ArticleInfection and immunity2015
Borrelia burgdorferi RevA Significantly Affects Pathogenicity and Host Response in the Mouse Model of Lyme Disease.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Revolutionizing Lyme disease vaccination: a systematic review and meta-analysis of promising candidates.Frontiers in cellular and infection microbiology · 2025Pooled it
- Colonization of 3D-organotypic human skin by the Lyme Disease pathogen,bioRxiv : the preprint server for biology · 2026Article
- Machine learning-driven identification of virulence determinants in Borrelia burgdorferi associated with human dissemination.PLoS computational biology · 2026Article
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- Pathogenicity and virulence ofVirulence · 2023Review
- Borrelia burgdorferi Outer Surface Protein C Is Not the Sole Determinant of Dissemination in Mammals.Infection and immunity · 2023Article
- Erp and Rev Adhesins of the Lyme Disease Spirochete's Ubiquitous cp32 Prophages Assist the Bacterium during Vertebrate Infection.Infection and immunity · 2023Review
- Past, present, and future of Lyme disease vaccines: antigen engineering approaches and mechanistic insights.Expert review of vaccines · 2022Review
- Nanomechanical mechanisms of Lyme disease spirochete motility enhancement in extracellular matrix.Communications biology · 2021Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Interactions between Borrelia burgdorferi and ticks.Nature reviews. Microbiology · 2020Review
- Strain-specific joint invasion and colonization by Lyme disease spirochetes is promoted by outer surface protein C.PLoS pathogens · 2020Article
- The Lyme disease spirochete's BpuR DNA/RNA-binding protein is differentially expressed during the mammal-tick infectious cycle, which affects translation of the SodA superoxide dismutase.Molecular microbiology · 2019Article
- Rhesus Brain Transcriptomic Landscape in anFrontiers in neuroscience · 2019Article
- The RpoS Gatekeeper inFrontiers in microbiology · 2019Article
- mRNA transcript distribution bias between Borrelia burgdorferi bacteria and their outer membrane vesicles.FEMS microbiology letters · 2018Article
- Borrelia burgdorferi SpoVG DNA- and RNA-Binding Protein Modulates the Physiology of the Lyme Disease Spirochete.Journal of bacteriology · 2018Article
- Multifunctional and Redundant Roles ofFrontiers in immunology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The Lyme disease spirochete, Borrelia burgdorferi, expresses RevA and numerous outer surface lipoproteins during mammalian infection. As an adhesin that promotes bacterial interaction with fibronectin, RevA is poised to interact with the extracellular matrix of the host. To further define the role(s) of RevA during mammalian infection, we created a mutant that is unable to produce RevA. The mutant was still infectious to mice, although it was significantly less well able to infect cardiac tissues. Complementation of the mutant with a wild-type revA gene restored heart infectivity to wild-type levels. Additionally, revA mutants led to increased evidence of arthritis, with increased fibrotic collagen deposition in tibiotarsal joints. The mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, and this increase was abolished in the complemented strain. Therefore, while revA is not absolutely essential for infection, deletion of revA had distinct effects on dissemination, arthritis severity, and host response.
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Registered trials
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.