ArticlePloS one2008
Borrelia burgdorferi complement regulator-acquiring surface protein 2 does not contribute to complement resistance or host infectivity.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 66 citations in OpenAlex.
- Developing a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rational adjuvant selection.NPJ vaccines · 2026Article
- Develop a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rationale adjuvant selection.bioRxiv : the preprint server for biology · 2026Article
- Mechanistic insights into the structure-based design of a CspZ-targeting Lyme disease vaccine.Nature communications · 2025Article
- 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
- Article
- Immune evasion strategies of major tick-transmitted bacterial pathogens.Trends in microbiology · 2023Review
- Past, present, and future of Lyme disease vaccines: antigen engineering approaches and mechanistic insights.Expert review of vaccines · 2022Review
- CspZ FH-Binding Sites as Epitopes Promote Antibody-Mediated Lyme Borreliae Clearance.Infection and immunity · 2022Article
- Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system.PLoS pathogens · 2021Article
- The Brilliance ofPathogens (Basel, Switzerland) · 2021Review
- Investigating BB0405 as a novel Borrelia afzelii vaccination candidate in Lyme borreliosis.Scientific reports · 2021Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Complement Evasion by Lyme Disease Spirochetes.Trends in microbiology · 2020Review
- Complement Evasion Contributes to Lyme Borreliae-Host Associations.Trends in parasitology · 2020Review
- The Factor H-Binding Site of CspZ as a Protective Target against Multistrain, Tick-Transmitted Lyme Disease.Infection and immunity · 2020Article
- New Insights Into CRASP-Mediated Complement Evasion in the Lyme Disease Enzootic Cycle.Frontiers in cellular and infection microbiology · 2020Review
- Outer surface protein polymorphisms linked to host-spirochete association in Lyme borreliae.Molecular microbiology · 2019Review
- Blood treatment of Lyme borreliae demonstrates the mechanism of CspZ-mediated complement evasion to promote systemic infection in vertebrate hosts.Cellular microbiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Borrelia burgdorferi, the pathogen of Lyme disease, cycles in nature through Ixodes ticks and mammalian hosts. At least five Complement Regulator-Acquiring Surface Proteins (BbCRASPs) are produced by B. burgdorferi, which are thought to assist spirochetes in host immune evasion. Recent studies established that BbCRASP-2 is preferentially expressed in mammals, and elicits robust antibody response in infected hosts, including humans. We show that BbCRASP-2 is ubiquitously expressed in diverse murine tissues, but not in ticks, reinforcing a role of BbCRASP-2 in conferring B. burgdorferi defense against persistent host immune threats, such as complement. BbCRASP-2 immunization, however, fails to protect mice from B. burgdorferi infection and does not modify disease, as reflected by the development of arthritis. An infectious BbCRASP-2 mutant was generated, therefore, to examine the precise role of the gene product in spirochete infectivity. Similar to wild type B. burgdorferi, BbCRASP-2 mutants remain insensitive to complement-mediated killing in vitro, retain full murine infectivity and induce arthritis. Quantitative RT-PCR assessment indicates that survivability of BbCRASP-2-deficient B. burgdorferi is not due to altered expression of other BbCRASPs. Together, these results suggest that the function of a selectively expressed B. burgdorferi gene, BbCRASP-2, is not essential for complement resistance or infectivity in the murine host.
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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.