William C. Nierman1, David DeShazer1, Masayuki Machida1, Hervé Tettelin1, William Nelson1, Tamara V. Feldblyum1, Ricky L. Ulrich1, Catherine M. Ronning1, Lauren Brinkac1, Sean C. Daugherty1, Tanja Davidsen1, Robert T. DeBoy1, George Dimitrov1, Robert J. Dodson1, A. Scott Durkin1, Michelle Gwinn1, Daniel H. Haft1, Hoda Khouri1, James F. Kolonay1, Ramana Madupu1, Yasmin Mohammoud1, Diana Radune1, Claudia Mabel Terenti Romero1, Saul Sarria1, Jeremy Selengut1, Christine Shamblin1, Steven A. Sullivan1, Owen White1, Yan Yu1, Nikhat Zafar1, Li‐Wei Zhou1, Claire M. Fraser1,2
1Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850; Departments of Biochemistry and Molecular Biology, Pharmacology, and Microbiology and Tropical Medicine, George Washington University School of Medicine, 2300 Eye Street NW, Washington, DC 20037; and U.S. Army Medical Research Institute for Infectious Diseases, 1425 Porter Street, Fort Detrick, MD 21702-5011
2J. Craig Venter Institute
Tóm tắt
The complete genome sequence of
Burkholderia mallei
ATCC 23344 provides insight into this highly infectious bacterium's pathogenicity and evolutionary history.
B. mallei
, the etiologic agent of glanders, has come under renewed scientific investigation as a result of recent concerns about its past and potential future use as a biological weapon. Genome analysis identified a number of putative virulence factors whose function was supported by comparative genome hybridization and expression profiling of the bacterium in hamster liver
in vivo
. The genome contains numerous insertion sequence elements that have mediated extensive deletions and rearrangements of the genome relative to
Burkholderia pseudomallei
. The genome also contains a vast number (>12,000) of simple sequence repeats. Variation in simple sequence repeats in key genes can provide a mechanism for generating antigenic variation that may account for the mammalian host's inability to mount a durable adaptive immune response to a
B. mallei
infection.
