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1                                              F. tularensis activates complement, and recent data sugg
2                                              F. tularensis also significantly impaired apoptosis trig
3                                              F. tularensis and B. anthracis were grown in liquid brot
4                                              F. tularensis DNA in buffer or CFU of F. tularensis was
5                                              F. tularensis has long been developed as a biological we
6                                              F. tularensis infects leukocytes and exhibits an extrace
7                                              F. tularensis LVS::Deltawzy expressed only 1 repeating u
8                                              F. tularensis represses inflammasome; a cytosolic multi-
9                                              F. tularensis subspecies encode a series of acid phospha
10                                              F. tularensis subspecies holarctica was isolated from th
11                                              F. tularensis Types A and B form poor biofilms, but F. t
12                                              F. tularensis virulence stems from genes encoded on the
13 eriments in F. tularensis identified over 50 F. tularensis DsbA substrates, including outer membrane
14 d protective effects against virulent type A F. tularensis challenge.
15 ainst aerosol challenge with virulent type A F. tularensis in a species other than a rodent since the
16 7 is dispensable for host immunity to type A F. tularensis infection, and that induced and protective
17  during intracellular infections with type A F. tularensis.
18             Infection of mice in vivo with a F. tularensis LVS FTL_0724 mutant resulted in diminished
19 In contrast, infection of macrophages with a F. tularensis LVS rluD pseudouridine synthase (FTL_0699)
20 t against intentional release of aerosolized F. tularensis, the most dangerous type of exposure.
21 cyte-derived DCs (Mo-DCs) in the lungs after F. tularensis LVS pulmonary infection.
22 roader spectrum of growth inhibition against F. tularensis , Bacillus anthracis , and Staphylococcus
23 y potential correlates of protection against F. tularensis and to expand and refine a comprehensive s
24 ific immune responses and protection against F. tularensis challenge.
25 nous interleukin 12 (IL-12) protects against F. tularensis infection; this protection was lost in MII
26 ous vaccine-induced immune responses against F. tularensis.
27                                     Although F. tularensis is a recognized biothreat agent with broad
28 ltiple differences between species and among F. tularensis subspecies and subpopulations.
29 inase activities were observed to vary among F. tularensis and F. novicida strains.
30     Furthermore, sequencing of the amplified F. tularensis targets provides clade confirmation and in
31                                           An F. tularensis subsp. tularensis trpB mutant is also atte
32 ole of OAg size in protection, we created an F. tularensis live vaccine strain (LVS) mutant with a si
33            Consistent with this function, an F. tularensis subsp. novicida trpB mutant is unable to g
34                                     Using an F. tularensis Schu S4 mutant library, we identified stra
35 F. tularensis subsp. tularensis (type A) and F. tularensis subsp. holarctica (type B).
36 hown to modulate both isomerase activity and F. tularensis virulence.
37 holarctica (also referred to as type B), and F. tularensis subsp. mediasiatica, as well as opportunis
38  polar bears to C. burnetii, N. caninum, and F. tularensis.
39 othenate pathway in Francisella novicida and F. tularensis and identified an unknown and previously u
40 s in human virulence between F. novicida and F. tularensis may be due in part to the absence of cdGMP
41 ture supernatant in vitro by F. novicida and F. tularensis subsp. holarctica LVS.
42     Such outbreaks are exceedingly rare, and F. tularensis is seldom recovered from clinical specimen
43 nd to differ between Francisella species and F. tularensis subspecies and subpopulations.
44 tial for misidentification of F. novicida as F. tularensis.
45 en identified 95 lung infectivity-associated F. tularensis genes, including those encoding the Lon an
46 rotective immune response against attenuated F. tularensis versus F. tularensis type A differs.
47 tion of antibodies from patients with type B F. tularensis infections and that these can be used for
48 rensis Types A and B form poor biofilms, but F. tularensis mutants lacking lipopolysaccharide O-antig
49 eration of AA to be converted into PGE(2) by F. tularensis-infected macrophages.
50 ecessary for classical pathway activation by F. tularensis in nonimmune human serum nor the receptors
51 veals novel pathogenic mechanisms adopted by F. tularensis to modulate macrophage innate immune funct
52  tularensis vs Pseudomonas aeruginosa and by F. tularensis live bacteria vs the closely related bacte
53 e previous reports, induction of IFN-beta by F. tularensis was not required for activation of the inf
54 hat metabolic reprogramming of host cells by F. tularensis is a key component of both inhibition of h
55 ector memory (EM) CD4(+) T cells elicited by F. tularensis infection (postimmunization) is increased
56 e FabI enoyl-ACP-reductase enzyme encoded by F. tularensis is essential and not bypassed by exogenous
57  mechanisms of host innate immune evasion by F. tularensis.
