Whole-genome DNA array analysis of the response of Borrelia
burgdorferi to a bactericidal monoclonal antibody.

    Anderton JM, Tokarz R, Thill CD, Kuhlow CJ, Brooks CS, Akins DR,
Katona LI, Benach JL.

    Center for Infectious Diseases and Department of Molecular Genetics
and Microbiology, Stony Brook University, Stony Brook, New York 11794,
USA.

    Identification and characterization of genes that contribute to
infection with Borrelia burgdorferi and, of those, genes that are
targets of host responses is important for understanding the
pathogenesis of Lyme disease. The complement-independent bactericidal
monoclonal antibody (MAb) CB2 recognizes a carboxy-terminal,
hydrophilic epitope of the outer surface protein B (OspB). CB2 kills B.
burgdorferi by an unknown bactericidal mechanism. Upon binding of CB2
to OspB, differentially expressed gene products may be responsible for,
or associated with, the death of the organism. A time course of the
response of B. burgdorferi to CB2 was completed to analyze the
differential gene expression in the bacteria over a period of visual
morphological changes. Bacteria were treated with a sublethal
concentration in which spirochetes were visibly distressed by the
antibody but not lysed. Preliminary whole-genome DNA arrays at various
time points within 1 h of incubation of B. burgdorferi with the
antibody showed that most significant changes occurred at 25 min.
Circular plasmid 32 (cp32)-encoded genes were active in this period of
time, including the blyA homologs, phage holin system genes. DNA array
data show that three blyA homologs were upregulated significantly,

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