Role of selection in the emergence of lineages and the evolution of virulence in Neisseria meningitidis
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články
Grantová podpora
047072
Wellcome Trust - United Kingdom
PubMed
18815379
PubMed Central
PMC2553036
DOI
10.1073/pnas.0712019105
PII: 0712019105
Knihovny.cz E-zdroje
- MeSH
- alely MeSH
- dítě MeSH
- dospělí MeSH
- genetická variace MeSH
- kojenec MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- molekulární epidemiologie MeSH
- molekulární evoluce * MeSH
- Neisseria meningitidis klasifikace genetika izolace a purifikace patogenita MeSH
- předškolní dítě MeSH
- selekce (genetika) * MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- virulence genetika MeSH
- Check Tag
- dítě MeSH
- dospělí MeSH
- kojenec MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika epidemiologie MeSH
Neisseria meningitis is a human commensal bacterium that occasionally causes life-threatening disease. As with a number of other bacterial pathogens, meningococcal populations comprise distinct lineages, which persist over many decades and during global spread in the face of high rates of recombination. In addition, the propensity to cause invasive disease is associated with particular "hyperinvasive" lineages that coexist with less invasive lineages despite the fact that disease does not contribute to host-to-host transmission. Here, by combining a modeling approach with molecular epidemiological data from 1,108 meningococci isolated in the Czech Republic over 27 years, we show that interstrain competition, mediated by immune selection, can explain both the persistence of multiple discrete meningococcal lineages and the association of a subset of these with invasive disease. The model indicates that the combinations of allelic variants of housekeeping genes that define these lineages are associated with very small differences in transmission efficiency among hosts. These findings have general implications for the emergence of lineage structure and virulence in recombining bacterial populations.
Zobrazit více v PubMed
Maiden MC. Multilocus sequence typing of bacteria. Annu Rev Microbiol. 2006;60:561–588. PubMed
Selander RK, et al. Methods of multilocus enzyme electrophoresis for bacterial population genetics and systematics. Appl Environ Microbiol. 1986;51:837–884. PubMed PMC
Achtman M, et al. Microevolution and history of the plague bacillus, Yersinia pestis. Proc Natl Acad Sci USA. 2004;101:17837–17842. PubMed PMC
Kidgell C, et al. Salmonella typhi, the causative agent of typhoid fever, is approximately 50,000 years old. Infect Genet Evol. 2002;2:39–45. PubMed
Falush D, et al. Recombination and mutation during long-term gastric colonization by Helicobacter pylori: Estimates of clock rates, recombination size, and minimal age. Proc Natl Acad Sci USA. 2001;98:15056–15061. PubMed PMC
Maynard Smith J, Feil EJ, Smith NH. Population structure and evolutionary dynamics of pathogenic bacteria. BioEssays. 2000;22:1115–1122. PubMed
Feil EJ, Spratt BG. Recombination and the population structures of bacterial pathogens. Annu Rev Microbiol. 2001;55:561–590. PubMed
Caugant DA, et al. Intercontinental spread of a genetically distinctive complex of clones of Neisseria meningitidis causing epidemic disease. Proc Natl Acad Sci USA. 1986;83:4927–4931. PubMed PMC
Maynard Smith J, Smith NH, O'Rourke M, Spratt BG. How clonal are bacteria? Proc Natl Acad Sci USA. 1993;90:4384–4388. PubMed PMC
Olyhoek T, Crowe BA, Achtman M. Clonal population structure of Neisseria meningitidis serogroup A isolated from epidemics and pandemics between 1915 and 1983. Rev Infect Dis. 1987;9:665–682. PubMed
Jolley KA, Wilson DJ, Kriz P, McVean G, Maiden MC. The influence of mutation, recombination, population history, and selection on patterns of genetic diversity in Neisseria meningitidis. Mol Biol Evol. 2005;22:562–569. PubMed
Yazdankhah SP, et al. Distribution of serogroups and genotypes among disease-associated and carried isolates of Neisseria meningitidis from the Czech Republic, Greece, and Norway. J Clin Microbiol. 2004;42:5146–5153. PubMed PMC
Maiden MC. Dynamics of bacterial carriage and disease: Lessons from the meningococcus. Adv Exp Med Biol. 2004;549:23–29. PubMed
Maiden MCJ, et al. Multilocus sequence typing: A portable approach to the identification of clones within populations of pathogenic microorganisms. Proc Natl Acad Sci USA. 1998;95:3140–3145. PubMed PMC
Russell JE, Jolley KA, Feavers IM, Maiden MC, Suker J. PorA variable regions of Neisseria meningitidis. Emerg Infect Dis. 2004;10:674–678. PubMed PMC
Levin BR. Periodic selection, infectious gene exchange, and the genetic structure of E coli populations. Genetics. 1981;99:1–23. PubMed PMC
Fraser C, Hanage WP, Spratt BG. Neutral microepidemic evolution of bacterial pathogens. Proc Natl Acad Sci USA. 2005;102:1968–1973. PubMed PMC
Levin S, Pimentel D. Selection of intermediate rates of increase in parasite-host systems. Am Nat. 1981;117:308–315.