58 saccharides may promote biofilm formation by F. tularensis Types A and B.
59 e for this suppression of innate immunity by F. tularensis are not defined.
60 ation of host cell death during infection by F. tularensis and highlight how shifts in the magnitude
61 he establishment of a fulminate infection by F. tularensis.
62 unidentified mechanism for uptake of iron by F. tularensis.
63 the mechanisms of inflammasome repression by F. tularensis.
64 iously demonstrated that PGE(2) synthesis by F. tularensis-infected macrophages requires cytosolic ph
65 White (NZW) rabbits with aerosols containing F. tularensis We evaluated the relative humidity, aeroso
66 infected antigen presenting cells to control F. tularensis LVS intracellular growth.
67 VOCs from their fully virulent counterparts, F. tularensis subspecies tularensis strain SCHU S4 and B
68  (live vaccine strain) or catalase-deficient F. tularensis (DeltakatG) show distinct profiles in thei
69 new cartridge-based assay can rapidly detect F. tularensis in bloodstream infections directly in whol
70     In infected macaques, the assay detected F. tularensis on days 1 to 4 postinfection in 21%, 17%,
71 tection against challenge with two different F. tularensis subsp. holarctica (type B) live vaccine st
72 . coli cells yielded glycOMVs that displayed F. tularensis O-PS.
73 erosolizable nature and low infectious dose, F. tularensis is classified as a category A select agent
74                                       During F. tularensis subspecies novicida infection, AIM2, an in
75 ly with the extent of necrotic damage during F. tularensis infection.
76 eveal a novel intraerythrocytic phase during F. tularensis infection.
77 iagnosis of BALB/c mice infected with either F. tularensis SCHU S4 or Y. pestis CO92.
78 .n., with MAb-iFT immune complexes, enhances F. tularensis-specific immune responses and protection a
79                                 To establish F. tularensis FabI (FtFabI) as a clinically relevant dru
80 y, human neutrophil uptake of GFP-expressing F. tularensis strains live vaccine strain and Schu S4 wa
81 nes, immunotherapeutics, and diagnostics for F. tularensis requires a detailed knowledge of the sacch
82 ted first that C1q and C3 were essential for F. tularensis phagocytosis, whereas C5 was not.
83 nicity island genes tested are essential for F. tularensis Schu S4 virulence and further suggest that
84 igase gene (FTL_0724) as being important for F. tularensis live vaccine strain (LVS) virulence.
85             The assay LOD was 8.5 CFU/ml for F. tularensis, 10 CFU/ml for B. anthracis, and 4.5 CFU/m
86  kinase 3 (JAK3) signaling are necessary for F. tularensis-induced PGE2 production.
87                    The activity observed for F. tularensis strains was predominantly associated with
88     Distinct VOC profiles where observed for F. tularensis when compared with B. anthracis while the
89 ent delay in host cell death is required for F. tularensis to preserve its intracellular replicative
90 aled that lon and clpP are also required for F. tularensis tolerance to stressful conditions.
91 TL_1548 and FTL_1709, which are required for F. tularensis virulence.
92  Moreover, p38 MAPK activity is required for F. tularensis-induced COX-2 protein synthesis, but not f
93  for zoonotic infections, including that for F. tularensis.
94 to inhibit the activity of purified DXR from F. tularensis LVS (IC(50)=230 nM).
95 in inhibits purified MEP synthase (DXR) from F. tularensis LVS.
96 vel bacterial carboxylesterase (FTT258) from F. tularensis, a homologue of human acyl protein thioest
97 signal transducer and model drug by LPS from F. tularensis vs Pseudomonas aeruginosa and by F. tulare
98  and subsp. holarctica (type B) strains from F. tularensis subsp. novicida and other near neighbors,
99                                 Furthermore, F. tularensis LVS delayed pyroptotic cell death of the i
100       Since current methods used to genotype F. tularensis are time-consuming and require extensive l
101  The methods currently available to genotype F. tularensis cannot conclusively identify the associate
102 rately detect and identify the hypervirulent F. tularensis subsp. tularensis subtype A.I, the virulen
103      Several in vivo screens have identified F. tularensis genes necessary for virulence.
104                Our objective was to identify F. tularensis-activated host signaling pathways that reg
105 . tularensis subsp. tularensis subtype A.II, F. tularensis subsp. holarctica (also referred to as typ
106 atty acid biosynthetic components encoded in F. tularensis are transcriptionally active during infect
107 nal role of OxyR has not been established in F. tularensis.
