Point mutation in meningococcal por A gene associated with increased endemic disease
Point mutation in meningococcal por A gene associated with increased endemic disease
The por A gene, which encodes expression of meningococcal class 1 outer membrane protein, responsible for antigenic subtype specificity, has been cloned and sequenced in an isolate of Neisseria meningitidis (B:15:P1.7,16) from a patient in the Gloucester area with meningococcal meningitis. Comparison of the sequence with that of the equivalent gene from the P1.7,16 reference strain reveals a point mutation which generates a single aminoacid change in the epitope responsible for P1.16 specificity. Monoclonal antibodies with P1.16 specificity do not react with synthetic peptides that correspond to the altered epitope, and do not promote complement-mediated bactericidal killing of the isolate. Analysis of other strains shows widespread distribution of infections due to B:15:P1.7,16 meningococci with the altered epitope (P1.16b) in England and Wales.
514-517
McGuinness, B.T.
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Clarke, I.N.
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Lambden, P.R.
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Barlow, A.K.
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Heckels, J.E.
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Poolman, J.T.
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Jones, D.M.
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2 March 1991
McGuinness, B.T.
3ef40ca0-9030-4f82-a986-91bee018e346
Clarke, I.N.
ff6c9324-3547-4039-bb2c-10c0b3327a8b
Lambden, P.R.
e99ecc21-50d7-4a43-9e79-efba46592c77
Barlow, A.K.
37084842-5493-4cf1-8405-1d452aa51336
Heckels, J.E.
fcfcfafe-5ca8-4728-9c5e-cb67f9af7e31
Poolman, J.T.
3de9d9d4-1719-49c2-aa3d-65605032761a
Jones, D.M.
8387aaf0-0b0e-401a-af8c-743b96f52d73
McGuinness, B.T., Clarke, I.N., Lambden, P.R., Barlow, A.K., Heckels, J.E., Poolman, J.T. and Jones, D.M.
(1991)
Point mutation in meningococcal por A gene associated with increased endemic disease.
The Lancet, 337 (8740), .
(doi:10.1016/0140-6736(91)91297-8).
(PMID:1705642)
Abstract
The por A gene, which encodes expression of meningococcal class 1 outer membrane protein, responsible for antigenic subtype specificity, has been cloned and sequenced in an isolate of Neisseria meningitidis (B:15:P1.7,16) from a patient in the Gloucester area with meningococcal meningitis. Comparison of the sequence with that of the equivalent gene from the P1.7,16 reference strain reveals a point mutation which generates a single aminoacid change in the epitope responsible for P1.16 specificity. Monoclonal antibodies with P1.16 specificity do not react with synthetic peptides that correspond to the altered epitope, and do not promote complement-mediated bactericidal killing of the isolate. Analysis of other strains shows widespread distribution of infections due to B:15:P1.7,16 meningococci with the altered epitope (P1.16b) in England and Wales.
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Published date: 2 March 1991
Organisations:
Faculty of Medicine
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Local EPrints ID: 352640
URI: http://eprints.soton.ac.uk/id/eprint/352640
ISSN: 0140-6736
PURE UUID: 8a560939-4e36-49e4-ae5e-2e81b5d2855d
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Date deposited: 04 Jun 2013 12:37
Last modified: 15 Mar 2024 02:33
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Author:
B.T. McGuinness
Author:
P.R. Lambden
Author:
A.K. Barlow
Author:
J.T. Poolman
Author:
D.M. Jones
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