The absence of linear plasmid 25 or 28-1 of Borrelia burgdorferi dramatically alters the kinetics of experimental infection via distinct mechanisms.
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Biology of infection with Borrelia burgdorferiBorrelia burgdorferi OspC protein required exclusively in a crucial early stage of mammalian infectionBorrelia burgdorferi changes its surface antigenic expression in response to host immune responsesPhase and antigenic variation in bacteriaLyme Borreliosis: Is there a preexisting (natural) variation in antimicrobial susceptibility among Borrelia burgdorferi strains?Mini-review: Strategies for Variation and Evolution of Bacterial Antigensvls Antigenic Variation Systems of Lyme Disease Borrelia: Eluding Host Immunity through both Random, Segmental Gene Conversion and Framework HeterogeneityMicrobial antigenic variation mediated by homologous DNA recombinationA chromosomally encoded virulence factor protects the Lyme disease pathogen against host-adaptive immunityInvestigation of the genes involved in antigenic switching at the vlsE locus in Borrelia burgdorferi: an essential role for the RuvAB branch migrase.Central role of the Holliday junction helicase RuvAB in vlsE recombination and infectivity of Borrelia burgdorferi.Identification of potential virulence determinants by Himar1 transposition of infectious Borrelia burgdorferi B31.Borrelia burgdorferi adhesins identified using in vivo phage display.Common and unique contributions of decorin-binding proteins A and B to the overall virulence of Borrelia burgdorferi.Detailed analysis of sequence changes occurring during vlsE antigenic variation in the mouse model of Borrelia burgdorferi infection.Characterization of a conditional bosR mutant in Borrelia burgdorferi.The BosR regulatory protein of Borrelia burgdorferi interfaces with the RpoS regulatory pathway and modulates both the oxidative stress response and pathogenic properties of the Lyme disease spirochete.High-throughput plasmid content analysis of Borrelia burgdorferi B31 by using Luminex multiplex technology.Induction of type I and type III interferons by Borrelia burgdorferi correlates with pathogenesis and requires linear plasmid 36.Use of the Cre-lox recombination system to investigate the lp54 gene requirement in the infectious cycle of Borrelia burgdorferiRole of Borrelia burgdorferi linear plasmid 25 in infection of Ixodes scapularis ticks.Role of the surface lipoprotein BBA07 in the enzootic cycle of Borrelia burgdorferi.Genome stability of Lyme disease spirochetes: comparative genomics of Borrelia burgdorferi plasmids.Presence of multiple variants of Borrelia burgdorferi in the natural reservoir Peromyscus leucopus throughout a transmission season.Temporal analysis of the antigenic composition of Borrelia burgdorferi during infection in rabbit skin.How do lyme borrelia organisms cause disease? The quest for virulence determinants()Analysis of an ordered, comprehensive STM mutant library in infectious Borrelia burgdorferi: insights into the genes required for mouse infectivity.CsrA modulates levels of lipoproteins and key regulators of gene expression critical for pathogenic mechanisms of Borrelia burgdorferi.pncA and bptA are not sufficient to complement Ixodes scapularis colonization and persistence by Borrelia burgdorferi in a linear plasmid lp25-deficient background.Variable VlsE is critical for host reinfection by the Lyme disease spirochete.Transcriptional regulation of the Borrelia burgdorferi antigenically variable VlsE surface protein.Influence of arthritis-related protein (BBF01) on infectivity of Borrelia burgdorferi B31.Use