Meningococcal disease in Dallas County, Texas: results of a six-year population-based study

Pastor, Patricia; Medley, Francinne; Murphy, Trudy V.

doi:10.1097/00006454-200004000-00012

Cited by 29 publications

(7 citation statements)

References 7 publications

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“…This strain is a relatively high expresser of fHbp (37). Bactericidal responses to the group C polysaccharide protein conjugate vaccine were measured using group C strain 4243 (C:2a:P1.5,2; ST-11) (38), which is an invasive clinical isolate from Dallas County, TX (39, 40). …”

Section: Methodsmentioning

confidence: 99%

A Meningococcal Factor H Binding Protein Mutant That Eliminates Factor H Binding Enhances Protective Antibody Responses to Vaccination

Beernink¹,

Shaughnessy

Braga³

et al. 2011

The Journal of Immunology

126

245

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Certain pathogens recruit host complement inhibitors such as factor H (fH) to evade the immune system. Microbial complement inhibitor-binding molecules can be promising vaccine targets by eliciting antibodies that neutralize this microbial defense mechanism. One such antigen, meningococcal fH-binding protein (fHbp), was used in clinical trials before the protein was discovered to bind fH. The potential effect of fH binding on vaccine immunogenicity had not been assessed in experimental animals because fHbp binds human fH specifically. In this study, we developed a human fH transgenic mouse model. Transgenic mice immunized with fHbp vaccine had 4- to 8-fold lower serum bactericidal antibody responses than control mice whose native fH did not bind the vaccine. In contrast, antibody responses were unimpaired in transgenic mice immunized with a control meningococcal group C polysaccharide-protein conjugate vaccine. In transgenic mice, immunization with an fH non-binding mutant of fHbp elicited antibodies with higher bactericidal activity than fHbp vaccination itself. Antibodies elicited by the mutant fHbp more effectively blocked fH binding to wild-type fHbp than antibodies elicited by fHbp that bound fH. Thus, a mutant fHbp vaccine that does not bind fH, but which retains immunogenicity, is predicted to be superior in humans than an fHbp vaccine that binds human fH. In the case of mutant fHbp vaccination, the resultant antibody responses may be directed more at epitopes in or near the fH-binding site, which result in greater complement-mediated serum bactericidal activity; these epitopes may be obscured when human fH is bound to the wild-type fHbp vaccine.

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Section: Methodsmentioning

confidence: 99%

A Meningococcal Factor H Binding Protein Mutant That Eliminates Factor H Binding Enhances Protective Antibody Responses to Vaccination

Beernink¹,

Shaughnessy

Braga³

et al. 2011

The Journal of Immunology

126

245

View full text Add to dashboard Cite

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“…Three of the N. meningitidis strains were capsular group B; 2 (H44/76 and MC58) were sequence types (STs) 32 and 74, respectively (both from ST 32 complex [9 -11]); and 1 (NZ98/254) was representative of ST 41/44 complex [12]. The fourth strain, 4243 [13], was group C and ST 11. Our approach to increasing the expression of fHBP from strain NZ98/ 254 was similar to that described elsewhere [14,15], except that we used a different plasmid (pComPind; gift from I. Delany, Novartis Vaccines) that integrates into the chromosome and allows expression of fHBP under control of the strong promoter from nmb1523 [16].…”

Section: Methodsmentioning

confidence: 99%

Complement‐Dependent Synergistic Bactericidal Activity of Antibodies against Factor H–Binding Protein, a Sparsely Distributed Meningococcal Vaccine Antigen

Welsch¹,

Ram

Koeberling³

et al. 2008

J INFECT DIS

105

145

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Expression of fHBP is a prerequisite for bacterial survival in blood only by strains with naturally high fHBP expression. In low-expressing strains, combinations of 2 nonbactericidal anti-fHBP MAbs can bind to nonoverlapping epitopes, engage C1q, activate C4, and mediate classical complement pathway SBA. In the absence of sufficient C4b binding for SBA, an individual MAb can have opsonophagocytic bactericidal activity.

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“…Increased incidence of meningococcal disease and series of local outbreaks have been associated with serogroup C in several European countries [33][34][35] and in the USA [36,37] since the early 1990s. Increased incidence of meningococcal disease and series of local outbreaks have been associated with serogroup C in several European countries [33][34][35] and in the USA [36,37] since the early 1990s.…”

Section: Laboratory Datamentioning

confidence: 99%

Meningococcal Disease in Catalonia 1 Year after Mass Vaccination Campaign with Meningococcal Group C Polysaccharide Vaccine

et al. 2003

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Background:The aim of this study was to investigate the clinical and epidemiological characteristics of meningococcal disease in Catalonia (Spain) after vaccination with the polysaccharide vaccine. Patients and Methods: Cases were collected by the Statutory Diseases Reporting System. Results: 176 cases were reported, an overall incidence of 2.9/100,000 persons/year. 60% of cases occurred during winter and spring. The case fatality rate was 6.3%. The highest age incidence was in children under 2 years of age (48/100,000 persons/year). Comparison of the cases detected by the Statutory Diseases Reporting System with those obtained by the Microbiological Reporting System shows that meningococcal disease surveillance in Catalonia was relatively complete (95.7%), with a positive predictive value of 66.3%. 115 cases (65%) were culture-confirmed with a rate of 1.9/100,000 persons/year. 86 (75%) cases were due to Neisseria meningitidis serogroup B and 21 to serogroup C (18%). Conclusion: Although infections due to serogroup C have decreased after mass vaccination with the polysaccharide vaccine, it is likely that the number of infections will decrease further with the conjugate meningococcal group C vaccine.

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Meningococcal disease in Dallas County, Texas: results of a six-year population-based study

Abstract: The results underscore the importance of conjugate vaccines for serogroups C and Y.

Cited by 29 publications

References 7 publications

A Meningococcal Factor H Binding Protein Mutant That Eliminates Factor H Binding Enhances Protective Antibody Responses to Vaccination

A Meningococcal Factor H Binding Protein Mutant That Eliminates Factor H Binding Enhances Protective Antibody Responses to Vaccination

Complement‐Dependent Synergistic Bactericidal Activity of Antibodies against Factor H–Binding Protein, a Sparsely Distributed Meningococcal Vaccine Antigen

Meningococcal Disease in Catalonia 1 Year after Mass Vaccination Campaign with Meningococcal Group C Polysaccharide Vaccine

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