Anderson RM, May RM. Infectious Diseases of Humans. Oxford: Oxford Univ Press; 1991.
Selander RK, Levin BR. Genetic diversity and structure in Escherichia coli populations. Science. 1980;210:545–547. PubMed
Maynard Smith J, Dowson CG, Spratt BG. Localized sex in bacteria. Nature. 1991;349:29–31. PubMed
Caugant DA. Population genetics and molecular epidemiology of Neisseria meningitidis. APMIS. 1998;106:505–525. PubMed
Zhu P, et al. Fit genotypes and escape variants of subgroup III Neisseria meningitidis during three pandemics of epidemic meningitis. Proc Natl Acad Sci USA. 2001;98:5234–5239. PubMed PMC
Enright MC, et al. The evolutionary history of methicillin-resistant Staphylococcus aureus (MRSA) Proc Natl Acad Sci USA. 2002;99:7687–7692. PubMed PMC
Feil EJ, et al. Recombination within natural populations of pathogenic bacteria: Short-term empirical estimates and long-term phylogenetic consequences. Proc Natl Acad Sci USA. 2001;98:182–187. PubMed PMC
Achtman M, et al. Molecular epidemiology of serogroup a meningitis in Moscow, 1969 to 1997. Emerg Infect Dis. 2001;7:420–427. PubMed PMC
Noirot P, Noirot-Gros MF. Protein interaction networks in bacteria. Curr Opin Microbiol. 2004;7:505–512. PubMed
Fraser HB, Hirsh AE, Steinmetz LM, Scharfe C, Feldman MW. Evolutionary rate in the protein interaction network. Science. 2002;296:750–752. PubMed
Jolley KA, et al. Carried meningococci in the Czech Republic: A diverse recombining population. J Clin Microbiol. 2000;38:4492–4498. PubMed PMC
Claus H, Maiden MC, Maag R, Frosch M, Vogel U. Many carried meningococci lack the genes required for capsule synthesis and transport. Microbiology. 2002;148:1813–1819. PubMed
Stollenwerk N, Maiden MC, Jansen VA. Diversity in pathogenicity can cause outbreaks of meningococcal disease. Proc Natl Acad Sci USA. 2004;101:10229–10234. PubMed PMC
Gupta S, et al. The maintenance of strain structure in populations of recombining infectious agents. Nat Med. 1996;2:437–442. PubMed
Urwin R, et al. Distribution of surface protein variants among hyperinvasive meningococci: Implications for vaccine design. Infect Immun. 2004;72:5955–5962. PubMed PMC
Bygraves JA, et al. Population genetic and evolutionary approaches to the analysis of Neisseria meningitidis isolates belonging to the ET-5 complex. J Bacteriol. 1999;181:5551–5556. PubMed PMC
Bentley SD, Parkhill J. Comparative genomic structure of prokaryotes. Annu Rev Genet. 2004;38:771–792. PubMed
Jolley KA, Chan MS, Maiden MC. mlstdbNet: Distributed multi-locus sequence typing (MLST) databases. BMC Bioinformatics. 2004;5:86. PubMed PMC
Buckee CO, Koelle K, Mustard MJ, Gupta S. The effects of host contact network structure on pathogen diversity and strain structure. Proc Natl Acad Sci USA. 2004;101:10839–10844. PubMed PMC
Frosch M, Maiden MC. In: Handbook of Meningococcal Disease. Frosch M, Maiden MC, editors. Weinheim, Germany: Wiley-VCH; 2006. p. 21.
Blower SM, Dowlatabadi H. Sensitivity and uncertainty analysis of complex models of disease transmission: An HIV model, as an example. Int Stat Rev. 1994;2:229–243.
Long-term evolution of antigen repertoires among carried meningococci