Herpes Simplex Virus Infection Increases Beta-Amyloid Production and Induces the Development of Alzheimer’s Disease

Abstract

Background. Alzheimer’s disease, a neurodegenerative memory disease, primarily results from the formation of amyloid plaques (Aβ) that gradually inhibit neuron communications. The entire mechanism of Aβ production remains unclear to date, and it is of particular interest among scientists to find out the exact mechanism that leads to amyloid precursor protein (APP) cleavage through the amyloidogenic pathway so that effective treatments can be developed. Method. 2 sets of experiments with the use of human H4-N cell lines are proposed to fully investigate the validity of the hypothesis. All of the experiments would involve immunoblotting of Aβ using an anti-Aβ antibody, and the results would be analyzed with the assistance of an image analyzer. A significant amount of Aβ would be expected to be present in the cytoplasm of cells with herpes simplex virus (HSV-1) applied, as APP endocytosis would be induced by HSV-1, which leads to higher Aβ levels inside the cell. Results. In this paper, a new hypothesis is presented on how HSV-1 infection initiates APP endocytosis and causes an increase in APP cleavage and Aβ production inside the cells. It is also hypothesized that increased Aβ peptides exit the cell via exocytosis, therefore, leading to the development of Alzheimer’s disease. The findings will support the hypothesis if intracellular Aβ concentration is significantly higher after the introduction of dHSV-1 and subsequently if extracellular Aβ concentration becomes higher without TeNT exocytosis inhibition. Conclusion. The results of this study would provide valuable insights into the mechanisms underlying Alzheimer’s disease and open new scopes of research for its potential treatments. Further studies on virus infection and the development of memory diseases should be conducted to investigate possible correlations.