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Lyme disease is a tick-transmitted
disease caused by the spirochete Borrelia burgdorferi. The bacterium adopts different strategies for its survival inside the immunocompetent host from the time of infection until dissemination in different parts of body tissues. The success of this spirochete depends on its ability to colonise the host tissues and counteract the host’s defence mechanisms. During this process borrelia seems to maintain its vitality to ensure long-term survival in the host. Borrelia’s proteins are encoded by plasmid and chromosomal genes. These genes are differentially regulated and expressed by different environmental factors in ticks as well as in the mammalian host during infection. In addition, antigenic diversity enables the spirochete to escape host defence mechanisms and maintain infection. In this review we focus on the differential expression of proteins and genes, and further molecular mechanisms used by borrelia to maintain its survival in the host. In light of these pathogenetic mechanisms, further studies on spirochete host interaction are needed to understand the complex interplay that finally lead to host autoimmunity.