ArticleInfection and immunity2004
Effects of vlsE complementation on the infectivity of Borrelia burgdorferi lacking the linear plasmid lp28-1.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 75 citations in OpenAlex.
- Testing the capacity of humanized immune system mice to induce a protective antibody response against the Lyme disease pathogen.Microbiology spectrum · 2026Article
- Navigating infection by pathogenic spirochetes: The host-bacteria interface at the atomic level.Protein science : a publication of the Protein Society · 2025Review
- Complex exchanges among plasmids and clonal expansion of lineages shape the population structure and virulence ofbioRxiv : the preprint server for biology · 2025Article
- Breaking a barrier: In trans vlsE recombination and genetic manipulation of the native vlsE gene of the Lyme disease pathogen.PLoS pathogens · 2025Article
- Hitchhiker's Guide toJournal of bacteriology · 2024Review
- Meta-analysis of the Vmp-like sequences of Lyme diseaseFrontiers in microbiology · 2024Article
- The Putative Endonuclease Activity of MutL Is Required for the Segmental Gene Conversion Events That Drive Antigenic Variation of the Lyme Disease Spirochete.Frontiers in microbiology · 2022Article
- Evolutionary Genetics ofCurrent issues in molecular biology · 2021Review
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- YebC regulates variable surface antigen VlsE expression and is required for host immune evasion in Borrelia burgdorferi.PLoS pathogens · 2020Article
- The Borrelia burgdorferi VlsE Lipoprotein Prevents Antibody Binding to an Arthritis-Related Surface Antigen.Cell reports · 2020Article
- Novel targets and strategies to combat borreliosis.Applied microbiology and biotechnology · 2020Review
- Changing of the guard: How the Lyme disease spirochete subverts the host immune response.The Journal of biological chemistry · 2020Review
- Article
- Delineating Surface Epitopes of Lyme Disease Pathogen Targeted by Highly Protective Antibodies of New Zealand White Rabbits.Infection and immunity · 2019Article
- New Zealand White Rabbits Effectively Clear Borrelia burgdorferi B31 despite the Bacterium's FunctionalInfection and immunity · 2019Article
- Recent discoveries and advancements in research on the Lyme disease spirocheteF1000Research · 2019Review
- Identification of Surface Epitopes Associated with Protection against Highly Immune-Evasive VlsE-Expressing Lyme Disease Spirochetes.Infection and immunity · 2018Article
- Host Immune Evasion by Lyme and Relapsing Fever Borreliae: Findings to Lead Future Studies forFrontiers in immunology · 2017Review
- Antigenic Variation and Immune Escape in the MTBC.Advances in experimental medicine and biology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The loss of linear plasmid lp28-1, which contains the vls antigenic variation locus, is associated with reduced infectivity of Borrelia burgdorferi in immunocompetent mice. The recombinant shuttle vector pBBE22, which includes the virulence determinant BBE22 from lp25 and restores infectivity to readily transformable B. burgdorferi lacking lp25 and lp56, was used to determine the effect of trans expression of vlsE on virulence. Spirochetes lacking lp28-1 were complemented with the plasmid pBBE22:vlsE, containing both BBE22 and vlsE. VlsE protein produced by this construct was expressed and surface accessible in in vitro-cultured B. burgdorferi, as determined by surface proteolysis and immunoblot analysis. Clones lacking lp25 but containing lp28-1 and either pBBE22 or pBBE22:vlsE were reisolated consistently from immunocompetent mice 8 weeks after infection. In contrast, a clone lacking both lp25 and lp28-1 and complemented with pBBE22:vlsE was isolated from only a single tissue of one of six C3H/HeN mice 8 weeks postinfection. These results indicate that either an intact vls antigenic variation locus or another determinant on lp28-1 is required to restore complete infectivity. In addition, an isogenic clone that retained lp28-1 was complemented with the vlsE shuttle plasmid and was examined for vlsE sequence variation and infectivity. Sequence variation was not observed for the shuttle plasmid, indicating that the cis arrangement of vlsE and the vls silent cassettes in lp28-1 facilitate vlsE gene conversion. Lack of vlsE sequence variation on the shuttle plasmid thus did not result in clearance of the trans-complemented strain in immunocompetent mice under the conditions tested.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.