ArticlePLoS pathogens2018
Polymorphic factor H-binding activity of CspA protects Lyme borreliae from the host complement in feeding ticks to facilitate tick-to-host transmission.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 citations in OpenAlex.
- Developing a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rational adjuvant selection.NPJ vaccines · 2026Article
- Natural genetic variation impacts complement inhibitory activity of PFam54 orthologs of Asian Borrelia bavariensis.Scientific reports · 2026Article
- Develop a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rationale adjuvant selection.bioRxiv : the preprint server for biology · 2026Article
- The wild, wild west of plasmids: First insights into comparative genomics of Borrelia burgdorferi sensu lato.PloS one · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Complement therapeutic factor H-IgG proteins as pre-exposure prophylaxes against Lyme borreliae infections.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- CCL17 Influences Borrelia burgdorferi Infection in the Heart.The Journal of infectious diseases · 2025Article
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- BBK32 attenuates antibody-dependent complement-mediated killing of infectious Borreliella burgdorferi isolates.PLoS pathogens · 2025Article
- Mechanistic insights into the structure-based design of a CspZ-targeting Lyme disease vaccine.Nature communications · 2025Article
- Current Progress in the Development of mRNA Vaccines Against Bacterial Infections.International journal of molecular sciences · 2024Review
- 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
- Lizards and the enzootic cycle of Borrelia burgdorferi sensu lato.Molecular microbiology · 2024Review
- Unprecedented genetic variability of PFam54 paralogs among Eurasian Lyme borreliosis-causing spirochetes.Ecology and evolution · 2024Article
- Article
- A high fidelity approach to assembling the complex Borrelia genome.BMC genomics · 2023Article
- Structural evolution of an immune evasion determinant shapes pathogen host tropism.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A tick C1q protein alters infectivity of the Lyme disease agent by modulating interferon γ.Cell reports · 2022Article
- Large-Scale Sequencing ofGenes · 2022Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Borrelia burgdorferi sensu lato (Bbsl), the causative agent of Lyme disease, establishes an initial infection in the host's skin following a tick bite, and then disseminates to distant organs, leading to multisystem manifestations. Tick-to-vertebrate host transmission requires that Bbsl survives during blood feeding. Complement is an important innate host defense in blood and interstitial fluid. Bbsl produces a polymorphic surface protein, CspA, that binds to a complement regulator, Factor H (FH) to block complement activation in vitro. However, the role that CspA plays in the Bbsl enzootic cycle remains unclear. In this study, we demonstrated that different CspA variants promote spirochete binding to FH to inactivate complement and promote serum resistance in a host-specific manner. Utilizing a tick-to-mouse transmission model, we observed that a cspA-knockout B. burgdorferi is eliminated from nymphal ticks in the first 24 hours of feeding and is unable to be transmitted to naïve mice. Conversely, ectopically producing CspA derived from B. burgdorferi or B. afzelii, but not B. garinii in a cspA-knockout strain restored spirochete survival in fed nymphs and tick-to-mouse transmission. Furthermore, a CspA point mutant, CspA-L246D that was defective in FH-binding, failed to survive in fed nymphs and at the inoculation site or bloodstream in mice. We also allowed those spirochete-infected nymphs to feed on C3-/- mice that lacked functional complement. The cspA-knockout B. burgdorferi or this mutant strain complemented with cspA variants or cspA-L246D was found at similar levels as wild type B. burgdorferi in the fed nymphs and mouse tissues. These novel findings suggest that the FH-binding activity of CspA protects spirochetes from complement-mediated killing in fed nymphal ticks, which ultimately allows Bbsl transmission to mammalian hosts.
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