108 tern of endogenous protein-tagging events in F. tularensis that are likely to be a universal feature
109                      Trapping experiments in F. tularensis identified over 50 F. tularensis DsbA subs
110 gh molecular weight (VHMW)] by expressing in F. tularensis a heterologous chain-length regulator gene
111 described as virulence-associated factors in F. tularensis Identification of these Lon substrates has
112  and FTT_0615c, the homologue of FTL_0883 in F. tularensis subsp. tularensis Schu S4 (Schu S4), elici
113                                  However, in F. tularensis-infected macrophages we observed a tempora
114 is also required for lipid A modification in F. tularensis as well as Bordetella bronchiseptica.
115     Analysis of the MglA and SspA mutants in F. tularensis reveals that interaction between PigR and
116          Only the OxyR homolog is present in F. tularensis, while the SoxR homologs are absent.
117 S transporters may play an important role in F. tularensis pathogenesis and serve as good targets for
118 in part to the absence of cdGMP signaling in F. tularensis.
119 amework for understanding the role of T4P in F. tularensis virulence.
120 susceptible than IgA(+/+) mice to intranasal F. tularensis LVS infection, despite developing higher l
121 ase, implicate the enzyme as a potential key F. tularensis effector protein, and may help elucidate a
122 membrane protein 2 localization with labeled F. tularensis in the lungs was greater in wild-type than
123 s involved in bacterial immune evasion, like F. tularensis clpB, can serve as a model for the rationa
124 ion in neutrophils is necessary for limiting F. tularensis colonisation and proliferation.
125  equivalents (GE) per reaction and 10 CFU/ml F. tularensis in both human and macaque blood.
126     Collectively, this study reports a novel F. tularensis factor that is required for innate immune
127 pic differences by evaluating the ability of F. tularensis and F. novicida to degrade chitin analogs
128                               The ability of F. tularensis subsp. novicida to recapitulate the key ph
129 echanism of immune evasion is the ability of F. tularensis to induce the synthesis of the small lipid
130 efense mechanisms, as well as the ability of F. tularensis to prolong neutrophil lifespan.
131                      Based on the ability of F. tularensis to resist high ROS/RNS levels, we have hyp
132         Multiple independent acquisitions of F. tularensis from the environment over a short time per
133 wever, the factors that govern adaptation of F. tularensis to the intrahepatocytic niche have not bee
134 del wherein the immunomodulatory capacity of F. tularensis relies, at least in part, on TolC-secreted
135        F. tularensis DNA in buffer or CFU of F. tularensis was spiked into human or macaque blood.
136 The outbreak was caused by diverse clones of F. tularensis that occurred concomitantly, were widespre
137 ypothesized that the antioxidant defenses of F. tularensis maintain redox homeostasis in infected mac
138  multiplex nested PCR assay for detection of F. tularensis, B. anthracis, and Y. pestis directly from
139 curate identification and differentiation of F. tularensis subpopulations during epidemiological inve
140   We demonstrate that antioxidant enzymes of F. tularensis prevent the activation of redox-sensitive
141                                    Escape of F. tularensis from the phagosome into the cytosol of the
142          One significant virulence factor of F. tularensis is the O-polysaccharide (O-PS) portion of
143 ur results also demonstrate that FTL_0325 of F. tularensis impacts proIL-1beta expression as early as
144 ) form of the enzyme and inhibited growth of F. tularensis SchuS4 at concentrations near that of thei
145                                A hallmark of F. tularensis virulence is its ability to quickly grow t
146 reased cell death with a 2-3 log increase of F. tularensis replication, but could be rescued with rIL
147 uding spermine, regulate the interactions of F. tularensis with host cells.
