ArticleClinical and vaccine immunology : CVI2011
Characterization of Neisseria meningitidis isolates that do not express the virulence factor and vaccine antigen factor H binding protein.
Article in Clinical and vaccine immunology : CVI, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 96 citations in OpenAlex.
- Meningococcal Serogroup B Bivalent rLP2086 Vaccine Elicits Broad and Robust Serum Bactericidal Responses in Healthy Adolescents.Journal of the Pediatric Infectious Diseases Society · 2016Trial
- Interlaboratory study to assess precision and reproducibility of the meningococcal antigen surface expression (MEASURE) assay to quantify factor H binding protein expression at the surface of meningococcal serogroup B strains.Diagnostic microbiology and infectious disease · 2025Article
- Methods to evaluate the performance of a multicomponent meningococcal serogroup B vaccine.mSphere · 2025Review
- Factor H binding protein (FHbp): An evaluation of genotypic diversity acrossHuman vaccines & immunotherapeutics · 2024Review
- Molecular characteristics of Neisseria meningitidis carriage strains in university students in Lithuania.BMC microbiology · 2023Article
- Meningococcal factor H-binding protein: implications for disease susceptibility, virulence, and vaccines.Trends in microbiology · 2023Review
- PathogenicInfection and immunity · 2022Article
- Deconvolution of intergenic polymorphisms determining high expression of Factor H binding protein in meningococcus and their association with invasive disease.PLoS pathogens · 2021Article
- Factor H binding protein (fHbp)-mediated differential complement resistance of a serogroup CAccess microbiology · 2021Article
- Broad vaccine protection against Neisseria meningitidis using factor H binding protein.Vaccine · 2020Review
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- Meningococcal Group B Vaccine For The Prevention Of Invasive Meningococcal Disease Caused ByInfection and drug resistance · 2019Article
- Neisseria cinerea Expresses a Functional Factor H Binding Protein Which Is Recognized by Immune Responses Elicited by Meningococcal Vaccines.Infection and immunity · 2017Article
- Frequent capsule switching in 'ultra-virulent' meningococci - Are we ready for a serogroup B ST-11 complex outbreak?The Journal of infection · 2017Article
- Utilizing complement evasion strategies to design complement-based antibacterial immunotherapeutics: Lessons from the pathogenic Neisseriae.Immunobiology · 2016Review
- Meningococcal Factor H Binding Protein Vaccine Antigens with Increased Thermal Stability and Decreased Binding of Human Factor H.Infection and immunity · 2016Article
- Expression of factor H binding protein in meningococcal strains can vary at least 15-fold and is genetically determined.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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- 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
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Neisseria meningitidis remains a leading cause of bacterial sepsis and meningitis. Complement is a key component of natural immunity against this important human pathogen, which has evolved multiple mechanisms to evade complement-mediated lysis. One approach adopted by the meningococcus is to recruit a human negative regulator of the complement system, factor H (fH), to its surface via a lipoprotein, factor H binding protein (fHbp). Additionally, fHbp is a key antigen in vaccines currently being evaluated in clinical trials. Here we characterize strains of N. meningitidis from several distinct clonal complexes which do not express fHbp; all strains were recovered from patients with disseminated meningococcal disease. We demonstrate that these strains have either a frameshift mutation in the fHbp open reading frame or have entirely lost fHbp and some flanking sequences. No fH binding was detected to other ligands among the fHbp-negative strains. The implications of these findings for meningococcal pathogenesis and prevention are discussed.
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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.