The authors reported a significant uptick in Iba1 and substance P (associated with neuroinflammation) expression and concluded that microglial cells were permissive to HHV-6A infection, which ultimately resulted in increased Aβ1-42 (beta-amyloid; implicated in Alzheimer’s disease) expression [45]. This evidence concerns the gene TAC1 and early-onset autosomal dominant Alzheimer disease.