Mimicry by Virus of Host Molecules: Implications for Autoimmune Disease

Molecular mimicry defines the shared identity of molecules from disparate genes or proteins. Thus, although their origins are as separate as a virus and the self-determinant of a human or lower animal, two molecules' linear amino acid sequences or their conformational fits may be shared. Such molecular homologies between proteins occur frequently and likely play roles in the processing of viral proteins inside cells. The homologies shared between viruses and host cytoskeletal proteins likely indicate that shared determinants on cell linker proteins guided viral proteins along highways and stop points inside cells. Most importantly, these unexpected cross-reactivities have broad and major implications for understanding autoimmune disease. Molecular mimicry is detected either by using humoral or cellular immune components, that cross-react with two presumably unrelated protein structures, or by computer searches to match descriptions of proteins in storage banks. The use of both these approaches to define molecular mimicry and establish its potential role in autoimmune disease is the topic of this chapter.