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http://www.blackwell-synergy.com/doi/full/10.1111/j.1365-2958.2006.05204.x
Mol Microbiol. 2006 Jun;60(6):1319-22.
Comment on:
Mol Microbiol. 2006 Jun;60(6):1329-43.
Antigenic variation with a twist--the Borrelia story.
* Norris SJ.
Department of Pathology. University of Texas Medical School at
Houston, PO Box 20708, Houston, TX 77225-0708, USA.
Steven....@uth.tmc.edu
A common mechanism of immune evasion in pathogenic bacteria and
protozoa is antigenic variation, in which genetic or epigenetic changes
result in rapid, sequential shifts in a surface-exposed antigen. In this
issue of Molecular Microbiology, Dai et al. provide the most complete description to date of the vlp/vsp antigenic variation system of the
relapsing fever spirochaete, Borrelia hermsii. This elaborate,
plasmid-encoded system involves an expression site that can acquire
either variable large protein (vlp) or variable small protein (vsp)
surface lipoprotein genes from 59 different archival copies. The
archival vlp and vsp genes are arranged in clusters on at least five
different plasmids. Gene conversion occurs through recombination events
at upstream homology sequences (UHS) found in each gene copy, and at
downstream homology sequences (DHS) found periodically among the vlp/vsp archival genes. Previous studies have shown that antigenic variation in relapsing fever Borrelia not only permits the evasion of host antibody responses, but can also result in changes in neurotropism and other
pathogenic properties. The vlsE antigenic variation locus of Lyme
disease spirochaetes, although similar in sequence to the relapsing
fever vlp genes, has evolved a completely different antigenic variation mechanism involving segmental recombination from a contiguous array of
vls silent cassettes. These two systems thus appear to represent
divergence from a common precursor followed by functional convergence to
create two distinct antigenic variation processes.
PMID: 16796669 [PubMed - indexed for MEDLINE]
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