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Antigen polymorphism in Borrelia hermsii, a clonal pathogenic bacterium
S M Rich1, S A Sawyer, A G Barbour
1Division of Infectious Diseases, Tufts University School of Veterinary Medicine, 200 Westboro Road, North Grafton, MA 01536, USA. stephen.rich@tufts.edu
Summary
Borrelia hermsii evades immune detection by switching surface lipoproteins. This immune evasion is driven by recombination within the vsp gene family, creating significant antigenic diversity.
Area of Science:
- Microbiology
- Immunology
- Evolutionary Biology
Background:
- Relapsing fever spirochetes like Borrelia hermsii evade immune responses by altering surface lipoprotein expression.
- This immune evasion mechanism involves duplicative transposition of surface lipoprotein-encoding genes into a single expression site.
- A large gene family encodes these lipoproteins, with some diversity predating major Borrelia species divergences.
Purpose of the Study:
- To investigate the evolutionary mechanisms driving diversification within the vsp (variable surface protein) gene subfamily of Borrelia hermsii.
- To understand how recombination and immune selection contribute to the antigenic diversity of vsp alleles.
Main Methods:
- Sequencing of over 90% of vsp alleles within the Borrelia hermsii strain HS1.
- Analysis of allelic mosaicism to infer recombination events.
- Assessment of amino acid differentiation to quantify serotype variation.
Main Results:
- A high degree of allelic mosaicism was observed within the vsp gene family.
- Intragenic recombination, influenced by host immune selection, appears to be the primary driver of vsp allele diversification.
- Recombinational diversification resulted in significant amino acid changes (30-40%), sufficient to overcome antibody cross-reactivity.
Conclusions:
- The evolution of the vsp gene family in Borrelia hermsii is characterized by punctuated events of allelic differentiation.
- This diversification strategy allows the spirochete to effectively evade host immune responses.
- Evolutionary diversification is driven by recombination rather than gradual accumulation of point mutations.