ArticleInfection and immunity2011
Effect of factor H-binding protein sequence variation on factor H binding and survival of Neisseria meningitidis in human blood.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 30 citations in OpenAlex.
- Cloning and expression of natively paired antibody fragments from single B cells of immunized rhesus macaques.Frontiers in immunology · 2026Article
- Deconvolution of intergenic polymorphisms determining high expression of Factor H binding protein in meningococcus and their association with invasive disease.PLoS pathogens · 2021Article
- Molecular characterization of two sub-family specific monoclonal antibodies to meningococcal Factor H binding protein.Heliyon · 2018Article
- Meningococcal Factor H Binding Protein Vaccine Antigens with Increased Thermal Stability and Decreased Binding of Human Factor H.Infection and immunity · 2016Article
- Binding of Complement Factor H (FH) Decreases Protective Anti-FH Binding Protein Antibody Responses of Infant Rhesus Macaques Immunized With a Meningococcal Serogroup B Vaccine.The Journal of infectious diseases · 2015Article
- Resistance of Neisseria meningitidis to human serum depends on T and B cell stimulating protein B.Infection and immunity · 2015Article
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- fH-dependent complement evasion by disease-causing meningococcal strains with absent fHbp genes or frameshift mutations.Vaccine · 2013Article
- Does binding of complement factor H to the meningococcal vaccine antigen, factor H binding protein, decrease protective serum antibody responses?Clinical and vaccine immunology : CVI · 2013Review
- Role of factor H binding protein in Neisseria meningitidis virulence and its potential as a vaccine candidate to broadly protect against meningococcal disease.Microbiology and molecular biology reviews : MMBR · 2013Review
- Vaccines, reverse vaccinology, and bacterial pathogenesis.Cold Spring Harbor perspectives in medicine · 2013Article
- Defining a protective epitope on factor H binding protein, a key meningococcal virulence factor and vaccine antigen.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- An analysis of the sequence variability of meningococcal fHbp, NadA and NHBA over a 50-year period in the Netherlands.PloS one · 2013Article
- Design of meningococcal factor H binding protein mutant vaccines that do not bind human complement factor H.Infection and immunity · 2012Article
- The relative roles of factor H binding protein, neisserial surface protein A, and lipooligosaccharide sialylation in regulation of the alternative pathway of complement on meningococci.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Activation of the classical complement pathway by Bacillus anthracis is the primary mechanism for spore phagocytosis and involves the spore surface protein BclA.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Enhanced bacteremia in human factor H transgenic rats infected by Neisseria meningitidis.Infection and immunity · 2012Article
- The effect of human factor H on immunogenicity of meningococcal native outer membrane vesicle vaccines with over-expressed factor H binding protein.PLoS pathogens · 2012Article
- Meningococcal factor H binding protein fHbpd184 polymorphism influences clinical course of meningococcal meningitis.PloS one · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Binding of the complement inhibitor factor H (fH) to the surface of Neisseria meningitidis is critical for evasion of innate host defenses. The meningococcal vaccine candidate factor H-binding protein (fHbp) serves as an fH ligand. We prepared 16 recombinant fHbp natural sequence variants. By enzyme-linked immunosorbent assay (ELISA), the variants from a New Zealand epidemic strain (fHbp ID 14) and from an endemic United Kingdom strain (ID 15) showed 10-fold lower fH binding than a reference fHbp from an epidemic Norwegian strain (ID 1). By surface plasmon resonance, association rate constants (k(a)) for fHbp ID 14 and 15 were similar to those for ID 1, but dissociation rate constants (k(d)) were 4- to 10-fold higher than those for ID 1. To determine the effect of fH affinity on fHbp fitness, we prepared isogenic mutants of strain H44/76 that expressed fHbp ID 1, 14, or 15. By flow cytometry, mutants expressing fHbp ID 14 or 15 had lower fH binding than ID 1. When incubated in plasma or blood of nonimmune donors, all three mutants showed similar increases in CFU/ml. In contrast, an isogenic fHbp knockout mutant, which grew well in broth, was rapidly killed in plasma or blood. Thus, although fHbp expression was required for survival of strain H44/76 in blood or plasma, expression of two natural fHbp sequence variants with lower fH affinity had minimal or no effect on nonimmune clearance. One reason may be the high fH concentrations in normal serum, which favor saturation of fH binding to fHbp, even when dissociation rates varied over 10-fold.
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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.