APP processing induced by herpes simplex virus type 1 (HSV-1) results in the production of several APP fragments and Aβ accumulation in human and rat neuronal cells

Background: HSV-1 is a neurotropic virus that, following primary infection, usually establishes a lifelong latent infection in the trigeminal ganglion. Following periodic reactivations, the newly produced viral particles may be transported to the central nervous system (CNS), resulting in productive but usually asymptomatic infections. Possible links between recurrent HSV-1 infections and Alzheimer's disease (AD) have emerged from epidemiological studies and experimental findings. We have recently found that HSV-1 produces marked changes in neuronal excitability and intracellular Ca2+ signalling which affect the phosphorylation of amyloid precursor protein (APP) and result in intracellular accumulation of amyloid-β peptide (Aβ).