148 y and was applicable to multiple isolates of F. tularensis Further improvements in the accuracy and p
149  screening a transposon insertion library of F. tularensis LVS in the presence of hydrogen peroxide,
150 re region of the lipopolysaccharide (LPS) of F. tularensis to probe antigenic responses elicited by a
151  profile of the live vaccine strain (LVS) of F. tularensis grown in the FL83B murine hepatocytic cell
152 nfection by the live vaccine strain (LVS) of F. tularensis Resistance is characterized by reduced let
153 f mice with the live vaccine strain (LVS) of F. tularensis, splenic IL-10 levels increased rapidly an
154  cells with the live vaccine strain (LVS) of F. tularensis.
155 oterrorism, but the pathogenic mechanisms of F. tularensis are largely unknown.
156 ovide fundamental insight into mechanisms of F. tularensis phagocytosis and support a model whereby n
157 ty and the antioxidant defence mechanisms of F. tularensis.
158            Through transposon mutagenesis of F. tularensis subsp. holarctica live vaccine strain (LVS
159                        Utilizing a mutant of F. tularensis in FTL_0325 gene, this study investigated
160  Significantly, trans-translation mutants of F. tularensis are impaired in replication within macroph
161  lipopolysaccharide (LPS) O antigen (OAg) of F. tularensis has been considered for use in a glycoconj
162 ignment of the inner core oligosaccharide of F. tularensis .
163 ays an important role in the pathogenesis of F. tularensis and suggest that a focus on the developmen
164             Essential to the pathogenesis of F. tularensis is its ability to escape the destructive p
165                         The pathogenicity of F. tularensis depends on its ability to persist inside h
166 surface capsular and O-Ag polysaccharides of F. tularensis and initiates the classical complement cas
167 y, whole-genome transcriptional profiling of F. tularensis with DNA microarrays from infected tissues
168 ory role in the oxidative stress response of F. tularensis.
169 r studies, using a virulent type A strain of F. tularensis (SchuS4), indicate that IL-17Ralpha(-/-) m
170                  A REP34 knock-out strain of F. tularensis has a reduced ability to both induce encys
171 s study, the highly human virulent strain of F. tularensis SCHU S4 and the live vaccine strain were u
172 lenge with both type A and type B strains of F. tularensis and induced functional immunity through bo
173 s between attenuated and virulent strains of F. tularensis.
174 t respiratory infection by type A strains of F. tularensis.
175 ether biofilm formation enhances survival of F. tularensis in aquatic or other environmental niches h
176 h the intramacrophage growth and survival of F. tularensis.
177 ne hepatocytic cell line compared to that of F. tularensis cultured in broth.
178  the uptake and intracellular trafficking of F. tularensis Live Vaccine Strain (LVS) and LVS with dis
179 elp elucidate a mechanistic understanding of F. tularensis infection of phagocytic cells.
180 asked whether complement-dependent uptake of F. tularensis strain SCHU S4 affects the survival of pri
181 larly that of ferrous iron, for virulence of F. tularensis in the mammalian host.
182         Extreme infectivity and virulence of F. tularensis is due to its ability to evade immune dete
183     We propose that the extreme virulence of F. tularensis is partially due to the bifunctional natur
184 h crucial for normal growth and virulence of F. tularensis.
185 ubsp. mediasiatica, as well as opportunistic F. tularensis subsp. novicida from each other and near n
186 gs indicate that recognition of C3-opsonized F. tularensis, but not extensive cytosolic replication,
187 ted in concert for phagocytosis of opsonized F. tularensis by human neutrophils, whereas CR3 and CR4
188 ly inoculated with F. novicida U112, LVS, or F. tularensis Schu S4.
189 the presence of complement, whereas parental F. tularensis LVS is internalized within spacious pseudo
190        Because of its extreme pathogenicity, F. tularensis is classified as a category A bioweapon by
191  have now evaluated the lethality of primary F. tularensis live vaccine strain (LVS) pulmonary infect
192  CD4(+) T cells to the lungs after pulmonary F. tularensis LVS infection.
193 te processes in the lung following pulmonary F. tularensis infection and provide additional insight i
194                       Importantly, pulmonary F. tularensis LVS infection of MR1-deficient (MR1(-/-))
195 the infected lungs, and control of pulmonary F. tularensis LVS growth.
196     We found that the lethality of pulmonary F. tularensis LVS infection was exacerbated under condit
197               Many of these mutations render F. tularensis defective for intracellular growth.
198 ve a critical protective role in respiratory F. tularensis LVS infection.
