Over the past 30 years, organ transplantation has evolved from an interesting experiment in human immunobiology to the most practical means of rehabilitating patients with end-stage dysfunction.1 At the same time, the requirement for chronic antirejection therapy, the presence of chronic or relapsing viral infection, and environmental exposures to a variety of opportunistic pathogens, have created a pathophysiological state and set of vulnerabilities rarely seen before.2,3 It has been estimated that 75% or more of organ transplant patients will have evidence of microbial replication and invasion in the first year posttransplant.4- 6 Several principles have emerged from this experience.
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