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1  LipoP, SignalP, and Phobius, a total of 191 R. typhi proteins were predicted to contain signal pepti
2 f PI(3,4,5)P3 and PI(3)P, negatively affects R. typhi infection.
3 ot analyses of ELB, with typing sera against R. typhi indicate that ELB surface antigens are more clo
4                                        Among R. typhi PCR-positive patients, the area under the time-
5 d LDH release demonstrated that R. akari and R. typhi caused negligible cytotoxicity in mouse periton
6 more, macrophage infection with R. akari and R. typhi resulted in differential synthesis and expressi
7 cytokines was observed between R. akari- and R. typhi-infected macrophages, which may correlate with
8            Both the R. prowazekii Breinl and R. typhi Wilmington metK genes complemented at a level c
9 . typhi, 15 are found only in R. conorii and R. typhi, and 24 are unique to R. typhi.
10 occurred after the typhus (R. prowazekii and R. typhi) and spotted fever (R. conorii) groups diverged
11 enes: 23 are found only in R. prowazekii and R. typhi, 15 are found only in R. conorii and R. typhi,
12 ettsiae, including Rickettsia prowazekii and R. typhi, produce visible plaques on primary chick embry
13 The cloned lepB genes from R. rickettsii and R. typhi have been demonstrated to possess signal peptid
14 the cloned lepB genes from R. rickettsii and R. typhi shows open reading frames of 801 and 795 nucleo
15  and in vivo culture of O. tsutsugamushi and R. typhi would require that only high-risk activities (a
16 factor was observed for O. tsutsugamushi and R. typhi, underscoring the importance of both time and t
17                     Accordingly, we assessed R. typhi-mediated flea IMD pathway activation in vivo us
18 s are more closely related to the flea-borne R. typhi than to the mite-borne R. akari.
19                     Complementation assay by R. typhi groESL in a temperature sensitive Escherichia c
20 ar mechanism underlying erythrocyte lysis by R. typhi has not been defined.
21                       RARP-1 was secreted by R. typhi into the host cytoplasm during in vitro infecti
22               The availability of the cloned R. typhi tlyC will permit further characterization and d
23      No patients returned with PCR-confirmed R. typhi relapse.
24 ctive was to characterize such Sec-dependent R. typhi proteins in the context of a mammalian host cel
25                        Secreted early during R. typhi infection, RalF localizes to the host plasma me
26 of growth suggests its potential role during R. typhi infection of host cells.
27 sponding to the requirement of PI(4,5)P2 for R. typhi entry.
28 -specific restimulation of spleen cells from R. typhi(GFPuv)-infected BALB/c mice elicits gamma inter
29 of the gene (tlyC) encoding a hemolysin from R. typhi.
30 netic complementation, recombinant lspA from R. typhi significantly restores the growth of temperatur
31  RT0776, and (ii) native OmpBs purified from R. typhi and R. prowazekii strains Breinl, RP22, and Mad
32                   We identified 877 genes in R. typhi encoding 3 rRNAs, 33 tRNAs, 3 noncoding RNAs, a
33 ich is close to the replication terminus, in R. typhi, compared to R. prowazekii and R. conorii.
34        Knockdown of Relish and Imd increased R. typhi infection levels, implicating the IMD pathway a
35               In addition, we found a 124-kb R. typhi-specific inversion, starting 19 kb from the ori
36                     DNA sequence analysis of R. typhi tlyC revealed an open reading frame of 912 bp,
37 es of Rickettsia prowazekii RP027-028 and of R. typhi RT0101 and to monomethyltransferases of R. prow
38 yltransferases of R. prowazekii RP789 and of R. typhi RT0776, and (ii) native OmpBs purified from R.
39                   Importantly, expression of R. typhi tolC in the E. coli tolC mutant restored the se
40 bed at all stages of intracellular growth of R. typhi in Vero cells.
41 igation of genomic and phenotypic markers of R. typhi azithromycin resistance is needed.
42                            Overexpression of R. typhi lspA in Escherichia coli confers increased glob
43 al transcript abundance at various phases of R. typhi intracellular growth.
44 ntified it as a secreted effector protein of R. typhi.
45 g the IMD pathway as a critical regulator of R. typhi burden in C. felis These data suggest that targ
46 e we present the complete genome sequence of R. typhi (1,111,496 bp) and compare it to the two publis
47           The deduced amino acid sequence of R. typhi GroES and GroEL shows a high degree of identity
48 the IMD pathway could minimize the spread of R. typhi, and potentially other human pathogens, vectore
49 t of the putative type 1 secretion system of R. typhi is involved in the secretion process of RARP-1.
50 ere for the first time the transformation of R. typhi with the pRAM18dRGA plasmid that originally der
51 of BA6163) transformed with R. typhi tlyC or R. typhi GFPuv-tlyC constructs.
52 e patient had a positive O. tsutsugamushi or R. typhi rapid diagnostic test (RDT), serology, or PCR.
53 a genome sequence, little is known regarding R. typhi biology in flea vectors that, importantly, do n
54                    Typhus group rickettsiae (R. typhi and R. prowazekii) adhere to and lyse human and
55 se to R. typhi Initially, we determined that R. typhi infects Drosophila cells and increases antimicr
56                             To associate the R. typhi tlyC gene product with hemolytic activity, we p
57 l analysis indicated that at least 54 of the R. typhi extracytoplasmic proteins undergo active gene e
58 n functionally characterized; therefore, the R. typhi Sec apparatus represents a mechanism for the se
59 ection, with GTP-bound Arf6 localized to the R. typhi entry foci.
60                                        Thus, R. typhi(GFPuv) bacteria are a novel, potent tool to stu
61 reduction factor at 56 degrees C compared to R. typhi, R. conorii, and R. honei.
62  importantly, do not suffer lethality due to R. typhi infection.
63 ion in the R. prowazekii genome, relative to R. typhi and R. conorii, which appears to have occurred
64 ocephalides felis) innate immune response to R. typhi Initially, we determined that R. typhi infects
65 . conorii and R. typhi, and 24 are unique to R. typhi.
66                                  Transformed R. typhi (R. typhi(GFPuv)) bacteria are viable, replicat
67 tection of GFPUV expression, and transformed R. typhi were isolated in a fluorescence-activated cell
68 ime required to inactivate O. tsutsugamushi, R. typhi, R. conorii, and R. honei.
69 to those for animals infected with wild-type R. typhi and develop comparable pathology and bacterial
70  with kinetics similar to those of wild-type R. typhi in cell culture, and stably maintain the plasmi
71                        Transformed R. typhi (R. typhi(GFPuv)) bacteria are viable, replicate with kin
72                    Native OmpB from virulent R. typhi contains mono- and trimethyllysines at location
73  single cluster in OmpB from mildly virulent R. typhi.
74 confirmed murine typhus, and 52 (24.1%) were R. typhi PCR positive.
75                 CB17 SCID mice infected with R. typhi(GFPuv) succumb to the infection with kinetics s
76 a HpmA(-) mutant of BA6163) transformed with R. typhi tlyC or R. typhi GFPuv-tlyC constructs.