 ignificant protection against aerosolized C. burnetii, suggesting that 1E4 may be useful for preventi

268 lysosomal hydrolases are not required for C. burnetii survival and growth but are needed for normal C

269 imilar role for PmrA in regulation of the C. burnetii T4BSS has been proposed.

270 ar effector proteins, a list of predicted C. burnetii T4BSS substrates was compiled using bioinformat

271 Infection with Coxiella burnetii, the causative agent of Q fever, can result in

272 Coxiella burnetii, the causative agent of Q fever, establishes a

273 Coxiella burnetii, the causative agent of Q fever, is a human int

274 Coxiella burnetii, the causative agent of Q fever, is a zoonotic

275 ccessful macrophage colonization by Coxiella burnetii, the cause of human Q fever, requires pathogen-

276 Coxiella burnetii, the etiologic agent of Q fever, replicates in

277 Coxiella burnetii, the etiological agent of acute and chronic Q f

278 Coxiella burnetii, the etiological agent of Q fever in humans, is

279 Coxiella burnetii, the etiological agent of Q fever, is a Gram-ne

280 (pppy), hence the risk of transmission of C. burnetii through inhalation of drinking water aerosols i

281 ombinant protein subunit vaccines against C. burnetii To accomplish this, we formulated C. burnetii A

282 The sensitivity of C. burnetii to progesterone, but not structurally related m

283 ellular bacterial agent of Q fever, Coxiella burnetii, translocates effector proteins into its host c

284 lytic cell death did not occur following C. burnetii-triggered inflammasome activation, indicating a

285 fection in vitro and found that avirulent C. burnetii triggers sustained interleukin-1beta (IL-1beta)

286 and the engagement of this pathway by the C. burnetii type 4B secretion system substrate Coxiella vac

287 oteins injected into the host cell by the C. burnetii type IVB secretion system (T4BSS) are required

288 The Q fever agent Coxiella burnetii uses a defect in organelle trafficking/intracel

289 In human alveolar macrophages, C. burnetii uses a Dot/Icm type IV secretion system (T4SS)

290 as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, ruptu

291 , such as M6PR and LRP1, are critical for C. burnetii virulence.

292 C burnetii was detected in CD68(+) macrophages within both

293 Serodiagnosis for Coxiella burnetii was performed for all patients.

294 The presence of Coxiella burnetii was tested using immunofluorescence and fluores

295 vaccine-mediated protection against Coxiella burnetii, we evaluated the protective efficacy of a form

296 In C. burnetii, we found that four different types of covalent

297 th a known role in initial recognition of C. burnetii were included.

298 In addition, treatment of C. burnetii with Fab1E4, muscFv1E4, or huscFv1E4 can block

299 Interestingly, treatment of C. burnetii with huscFv1E4 can significantly reduce C. burn

300 tudy demonstrated that treatment of Coxiella burnetii with the phase I lipopolysaccharide (PI-LPS)-ta