of an endogenous plasmid locus for stable in trans complementation in Borrelia burgdorferi.In vivo expression technology identifies a novel virulence factor critical for Borrelia burgdorferi persistence in mice.Protective niche for Borrelia burgdorferi to evade humoral immunityOligopeptide permease A5 modulates vertebrate host-specific adaptation of Borrelia burgdorferi.Borrelia burgdorferi linear plasmid 38 is dispensable for completion of the mouse-tick infectious cycle.Borrelia burgdorferi genetic markers and disseminated disease in patients with early Lyme disease.Bioluminescent imaging of Borrelia burgdorferi in vivo demonstrates that the fibronectin-binding protein BBK32 is required for optimal infectivityThe coenzyme A disulphide reductase of Borrelia burgdorferi is important for rapid growth throughout the enzootic cycle and essential for infection of the mammalian host
P2860
Q22252198-4C6DB7F9-DE2C-4E6B-A928-69A2F914E06FQ24548272-DFC6FA39-7FC6-47C9-8C77-2FF173DF26D6Q24561576-FF4B1A2C-C663-4007-AA35-683D23D77102Q24561666-D0C13872-25B1-409E-8DB3-BAC82F3D6D59Q26795774-71DA50D7-43E1-4D6F-BBBE-C872C0AF775EQ26796459-D7B05BC1-C583-4BF8-A7C7-B16E5BC0C407Q26829575-7666AAF5-8DBA-44A1-AF12-635187673F9BQ27009515-622B1D09-9F25-49DF-95A9-322E1CB8986AQ27317412-36964FAB-2A12-40CF-9333-EE9E053FED89Q30973496-B91C86B4-EE2A-403B-AEFE-8F086B759C07Q30974863-71041733-7FBF-405E-9C80-15941DEFDBC9Q33259140-FF2E3E4C-6292-41D2-82FC-3D1FB38D17EEQ33296896-F5475C58-5D46-40F3-A6D0-7BFA80D4499EQ33373693-F8063BD6-8D13-4827-98FA-4FAC0DAB8FD9Q33408773-7FCC8383-801E-4803-850B-0028B1D39FB1Q33557862-FC2A7BCB-9E4B-413C-877D-62CE39E185FCQ33585831-5D00D222-7443-4994-B24B-71E28120C278Q33775277-6197C1A1-1A04-426F-B0F4-92BC875796F8Q33778936-263BC496-C145-4C36-B239-9D24F99B710FQ33877080-16FE746E-306A-4FC4-ABE3-60B7797469A3Q33937487-0931A5E2-73B7-4348-BCB2-4C686C24330CQ33963206-2012E523-A922-4A54-A395-36C59554E886Q34202850-552393FA-E2E0-46F1-923D-86C7CFFC638CQ34296826-1F3A3DAC-9909-4D92-8C45-4F132D99A9FBQ34342409-7F276DA9-6AEF-4AEC-86AC-3EE214D8934AQ34455048-AE6A4D7F-BBE5-4B78-B715-3F163D725058Q34469139-99BC5FD9-79AD-4009-BD53-FEA4CA672393Q34529598-6E486E9F-A4CB-4ADF-BFA1-BC410ADEE59EQ34595762-98BD1DE9-F1DE-4001-BCF4-795D22BED1DFQ34674810-89DC9583-4FC0-411B-BC2E-21A62E677381Q34697832-ABE9A8C8-1485-49E0-A9BD-C7D8C3C7695FQ34709026-7F513AF7-6E2B-403B-BCEB-1D2E36ADEEDAQ34933876-B4E6AD89-2E8F-4015-AF27-E11A51E13586Q34979354-2485465F-BB9D-474A-9255-D366AE4463C3Q35103113-C6FD8DD5-477C-4F6F-AE68-8DFE355911E8Q35139390-950BF29E-66F8-42C6-B87A-278207AE8D54Q35191923-518D8865-E2F8-4199-8850-5078BECACE7EQ35221017-F452C691-644B-4BBA-9931-4552DC224375Q35242498-5DB3A704-52B1-4FA2-B5A6-1424931639B6Q35580725-5B8B1F09-84A1-426B-9EE8-309B4C78EB68
P2860
The absence of linear plasmid 25 or 28-1 of Borrelia burgdorferi dramatically alters the kinetics of experimental infection via distinct mechanisms.
description
2003 nî lūn-bûn
@nan
2003 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
name
The absence of linear plasmid ...... ction via distinct mechanisms.
@ast
The absence of linear plasmid ...... ction via distinct mechanisms.
@en
type
label
The absence of linear plasmid ...... ction via distinct mechanisms.
@ast
The absence of linear plasmid ...... ction via distinct mechanisms.
@en
prefLabel
The absence of linear plasmid ...... ction via distinct mechanisms.
@ast
The absence of linear plasmid ...... ction via distinct mechanisms.
@en
P2093
P2860
P1476
The absence of linear plasmid ...... ction via distinct mechanisms.
@en
P2093
Jonathan T Skare
Maria Labandeira-Rey
P2860
P304
P356
10.1128/IAI.71.8.4608-4613.2003
P407
P577
2003-08-01T00:00:00Z