Further supporting a potential role for herpesviral reactivation in AD pathophysiology, a 2019 study from De Chiara et al. [18] showed that wild-type mice infected with HSV-1 developed Aβ accumulation, tau hyperphosphorylation, and neuroinflammation after several cycles of reactivation with thermal stress (15 min in a 43 °C water bath) compared to controls exposed to the thermal stress but not infected with HSV-1. The gene discussed is MAPT; the disease is Alzheimer disease.