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Pathogen escape from host immunity by a genome program for antigenic variation.

Alan G Barbour1, Qiyuan Dai, Blanca I Restrepo

  • 1Department of Microbiology, University of California, Irvine, CA 92697-4028, USA. abarbour@uci.edu

Proceedings of the National Academy of Sciences of the United States of America
|November 15, 2006
PubMed
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Borrelia hermsii, a relapsing fever bacterium, modulates antigenic variation switch rates using genomic elements near genes. This controls immune evasion and transmission, creating a predictable variant order within hosts.

Area of Science:

  • Microbiology
  • Genetics
  • Immunology

Background:

  • Borrelia hermsii causes relapsing fever through antigenic variation of surface proteins.
  • Antigenic variation enables immune evasion and transmission, similar to systems in trypanosomes and Plasmodium falciparum.
  • Switch rates to different variants vary widely in these organisms.

Purpose of the Study:

  • To investigate the genomic mechanisms determining Borrelia hermsii antigenic variation switch rates.
  • To identify specific genetic elements that regulate the frequency of switching between antigenic variants.

Main Methods:

  • Studied switch rates in B. hermsii using experimental infections.
  • Identified variants by specific antisera and DNA sequencing.
  • Analyzed extragenic features of silent loci and their relationship to the expression site.

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Main Results:

  • Switch rates are determined by extragenic features of silent loci, not coding sequence similarity.
  • Two sets of elements regulate switch rates: 5' overlapping elements and 3' flanking elements.
  • Sequence identity at 5' elements and proximity of 3' elements correlate with higher switch rates.

Conclusions:

  • Genomic elements create a hierarchy of switch rates for silent loci.
  • This mechanism allows B. hermsii to modulate antigenic variation.
  • While cellular switching is stochastic, variant ordering within hosts is semi-predictable, aiding immune escape and transmission.