199 ld-type mice highly sensitive to respiratory F. tularensis infection, and depletion beginning at 3 da
200 eutrophil niche in CD200R(-/-) mice restores F. tularensis infection to levels seen in wild-type mice
201      Here, we demonstrate a highly sensitive F. tularensis assay that incorporates sample processing
202  Despite the monomorphic nature of sequenced F. tularensis genomes, there is a significant degree of
203              Previously, we identified seven F. tularensis proteins that induce a rapid encystment ph
204 ysis probe, providing sensitive and specific F. tularensis subspecies and subtype identification in a
205 Gr-1(+) CD11b(+) cells in mice that survived F. tularensis infection also suggests a potential role f
206 gs of mice infected with the LVS rather than F. tularensis type A, while IL-23p19 mRNA expression was
207 S represses inflammasome activation and that F. tularensis-encoded FTL_0325 mediates this effect.
208                    Here, we demonstrate that F. tularensis DsbA is a bifunctional protein that oxidiz
209              In summary, we demonstrate that F. tularensis profoundly impairs constitutive neutrophil
210                      We now demonstrate that F. tularensis significantly inhibited neutrophil apoptos
211                       Here we establish that F. tularensis limits Ca(2+) entry in macrophages, thereb
212 ur findings provide compelling evidence that F. tularensis catalase restricts reactive oxygen species
213 lectively, this study provides evidence that F. tularensis LVS represses inflammasome activation and
214       These findings further illustrate that F. tularensis LVS possesses numerous genes that influenc
215                  The data also indicate that F. tularensis pathogenesis is controlled by a highly int
216              We demonstrated previously that F. tularensis inhibits NADPH oxidase assembly and activi
217                          We also report that F. tularensis inhibits ROS-dependent autophagy to promot
218 rly infection has led to the suggestion that F. tularensis evades detection by host innate immune sur
219                                          The F. tularensis genome is predicted to encode 31 major fac
220                                          The F. tularensis subsp. tularensis DeltaFTT0798 and DeltaFT
221               As with phagosomal escape, the F. tularensis Type VI Secretion System (T6SS) was requir
222 nuated Listeria monocytogenes expressing the F. tularensis immunoprotective antigen IglC) as the boos
223 accharide antigen and 31 bacteria/mL for the F. tularensis bacteria were achieved.
224 DE-encoding protein genes are present in the F. tularensis genome.
225       We were particularly interested in the F. tularensis LVS (live vaccine strain) clpB (FTL_0094)
226 ate that AcpA, which contributes most of the F. tularensis acid phosphatase activity, is secreted int
227 and RNA-Seq we identify those regions of the F. tularensis chromosome occupied by PmrA and those gene
228  associates with 252 distinct regions of the F. tularensis chromosome, but exerts regulatory effects
229 erein we report the crystal structure of the F. tularensis FabI enzyme in complex with our most activ
230 identified TolC as a virulence factor of the F. tularensis live vaccine strain (LVS) and demonstrated
231 st by using unmarked deletion mutants of the F. tularensis live vaccine strain (LVS).
232 xperiments identified five substrates of the F. tularensis Lon protease (FTL578, FTL663, FTL1217, FTL
233 ator of the oxidative stress response of the F. tularensis LVS.
234 rtant clues for further understanding of the F. tularensis stress response and pathogenesis.
235  thereby contributing to the survival of the F. tularensis subsp. holarctica live vaccine strain (LVS
236 ogy revealed that the immune response to the F. tularensis mutant strains was significantly different
237             Intradermal inoculation with the F. tularensis live vaccine strain (LVS) results in a rob
238 growth, leading us to hypothesize that these F. tularensis mutants are attenuated because they induce
239 results demonstrate that trpB contributes to F. tularensis virulence by enabling intracellular growth
240 ophages and other cell types are critical to F. tularensis pathogenesis, and impaired intracellular s
241 cinated rabbits were seropositive for IgG to F. tularensis lipopolysaccharide (LPS).
242  critical and novel regulator of immunity to F. tularensis LVS infection, its effects were masked dur
243 g the mechanisms that recruit neutrophils to F. tularensis-infected lungs, opsonization and phagocyto
244            F. novicida is closely related to F. tularensis and exhibits high virulence in mice, but i
245 ch literature exists on the host response to F. tularensis infection, the vast majority of work has b
246 te to macrophage inflammation in response to F. tularensis.
247 del of CR3 and TLR2 signaling in response to F. tularensis.
248 equired for macrophage cytokine responses to F. tularensis.
249 a crucial role in innate immune responses to F. tularensis.
250 ungs of MAb-iFT-immunized mice subsequent to F. tularensis LVS challenge.
