Invasive Meningococcal Capsular Group Y Disease, England and Wales, 2007–2009
Shamez N. Ladhani , Jay Lucidarme, Lynne S. Newbold, Stephen J. Gray, Anthony D. Carr, Jamie Findlow, Mary E. Ramsay, Edward B. Kaczmarski, and Raymond Borrow
Author affiliations: Health Protection Agency, London, UK (S.N. Ladhani, M.E. Ramsay); Health Protection Agency, Manchester, UK (J. Lucidarme, L.S. Newbold, S.J. Gray, A.D. Carr, J. Findlow, E.B. Kaczmarski, R. Borrow); University of Manchester, Manchester (R. Borrow)
Figure 2. Newly identified lpxL1 mutations XV, XVI, and XVII. lpxL1 sequence data from isolates harboring each of the corresponding meningococcal capsular group Y mutations (in parentheses), England and Wales. Mutations are aligned with the full-length gene from strain MC58. All of the alleles share a common start codon (green arrow). Mutations and stop codons are denoted by red circles and red lines, respectively. Mutation XVI is a single-base deletion at nt A4 that causes a frame shift resulting in a premature stop codon at nt 74. Mutation XVII is a single base deletion at nt T813. This causes a frame shift resulting in a late stop codon at nt 919. Mutation XV is a polymorphism at the region of the prototypical stop codon (that of strain MC58). In affected isolates, 3 adenines occupy the site that comprises the stop codon, TGA, in MC58. The next available stop codon occurs 15 bp downstream. The encoded peptide has an additional 6 aa.
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