Last update:
20-Mar-2023

The herpes simplex virus type 1 (HSV-1), in addition to its harmful effects on the neurons of the peripheral nervous system, can penetrate the central nervous system (CNS), where it remains in a latent state, with the potential to later affect older persons to a higher degree. In the case of biological stress, immunosuppression and infection by another factor, HSV-1 appears to be reactivated, causing inflammation of the CNS, and damage affecting to a greater extent areas associated with the onset of Alzheimer's disease (AD). This results in the accumulation and generation of related factors linked directly with the pathophysiology of the disease, such as the Aβ-42 amyloid peptide and its precursor amyloid-β protein (APP), but also the hyperphosphorylated tau proteins, associated with the formation of amyloid plaques and neurofibrillary tangles, respectively. The increase in Aβ-42 appears to involve the immune system in an effort to encircle the virus and reduce it, contributing to the creation of oxidative stress and inflammation in the brain. In addition, viral DNA appears to be selectively present at the sites of amyloid plaques. Antiherpetic therapy appears to have beneficial effects on the cognitive deficits of the patients, with the action of drugs having a preventive effect on AD, rather than a therapeutic effect on the manifestation of symptoms. Despite the data supporting the correlation of the two diseases, certain factors raise questions, including the host individuals involved in the studies, but also other factors, such as the strain of the virus and the stage of AD, and do not allow definite conclusions about the relationship.

Key words: Alzheimer's disease, Herpes simplex virus 1, Neuroinflammation.