Please use this identifier to cite or link to this item:
|Title:||Genomic Analysis of Serogroup Y Neisseria meningitidis Isolates Reveals Extensive Similarities Between Carriage and Disease-Associated Organisms|
|Authors:||Oldfield, N. J.|
Harrison, O. B.
Bayliss, Christopher David
Maiden, M. C.
Ala'Aldeen, D. A.
Turner, D. P.
|Publisher:||Oxford University Press (OUP)|
|Citation:||Journal of Infectious Diseases, 2016 (Online First)|
|Abstract:||BACKGROUND: Neisseria meningitidis is a frequent colonizer of the human nasopharynx with asymptomatic carriage providing the reservoir for invasive, disease-causing strains. Serogroup Y (MenY) strains are a major cause of meningococcal disease. High resolution genetic analyses of carriage and disease isolates can establish epidemiological relationships and identify potential virulence factors. METHODS: Whole genome sequence data were obtained from UK MenY carriage isolates from 1997-2010 (n=99). Sequences were compared to those from MenY invasive isolates from 2010 and 2011 (n=73) using a gene-by-gene approach. RESULTS: Comparisons across 1,605 core genes resolved 91% of isolates into one of eight clusters containing closely related disease and carriage isolates. Six clusters contained carried meningococci isolated in 1997-2001 suggesting temporal stability. One cluster of isolates, predominately sharing the designation Y: P1.5-1,10-1: F4-1: ST-1655 (cc23), was resolved into a sub-cluster with 86% carriage isolates and a second with 90% invasive isolates. These sub-clusters were defined by specific allelic differences in five core genes encoding glycerate kinase (glxK), valine-pyruvate transaminase (avtA), superoxide dismutase (sodB) and two hypothetical proteins. CONCLUSIONS: High resolution genetic analyses detected long-term temporal stability and temporally-overlapping carriage and disease populations for MenY clones but also evidence of a disease-associated clone.|
|Embargo on file until:||7-Jan-2017|
|Rights:||Copyright © The Author 2016. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail email@example.com. This is a pre-copyedited, author-produced PDF of an article accepted for publication in Journal of Infectious Diseases following peer review. The version of record J Infect Dis. (2016) doi: 10.1093/infdis/jiw008 is available online at: dx.doi.org/10.1093/infdis/jiw008|
|Description:||The file associated with this record is under a 12-month embargo from publication in accordance with the publisher's self-archiving policy. The full text may be available through the publisher links provided above.|
|Appears in Collections:||Published Articles, Dept. of Genetics|
Files in This Item:
|Oldfield et al_J Infect Dis_v5.docx||Post-review (final submitted)||157.67 kB||Unknown||View/Open|
|Oldfield et al_J Infect Dis_v5.pdf||Post-review (final submitted)||377.32 kB||Adobe PDF||View/Open|
Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.