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.