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1 ificantly elevated upon removal of bioR from B. melitensis.
2 y of novel vaccines and therapeutics against B. melitensis.
3 against inhalational infection with virulent B. melitensis.
4 ting against intracellular organisms such as B. melitensis.
5 e against intranasal challenge with virulent B. melitensis.
6                                    Using the B. melitensis 16 M genome sequence, primers were designe
7 d in identifying genomic differences between B. melitensis 16M and Brucella abortus 2308.
8 re were both pro- and antiapoptosis effects, B. melitensis 16M appears to inhibit apoptosis of macrop
9  that (i) OPS-deficient strains derived from B. melitensis 16M are more resistant to the bactericidal
10 otect mice against intranasal challenge with B. melitensis 16M bacteria.
11 y this, deletion mutants were constructed in B. melitensis 16M by removing genes encoding phosphomann
12 mutant improved protection against wild-type B. melitensis 16M challenge compared to the nonencapsula
13         Deletion of wboA in smooth, virulent B. melitensis 16M results in a rough mutant designated W
14                         After challenge with B. melitensis 16M strain, two protective antigens were f
15 ies, we used the complete genome sequence of B. melitensis 16M, the species highly pathogenic to huma
16 otect mice against intranasal challenge with B. melitensis 16M.
17 ted mice upon nasal challenge with wild-type B. melitensis 16M.
18 6 animals after intranasal administration of B. melitensis 16M.
19 hybridization led to our conclusion that the B. melitensis 28-kDa protein was a group 3 protein disti
20  To investigate the role of cyclic-di-GMP in B. melitensis, all 11 predicted cyclic-di-GMP-metabolizi
21 he genome is basal with respect to all known B. melitensis and allows the calibration of the B. melit
22 trategies for the region should include both B. melitensis and B. abortus.
23 severity as WT mice following infection with B. melitensis and treatment with anti-IFN-gamma.
24                            Brucella abortus, B. melitensis, and B. suis are pathogenic to humans, whe
25 spensable for the persistence of B. abortus, B. melitensis, and B. suis in mice up to 4 weeks after i
26 is a rodent pathogen, and unlike B. abortus, B. melitensis, and B. suis, B. neotomae has not been obs
27 ree pathogenic Brucella species: B. abortus, B. melitensis, and B. suis.
28 on susceptibility tests of Brucella abortus, B. melitensis, and B. suis.
29 omplement fixation tests with B. abortus and B. melitensis antigens (CFA and CFM), USDA and Mexican m
30 Three patterns of antibody responses against B. melitensis antigens were seen for serum samples obtai
31 quired for food-borne infection of humans by B. melitensis are poorly understood.
32 B. abortus, both smooth and rough strains of B. melitensis are resistant to complement-mediated killi
33 c infections with either Brucella abortus or B. melitensis at various doses.
34 he homologous sequences of Brucella abortus, B. melitensis, B. canis, and B. suis.
35 d animal origin, including Brucella abortus, B. melitensis, B. ovis, B. neotomae, marine mammal isola
36                                  B. abortus, B. melitensis, B. suis, and B. canis produced identical
37 s of five Brucella species-Brucella abortus, B. melitensis, B. suis, B. canis, and B. ovis-using whol
38 me for the detection of Brucella melitensis (B. melitensis) based on the screening of its complementa
39 sts that the presence of surface OPS on live B. melitensis benefits the bacterium by preventing the d
40                                          The B. melitensis BioR ortholog was overexpressed and purifi
41                                 Furthermore, B. melitensis but not B. abortus nor B. suis interfered
42 ine whether oral administration of DeltaznuA B. melitensis can confer protection against nasal B. mel
43 litensis can confer protection against nasal B. melitensis challenge.
44 attenuation displayed by this strain and its B. melitensis counterpart in experimentally infected ani
45                                 There was no B. melitensis detected in this study.
46          RMs given an aerosol challenge with B. melitensis developed undulating fevers (6/6 phase I;
47                          Both B. abortus and B. melitensis DNA were detected in humans and in multipl
48         We have investigated how B. suis and B. melitensis enter human monocytes and in which compart
49 ve limited ability to control infection with B. melitensis, even when activated by IFN-gamma in the p
50 d host range (e.g., Brucella suis for swine, B. melitensis for sheep and goats, and Brucella abortus
51                      Several features of the B. melitensis genome are similar to those of the symbiot
52                            We report a 3.45X B. melitensis genome preserved in an ~8000 year old shee
53 tification of Brucella spp., B. abortus, and B. melitensis in a single test.
54 ides an alternative way for the detection of B. melitensis in less than 10min.
55 l genome to timestamp evolutionary events in B. melitensis, including pseudogenization events linked
56                                 Treatment of B. melitensis infected macrophages with rifampicin-conta
57 biotics was demonstrated in vivo by treating B. melitensis infected mice with the standard therapy of
58                                  Joints from B. melitensis-infected IFN-gamma(-/-) mice had markedly
59                                 In contrast, B. melitensis infection diminishes more rapidly, and hig
60 pproaches to classifying and prognosticating B. melitensis infection have ever been delineated.
61                                 Few cases of B. melitensis infection in goats have occurred in the Un
62 urther, loss of Tat significantly attenuates B. melitensis infection in murine macrophages ex vivo Us
63  confer protective immunity in the spleen to B. melitensis infection.