251 L-17Ralpha(-/-) mice are more susceptible to F. tularensis LVS infection, our studies, using a virule
252 re by bacterial taxa Francisella tularensis (F. tularensis) subspecies novicida and Bacillus anthraci
253 facultative anaerobe Francisella tularensis: F. tularensis subsp. tularensis (type A) and F. tularens
254 ile the observed profiles of each of the two F. tularensis and B. anthracis strains exhibited some si
255                        Analysis of wild-type F. tularensis isolates by DISA correlated with pulsed-fi
256 age growth that can be restored to wild-type F. tularensis LVS levels by either transcomplementation,
257 tive than the currently available unlicensed F. tularensis live vaccine strain (LVS) is needed to pro
258 es in virulence observed between the various F. tularensis subspecies and subtypes.
259 onse against attenuated F. tularensis versus F. tularensis type A differs.
260 vival during pulmonary infection by virulent F. tularensis.
261 monstrate that lipids enriched from virulent F. tularensis strain SchuS4, but not attenuated live vac
262 role in infection mediated by fully virulent F. tularensis is not known.
263 FtlC and SilC, present in the fully virulent F. tularensis Schu S4 strain for their contributions to
264  doses (LD50) of aerosolized highly virulent F. tularensis Schu S4 had a significantly higher surviva
265 on, both F. novicida and the highly virulent F. tularensis subsp. tularensis Schu S4 strain are able
266 e challenged via aerosol with human-virulent F. tularensis SCHU S4 that had been cultivated in either
267 trophy is also important in a human-virulent F. tularensis subspecies.
268  to detect and distinguish the more virulent F. tularensis subsp. tularensis (subtypes A.I and A.II)
269 were infected with the prototypical virulent F. tularensis strain, Schu S4.
270  In this study, we demonstrate that virulent F. tularensis impairs production of inflammatory cytokin
271 In this study, we demonstrated that virulent F. tularensis strain SchuS4 selectively inhibits product
272 25 and its ortholog FTT0831c in the virulent F. tularensis SchuS4 strain in intramacrophage survival
273 of B1a cells in defense against the virulent F. tularensis ssp. tularensis strain SchuS4.
274  subsp. tularensis subtype A.I, the virulent F. tularensis subsp. tularensis subtype A.II, F. tularen
275 trolling survival of infection with virulent F. tularensis.
276                                    In vitro, F. tularensis invaded human erythrocytes, as shown in th
277                                         When F. tularensis OAg was purified under standard conditions
278 s of intraocular inflammation in areas where F. tularensis is endemic.
279              It is unknown, however, whether F. tularensis can infect erythrocytes; thus, we examined
280 fsl operon are the only major means by which F. tularensis acquires iron.
281   However, the molecular mechanisms by which F. tularensis DsbA contributes to virulence are unknown.
282 ore, we sought an alternative means by which F. tularensis might obtain iron.
283                           The means by which F. tularensis modulates macrophage activation are not fu
284 Our understanding of the mechanisms by which F. tularensis senses and adapts to host environments is
285 lla factors and the mechanisms through which F. tularensis mediates these suppressive effects remain
286 unosensor formats for the detection of whole F. tularensis bacteria were developed and their performa
287         The severe morbidity associated with F. tularensis infections is attributed to its ability to
288 nged survival upon subsequent challenge with F. tularensis Schu S4 and provided complete protection a
289 onses generated in macrophages infected with F. tularensis live vaccine strain (LVS) or the virulent
290 ved monocytes and neutrophils, infected with F. tularensis LVS ex vivo, display enhanced restriction
291 d on blood drawn from macaques infected with F. tularensis Schu S4 at daily intervals.
292 ified from the spleens of mice infected with F. tularensis suppressed polyclonal T-cell proliferation
293 nthetic pathway in macrophages infected with F. tularensis.
294 ulation in the spleens of mice infected with F. tularensis.
295 ve immunity against pulmonary infection with F. tularensis live vaccine strain, its production is tig
296 sed mortality after pulmonary infection with F. tularensis live vaccine strain.
297 nd pathology during pulmonary infection with F. tularensis live vaccine strain.
298 eased resistance to pulmonary infection with F. tularensis.
299         Using PBLs from mice vaccinated with F. tularensis Live Vaccine Strain (LVS) and related atte
300  mutant strains compared with wild-type (WT) F. tularensis LVS.

 
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