ArticleInfection and immunity2002
Clonal polymorphism of Borrelia burgdorferi strain B31 MI: implications for mutagenesis in an infectious strain background.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
253 citing papers in PubMed, 329 citations in OpenAlex.
- Induction of indoleamine 2,3-dioxygenase by Borrelia burgdorferi in human immune cells correlates with pathogenic potential.Journal of leukocyte biology · 2015Trial
- Protective efficacy of mutant strains ofInfection and immunity · 2026Article
- Spatial Transcriptomic Profiling Reveals Microenvironment-Dependent Immune Signatures in a Lyme Arthritis model.bioRxiv : the preprint server for biology · 2026Article
- A lipid compendium of a metabolically compromised bacterium provides insights into lipid acquisition, biosynthesis, and metabolism.bioRxiv : the preprint server for biology · 2026Article
- Efficacy of Purified Borrelial Lipoproteins (PBL) as an oral formulation in reducing transmission of Lyme spirochetes from reservoir hosts tobioRxiv : the preprint server for biology · 2026Article
- Polyvalent mRNA vaccine targeting outer surface protein C affords multi-strain protection against Lyme disease.NPJ vaccines · 2025Article
- Article
- Article
- A type-specific B-cell epitope at the apex of outer surface protein C (OspC) of the Lyme disease spirochete,Microbiology spectrum · 2025Article
- Article
- Borrelia burgdorferi serine protease HtrA is a pleiotropic regulator of stress response, motility, flagellar hemostasis, and infectivity.Communications biology · 2025Article
- Article
- Breaking a barrier: In trans vlsE recombination and genetic manipulation of the native vlsE gene of the Lyme disease pathogen.PLoS pathogens · 2025Article
- Analysis of bb0556 Expression and Its Role During Borrelia burgdorferi Mammalian Infection.Molecular microbiology · 2024Article
- Novel recombinant vaccinia virus-vectored vaccine affords complete protection against homologousEmerging microbes & infections · 2024Article
- Broadly conserved FlgV controls flagellar assembly and Borrelia burgdorferi dissemination in mice.Nature communications · 2024Article
- Article
- Mechanistic insights into structure-based design of a Lyme disease subunit vaccine.bioRxiv : the preprint server for biology · 2024Article
- Complement therapeutic Factor H-IgG proteins as pre-exposure prophylaxes against Lyme borreliae infections.bioRxiv : the preprint server for biology · 2024Article
- Development and validation of systems for genetic manipulation of the Old World tick-borne relapsing fever spirochete, Borrelia duttonii.PLoS neglected tropical diseases · 2024Article
193 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
A major obstacle to studying the functions of particular gene products in the mouse-tick infectious cycle of Borrelia burgdorferi has been an inability to knock out genes in pathogenic strains. Here, we investigated conditions for site-directed mutagenesis in B31 MI, the low-passage-number, infectious B. burgdorferi strain whose genome was sequenced. We inactivated several plasmid and chromosomal genes in B31 MI and determined that clones carrying these mutations were not infectious for mice. However, we found extensive heterogeneity among clones and mutants derived from B31 MI based on colony phenotype, growth rate, plasmid content, protein profile, and transformability. Significantly, several B31 MI clones that were not subjected to mutagenesis but that lacked particular plasmids also exhibited defects at various stages in the infectious cycle. Therefore, the high degree of clonal polymorphism within B31 MI complicates the assessment of the contributions of individual genes to the observed phenotypes of the mutants. Our results indicate that B31 MI is not an appropriate strain background for genetic studies in infectious B. burgdorferi, and a well-defined isogenic clone is a prerequisite for targeted mutagenesis. To this end, we derived several wild-type clones from B31 MI that were infectious for mice, and gene inactivation was successful in one of these clones. Due to the instability of the genome with in vitro propagation, careful monitoring of plasmid content of derived mutants and complementation of inactivated genes will be crucial components of genetic studies with this pathogen.
Indexed as
Identifiers
What OpenQuestion holds
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.