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Published on: November 5, 2019
A multi-country evaluation of Neisseria meningitidis serogroup B factor H-binding proteins and implications for
Susan K Hoiseth1, Ellen Murphy, Lubomira Andrew
1From the *Pfizer Vaccine Research, Pearl River, NY; †Institute for Hygiene and Microbiology, University of Würzburg, Würzburg; ‡Robert Koch Institute, Berlin, Germany; §National Institute of Health, Carlos III, Madrid, Spain; ¶Health Protection Agency, Manchester Royal Infirmary, Manchester, United Kingdom; ‖Institut Pasteur, Paris, France; **Norwegian Institute of Public Health, Oslo, Norway; ††National Institute of Public Health, Prague, Czech Republic; ‡‡Centers for Disease Control and Prevention, Atlanta, GA; and §§Pfizer, Collegeville, PA.
Background:
Recombinant vaccines containing factor H-binding protein (fHBP) have been developed for the purpose of protection from invasive meningococcal serogroup B disease. Neisseria meningitidis fHBP sequences can be divided into 2 genetically and immunologically distinct subfamilies (A and B); thus, cross protection is conferred within but not between subfamilies. A comprehensive understanding of fHBP epidemiology is required to accurately assess the potential vaccine impact when considering different vaccination implementation strategies.
Methods:
Systematically collected invasive meningococcal serogroup B isolates from England, Wales, Northern Ireland, the United States, Norway, France and the Czech Republic were previously characterized for fHBP sequence. This study expanded the evaluation with additional meningococcal serogroup B disease isolates from Spain (n = 346) and Germany (n = 205). This expanded set (n = 1841), collected over a 6-year period (2001 to 2006), was evaluated for fHBP sequence and fHBP subfamily relative to patient age.
Results:
All 1841 isolates contained fhbp. fHBP sequences from Spain and Germany fell within the previously described subfamilies, with 69% of isolates belonging to subfamily B and 31% to subfamily A; prevalent sequence variants were also similar. Stratification of data by age indicated that disease in infants <1 year of age was caused by a significantly higher proportion of isolates with fHBP subfamily A variants than that seen in adolescents and young adults 11-25 years (47.7% versus 19.5%, P < 0.0001, respectively).
Conclusions:
These observations highlight a difference in epidemiology of fHBP subfamilies in different age groups, with fHBP subfamily A strains causing more disease in vulnerable populations, such as infants, than in adolescents.
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