Surface protein variation by expression site switching in the relapsing fever agent Borrelia hermsii
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Updated: Oct 10, 2026
Immuno-fluorescence Assay of Leptospiral Surface-exposed Proteins
Published on: July 1, 2011
A G Barbour1, C J Carter, C D Sohaskey
1Department of Microbiology & Molecular Genetics and Medicine, University of California-Irvine, Irvine, California 92697, USA. abarbour@uci.edu
Abstract:
Borrelia hermsii, an agent of relapsing fever, undergoes antigenic variation of serotype-specifying membrane proteins during mammalian infections. When B. hermsii is cultivated in broth medium, one serotype, 33, eventually predominates in the population. Serotype 33 has also been found to be dominant in ticks but not in mammalian hosts. We investigated the biology and genetics of two independently derived clonal populations of serotype 33 of B. hermsii. Both isolates infected immunodeficient mice, but serotype 33 cells were limited in number and were only transiently present in the blood. Probes for vsp33, which encodes the serotype-specifying Vsp33 outer membrane protein, revealed that the gene was located on a 53-kb linear plasmid and that there was only one locus for the gene in serotype 33. The vsp33 probe and probes for other variable membrane protein genes showed that expression of Vsp33 was determined at the level of transcription and that when the vsp33 expression site was active, an expression site for other variable proteins was silent. The study confirmed that serotype 33 is distinct from other serotypes of B. hermsii in its biology and demonstrated that B. hermsii can change its major surface protein through switching between two expression sites.
Insights
Borrelia hermsii, a relapsing fever agent, switches its major surface protein (Vsp33) via transcriptional control. This study reveals serotype 33
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Borrelia hermsii causes relapsing fever and exhibits antigenic variation of its surface proteins.
- Serotype 33 of B. hermsii predominates in vitro and in ticks but is transient in mammalian hosts.
- The mechanisms underlying serotype 33's biology and surface protein expression remain unclear.
Purpose of the Study:
- To investigate the biology and genetics of two clonal populations of Borrelia hermsii serotype 33.
- To elucidate the genetic basis and regulation of Vsp33 outer membrane protein expression.
- To understand the role of antigenic variation in B. hermsii infections.
Main Methods:
- Infection of immunodeficient mice with serotype 33 B. hermsii isolates.
- Gene mapping using probes for vsp33 and other variable membrane protein genes.
- Analysis of gene expression at the transcriptional level.
Main Results:
- Serotype 33 B. hermsii infected mice but cells were transient in blood.
- The vsp33 gene, encoding the Vsp33 protein, is located on a 53-kb linear plasmid.
- Vsp33 expression is regulated transcriptionally, with mutually exclusive expression of vsp33 and other variable protein genes.
Conclusions:
- Serotype 33 is biologically distinct, with transient presence in mammalian hosts.
- Borrelia hermsii switches its major surface protein by alternating between two expression sites.
- Transcriptional control governs the expression of variable membrane proteins in B. hermsii.
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