Powell P D
Med Hypotheses. 1998 May;50(5):399-407. doi: 10.1016/s0306-9877(98)90212-2.
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.
一种关于致病性逆转录病毒感染的机制涉及自身免疫。病毒蛋白和宿主蛋白之间可能会发生分子模拟，它们具有序列同源性。抗原肽的免疫加工可导致产生能够结合宿主组织的交叉反应性抗体。因此，由于非自身与自身之间的遗传相似性，免疫系统似乎可能会无意中对宿主发起攻击。定点诱变是分子生物学中一种常用于诱导感兴趣微生物发生基因变化的工具。由于逆转录病毒病因可能具有自身免疫成分，利用定点诱变对逆转录病毒基因组进行基因改造似乎是合理的。逆转录病毒在其生命周期中具有DNA中间体，这使得逆转录病毒感染问题可作为宿主的一种基因疾病来解决。通过改变导致有害自身免疫反应的遗传根源，可能会改善与逆转录病毒病理学相关的有害自身免疫反应。
