Send to

Choose Destination
Int J Med Microbiol. 2006 May;296 Suppl 40:185-94. Epub 2006 Mar 10.

Borrelia burgdorferi erp genes are expressed at different levels within tissues of chronically infected mammalian hosts.

Author information

Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, MS 415 Chandler Medical Center, Lexington, KY 40536-0298, USA.


The spirochete Borrelia burgdorferi is the causative agent of Lyme disease and is transmitted to humans and other vertebrate hosts through the bites of ixodid ticks. B. burgdorferi Erp (OspE-F related lipoprotein) family members are encoded on members of the 32 kb circular plasmid-like prophage family (cp32s). Many Erp proteins serve as receptors for the complement inhibitory factor H molecules of numerous vertebrate hosts, providing one mechanism by which the bacteria potentially evade the innate immune system. Indirect immunofluorescence analyses (IFA) have demonstrated that Erp expression is temporally regulated throughout the mammal-tick infectious cycle, indicating that Erp proteins perform an important role (or even roles) during mammalian infection. However, it was not previously known whether Erp proteins are continually produced by B. burgdorferi throughout the course of mammalian infection. To address this issue, quantitative RT-PCR (q-RT-PCR) was utilized to assess erp transcription levels by bacteria within numerous different tissues of both mice and non-human primates (NHPs) chronically infected with B. burgdorferi. Q-RT-PCR results obtained using both animal models indicated that while the majority of erp genes were detectably transcribed during chronic infection, differences in expression levels were noted. These data strongly suggest that Erp proteins contribute to B. burgdorferi persistence within chronically infected host tissues, perhaps by protecting the bacteria from complement-mediated killing.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center