Chronic infection as a major force in the evolution of the suppressor T-cell system

Abstract

This chapter focuses on molecular mimicry. Molecular mimicry has been defined in several different ways. The first formal definition states that molecular mimicry is the sharing of antigenic determinants between a parasite and its host. The term “adaptive mimicry” is essentially self-explanatory and means that a parasite molecule mimics a host molecule for a biological reason. The term “consequential mimicry” does not imply (but equally does not exclude) any adaptive force behind the observations of shared structures. Examples of molecular mimicry are now manifold and found in viruses, bacteria, protozoa, and helminthes. Molecular mimicry is a real phenomenon with definite consequences for host and parasite. The existence of molecular mimicry offers a mechanistic explanation for the occurrence of a plethora of autoimmune syndromes associated with microbial infection. The number and range of examples of this phenomenon is now large, although the evidence for a direct causal association is lacking in most cases. However, in some model syndromes the autoimmune basis has been established, and this is also been verified for Chagas' disease. Much work remains to be done in both the fields of adaptive and consequential mimicry. In the adaptive sphere, the emphasis must be to obtain a conclusive proof of function for the mimicked structure. The consequentialists are required to establish causation of disease by mimicry.