The Borrelia are the causative agents of several important human and animal infections including Lyme disease and relapsing fever. Recent studies from our lab and others have demonstrated that some species of the Lyme disease spirochetes bind the complement regulatory protein, factor H (fH). FH bound on the cell surface is able to interact with factor I and facilitate the efficient cleavage of the critical complement component C3b. In the context of bacterial pathogenesis, this cleavage event serves to protect the bacteria from opsonization and the alternate complement cascade. The relapsing fever spirochetes (RFS) are able to persist in their mammalian hosts for extended periods of time. Some species achieve high cell densities in the blood while others tend to invade the CNS. The ability to survive in the blood suggests that these bacteria are also able to circumvent complement. We have recently identified and characterized a new and novel fH binding protein (FHBP) in B. hermsii that we call FhbA (fH-binding protein A). In this proposal we will investigate the molecular interactions between FhbA and human fH and investigate the contribution of FhbA in pathogenesis through gene inactivation.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
1F31NS048769-01A1
Application #
6940966
Study Section
Special Emphasis Panel (ZRG1-F08 (20))
Program Officer
Nunn, Michael
Project Start
2005-04-25
Project End
2007-04-24
Budget Start
2005-04-25
Budget End
2006-04-23
Support Year
1
Fiscal Year
2005
Total Cost
$30,709
Indirect Cost
Name
Virginia Commonwealth University
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
105300446
City
Richmond
State
VA
Country
United States
Zip Code
23298