The spirochete Borrelia burgdorferi is the causative agent of Lyme disease, a multisystem disorder that can cause a variety of disorders in susceptible mammalian hosts. The immune response of infected mammals, including humans, is ineffective in clearing B. burgdorferi as demonstrated by the ability to reisolate the spirochete from naturally and experimentally infected hosts after extended periods of time. Recent evidence suggests that this pathogen evades the immune response in part through changes in antigenic reactivity.The purpose of this study was to determine if outer surface protein A (OspA) of B. burqdorferi varies in the course of infection in Syrian hamsters and thus potentially plays a role in evading the host immune response. To assess the degree of change, differences in the binding of a murine monoclonal antibody (H5332) were measured using IFA and ELISA techniques over a 9-week period of time.Results of this study suggest that OspA is persistently expressed in infected Syrian hamsters for at least 9-weeks. Moreover, this protein, or at least the epitope that H5332 binds with, is stably expressed. These results indicate OspA, or at least the epitope of OspA that I probed, does not appear to contribute to the evasive mechanisms of 8. burgdorferi in Syrian hamsters. / Department of Biology
| Identifer | oai:union.ndltd.org:BSU/oai:cardinalscholar.bsu.edu:handle/184420 |
| Date | January 1992 |
| Creators | Mummert, Mark E. |
| Contributors | Pinger, Robert R. |
| Source Sets | Ball State University |
| Detected Language | English |
| Format | vi, 54 leaves ; 28 cm. |
| Source | Virtual Press |
Page generated in 0.002 seconds