Herpes Simplex Virus 1 Infection Does Not Increase Amyloid-β Pathology in APP/PS1 Mice

Article type: Short Communication

Authors: Lapeyre, Lina^a | Piret, Jocelyne^a | Rhéaume, Chantal^a | Pons, Vincent^b | Uyar, Olus^a | Préfontaine, Paul^b | Rivest, Serge^b | Boivin, Guy^{a; *}

Affiliations: [a] Research Center in infectious diseases, Research center of the CHU de Québec-Laval University, Quebec City, QC, Canada | [b] Neuroscience laboratory, Research center of the CHU de Québec-Laval University, Quebec City, QC, Canada

Correspondence: [*] Correspondence to: Dr. Guy Boivin, CHU de Québec-Laval University, 2705 Boul. Laurier, R-0709, Quebec City (QC), G1V 4G2, Canada. Tel.: +1 418 654 2705; E-mail: [email protected].

Abstract: Using APP/PS1 mice that overproduce amyloid-β (Aβ) peptides, we investigated whether intranasal infection with a neurovirulent clinical strain of herpes simplex virus 1 (HSV-1) before Aβ deposition could accelerate or increase Alzheimer’s disease-like pathology. After HSV-1 infection, APP/PS1 mice presented a similar disease as wild type animals based on body weight changes, clinical symptoms, and survival rates. The number and volume of Aβ plaques, the number of microglia, and the percentages of circulating monocyte subsets were similar in APP/PS1 mice infected or not with HSV-1. Thus, intranasal infection with HSV-1 does not alter Aβ pathology in this mouse model.

Keywords: Alzheimer’s disease, amyloid-β , amyloid protein precursor, APP/PS1 mice, herpes simplex virus 1, microglia, monocytes, presenilin-1

DOI: 10.3233/JAD-230746

Journal: Journal of Alzheimer's Disease, vol. 97, no. 1, pp. 171-178, 2024