Tuesday, May 18, 2010, 11:00 am — John Dunn Seminar Room, Bldg. 463
Lyme disease is the most common vector-borne disease in the United States and is caused by the spirochete Borrelia burgdorferi, a bacterium transmitted by Ixodes ticks. The disease is a serious multisystem infection, with inflammatory complications commonly affecting the skin, joints, and central nervous system in humans. There is currently no vaccine available, no infection-induced protective immunity, varying information on antibiotic efficacy in late stages, no agreed upon diagnostic tests, and no 100% diagnostic clinical signs. Only recently have the Borrelia biology, genetics and molecular pathogenesis begun to become accessible to experimentation, stimulated by the sequencing and analysis of the first Borrelia genome sequence, that of the Borrelia burgdorferi strain B31, in 1997. The Borrelia B31 genome was found to be very unusual, comprised of one 910 Kbp linear chromosome and twenty-one (twelve linear and nine circular) plasmids that contain over 600 Kbp of sequence. We have since then completed the whole-genome sequence of the B. burgdorferi phenotypic variants JD1, N40, and 297, as well as that of 17 strains of Borrelia species that span the range of the Lyme agents' natural variation and include several non-Lyme relatives. Strains were chosen to include both closely and distantly-related Borrelia species, as well as strains that differ greatly in virulence and that were gathered from human cases in the USA and abroad. The overall objective of our comprehensive comparative genomics strategy is to develop a robust, genome-wide picture of Lyme agent diversity with the ultimate aim to understand how variations in sequence lead to variations in pathogenicity. My presentation will highlight the initial findings of our comparative study, which include the description of the Borrelia pangenome, and the implications of the Borrelia genome diversity in the pathogenicity and evolution of the Lyme agent.
Hosted by: John Dunn
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