Can site-directed mutagenesis eliminate autoimmunity arising from molecular mimicry?

One proposed mechanism of pathogenic retroviral infection involves autoimmunity. Molecular mimicry may occur between viral and host proteins which share sequence homologies. Immune processing of antigenic peptides can result in the generation of cross-reactive antibodies capable of binding to host tissues. Thus, it appears the immune system can inadvertently initiate an attack upon the host due to genetic similarities between non-self and self. Site-directed mutagenesis is a tool of molecular biology often utilized to induce genetic changes in a microbe of interest. Since retroviral etiology may possess an autoimmune component, it seems plausible to utilize site-directed mutagenesis to genetically shape the retroviral genome. Retroviruses possess a DNA intermediate in their lifecycle, allowing the problem of retroviral infection to be addressed as a genetic disorder of the host. Detrimental autoimmune responses associated with retroviral pathology might be ameliorated by shaping the genetic source of their existence.