64 lay an important role in the pathogenesis of B. melitensis infection.
65                  These results indicate that B. melitensis is able to spread systemically from the di
66  the most common bloodstream infection, with B. melitensis isolated from seven participants and B. ab
67 a pigs were challenged at mid-gestation with B. melitensis IT inoculation and monitored for fever and
68                   In contrast to B. suis and B. melitensis, it was found that B. neotomae is a partia
69 quences were identical and differed from the B. melitensis IVS sequences by a single base pair.
70 n this study, chronic infection of mice with B. melitensis led to CD8(+) T cell exhaustion, manifeste
71 ulin G (IgG) and IgA antibodies specific for B. melitensis LPS in lung lavages and specific IgG and I
72 udies show that intranasal immunization with B. melitensis LPS-GBOMP subunit vaccine significantly pr
73 us, which shares an immunogenic epitope with B. melitensis LPS.
74 e that Tat is required for full virulence of B. melitensis M28.
75 nts are the first to systematically identify B. melitensis MHC-II-restricted CD4(+) T cell epitopes r
76 ogenicity of three attenuated bioluminescent B. melitensis mutants, GR019 (virB4), GR024 (galE), and
77 e bactericidal action of NHS than were rough B. melitensis mutants.
78 nst killed B. abortus whole cells recognized B. melitensis Omp28 on Western blots (immunoblots).
79 ups of 10 goats experimentally infected with B. melitensis or B. abortus and monitored for 24 weeks.
80 mary and secondary intranasal infection with B. melitensis Our analysis of primary infection demonstr
81 ce and goats infected with smooth strains of B. melitensis produced Abs against Omp28.
82                                            A B. melitensis protein microarray comprised of nearly all
83 nized by IgG in human sera on a genome level B. melitensis protein microarray.
84                            We designated the B. melitensis protein Omp28.
85         Four peptide epitopes derived from 3 B. melitensis proteins (BMEI 1330, a DegP/HtrA protease;
86 as confirmed with DNA vaccines for these two B. melitensis proteins and, when combined, protection ag
87 onic brucellosis recognized some of the same B. melitensis proteins as those recognized by sera from
88        Computer-assisted analysis of the two B. melitensis proteomes revealed proteins expressed in e
89     A single oral vaccination with DeltaznuA B. melitensis rapidly cleared from mice within 2 weeks a
90 onfirming these results, deletion of blxR in B. melitensis reduced the transcriptional activities of
91 iated protein 1-positive inclusions, whereas B. melitensis replicated in the ER-derived compartment.
92 MEI1162 targets, specific for B. abortus and B. melitensis, respectively.
93  neotomae by using nirK, nirV, and nnrA from B. melitensis restored the ability of B. neotomae to red
94             A low dose of 1000 cfu/animal of B. melitensis resulted in 45% of mice with tissue burden
95             Genome sequencing of B. suis and B. melitensis revealed that both are complete denitrifie
96 ice inoculated with B. abortus 19 or 2308 or B. melitensis RM1 also produced antibodies to YajC.
97 rts previous indications that B. abortus and B. melitensis share a common ancestor that diverged from
98 melitensis and allows the calibration of the B. melitensis speciation time from the primarily cattle-
99 osorbent assay (iELISA) for the detection of B. melitensis-specific antibodies in goat milk.
100 use as a bulk milk test for the detection of B. melitensis-specific antibodies in goat milk.
101                                          The B. melitensis-specific CD8(+) T cells that produced IFN-
102 nged intranasally with 10(4) CFU of virulent B. melitensis strain 16 M 4 weeks after the second dose
103 . suis strain 1330 but no protection against B. melitensis strain 16 M.
104 e were challenged intranasally with virulent B. melitensis strain 16M 4 weeks after the second dose o
105                                              B. melitensis strain 16M was consistently recovered from
106                                The genome of B. melitensis strain 16M was sequenced and found to cont
107 s in the epidemiological genotyping of human B. melitensis strains.
108                       The mechanism by which B. melitensis subverts adaptive immunological memory is
109                                       Smooth B. melitensis survived and multiplied for at least 6 day
110  and had fewer nucleotide polymorphisms with B. melitensis than B. suis.
111 l deletions on chromosomes of B. abortus and B. melitensis that encoded proteins of various metabolic
112  To understand the mechanism of virulence in B. melitensis, the proteome of vaccine strain Rev 1 was
113  vitro lymphoepithelial cell (M-cell) model, B. melitensis transited rapidly through polarized entero
114 nization with the live, attenuated DeltaznuA B. melitensis vaccine provides an attractive strategy to
115 and camels (OR = 2.9, 95% CI 1.3-6.3), while B. melitensis was detected more in sheep (OR = 3.6, 95%
116 ly identified as unique to either B. suis or B. melitensis were present in the B. abortus genome.
117 blxR mutant was similar to that of wild-type B. melitensis, while the vjbR mutant was defective for s
118 e role of surface OPS in the interactions of B. melitensis with monocytes/macrophages (M/M), 16M and
119 istered live, attenuated, purine auxotrophic B. melitensis WR201 bacteria for their ability to elicit

 
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