ArticleInfection and immunity2006
Delineating the requirement for the Borrelia burgdorferi virulence factor OspC in the mammalian host.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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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Who cites it
78 citing papers in PubMed, 120 citations in OpenAlex.
- OspC phylogenetic analyses support the feasibility of a broadly protective polyvalent chimeric Lyme disease vaccine.Clinical and vaccine immunology : CVI · 2007Trial
- Mostly getting along -Borrelia burgdorferi and its manipulation of the host immune system.ImmunoHorizons · 2026Review
- Genomic characterization of clinical Borrelia burgdorferi sensu lato isolates in the Netherlands over a thirty-year period.BMC genomics · 2025Article
- Comparative Genomics of Two Newly Sequenced Rodent-Derived and One Previously Reported Tick-DerivedPathogens (Basel, Switzerland) · 2025Article
- Virulence Regulation inMicroorganisms · 2025Review
- Comparative genomics analysis of three conserved plasmid families in the Western Hemisphere soft tick-borne relapsing fever borreliae provides insight into variation in genome structure and antigenic variation systems.Microbiology spectrum · 2023Article
- Gac Is a Transcriptional Repressor of the Lyme Disease Spirochete's OspC Virulence-Associated Surface Protein.Journal of bacteriology · 2023Article
- Borrelia burgdorferi Outer Surface Protein C Is Not the Sole Determinant of Dissemination in Mammals.Infection and immunity · 2023Article
- Comparative genomics analysis of three conserved plasmid families in the Western Hemisphere soft tick-borne relapsing fever borreliae provides insight into variation in genome structure and antigenic variation systems.bioRxiv : the preprint server for biology · 2023Article
- The Consistent Tick-Vertebrate Infectious Cycle of the Lyme Disease Spirochete Enables Borrelia burgdorferi To Control Protein Expression by Monitoring Its Physiological Status.Journal of bacteriology · 2022Review
- DksA-dependent regulation of RpoS contributes to Borrelia burgdorferi tick-borne transmission and mammalian infectivity.PLoS pathogens · 2021Article
- Lyme Disease in Humans.Current issues in molecular biology · 2021Article
- Interactions Between Ticks and Lyme Disease Spirochetes.Current issues in molecular biology · 2021Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Article
- Strain-specific joint invasion and colonization by Lyme disease spirochetes is promoted by outer surface protein C.PLoS pathogens · 2020Article
- Transgenic functional complementation with a transmission -associated protein restores spirochete infectivity by tick bite.Ticks and tick-borne diseases · 2020Article
- Non-anticoagulant Heparin as a Pre-exposure Prophylaxis Prevents Lyme Disease Infection.ACS infectious diseases · 2020Article
- Delineating Surface Epitopes of Lyme Disease Pathogen Targeted by Highly Protective Antibodies of New Zealand White Rabbits.Infection and immunity · 2019Article
- Genome-wide screen identifies novel genes required for Borrelia burgdorferi survival in its Ixodes tick vector.PLoS pathogens · 2019Article
18 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
9 authors at 4 institutions in 1 country.
Funding
Abstract
We previously demonstrated that outer surface protein C (OspC) of Borrelia burgdorferi is essential for establishing mammalian infection. However, the role of OspC in mammalian infection is unknown. Here, we report experiments designed to distinguish between two models of OspC function in the mammalian host: (i) OspC fulfills an essential physiological role for growth and host adaptation or (ii) OspC provides a protective role for evasion of components of the innate immune response. We found that a B. burgdorferi ospC mutant, previously demonstrated to be noninfectious in both immunocompetent and SCID mice, could survive in the relatively immune-privileged environment of dialysis membrane chambers implanted within the peritoneum of a rat. The ospC mutant also adapts to the mammalian environment, as determined by the protein profiles of the chamber-cultivated spirochetes. Therefore, OspC does not appear to provide a physiological function for the survival of B. burgdorferi within the mammalian host. The second model, evasion of the innate immune system, was tested by assessing the infectivity of the ospC mutant in mice deficient for myeloid differentiation protein 88 (MyD88). Recent studies have shown that B. burgdorferi is prevented from reaching high cell numbers in the mammalian host by MyD88-dependent signaling pathways. The ospC mutant was incapable of infecting MyD88-deficient mice, suggesting that the role of OspC cannot be related solely to evasion of MyD88-mediated innate immunity. These results reiterate the importance of OspC in mammalian infection and eliminate simple models of function for this enigmatic protein.
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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.