Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29425-2230, USA.
J Alzheimers Dis. 2009;17(4):753-6. doi: 10.3233/JAD-2009-1094.
There is growing body of evidence for the involvement of herpes simplex virus type 1 (HSV1) in the etiology of Alzheimer's disease (AD). HSV1 has evolved strategies for decreasing the efficacy of the host immune response and interfering with viral clearance. Based on their putative role as the modulators of these immune avoidance strategies, I hypothesize that immunoglobulin (Ig) GM genes - genetic markers of IgG heavy chains located on chromosome 14 - are functional risk and protective factors for AD. Results from genome-wide association and linkage studies in support of this hypothesis, testable predictions, and possible therapeutic implications are discussed.
越来越多的证据表明,单纯疱疹病毒 1 型(HSV1)参与了阿尔茨海默病(AD)的发病机制。HSV1 已经进化出了降低宿主免疫反应效力和干扰病毒清除的策略。基于它们作为这些免疫逃避策略调节剂的假定作用,我假设免疫球蛋白(Ig)GM 基因——位于 14 号染色体上 IgG 重链的遗传标记——是 AD 的功能风险和保护因素。支持这一假设的全基因组关联和连锁研究结果、可检验的预测以及可能的治疗意义进行了讨论。