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ABSTRACT Infection with Borrelia burgdorferi often triggers pathophysiologic perturbations that are further augmented by the inflammatory responses of the host, resulting in the severe clinical conditions of Lyme disease

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Thus, disruption of the gene encoding either of these -type TrxRs is compensated by a partial re-distribution of product from the other gene into the deficient sub-cellular compartment (Meyer et al., 2008

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