Abstract
Evidence is reviewed which suggests that the sharing of antigens by parasite and host (molecular mimicry) is of common occurrence. Antigenic determinants of parasite origin which resemble those of their hosts and thus do not elicit antibody production are named eclipsed antigens. It is suggested that eclipsed antigens have arisen as the result of mutation and selection operating upon fortuitously similar antigens of the partners of an incipient host-parasite association. Consequences of molecular mimicry to the host are discussed. Autoimmunity is rejected on evolutionary and immunological grounds, and it is suggested that host antigenic polymorphism (e.g. blood groups) could have evolved as a host defense mechanism. Ways in which tills may have occurred are discussed. The heterosis model is shown to be inadequate. An alternative explanation, based on eclipsed antigens, is presented; namely, that the blood group genes could be maintained in a balanced polymorphic state by changes in selection pressure and direction dependent upon gene frequency. The selective agents would be parasites with antigens eclipsed by the blood group antigens. Differences in blood group frequencies among different races could be the result of different parasite environments in the various centers of racial development. Convergent molecular evolution among parasites adapted to the same hosts could occur and evidence in support of this conclusion is reviewed.