Protective Effect of Amyloid-β Peptides Against Herpes Simplex Virus-1 Infection in a Neuronal Cell Culture Model
Abstract
Senile amyloid plaques are one of the main hallmarks of Alzheimer’s disease (AD). They correspond to insoluble deposits of amyloid-β peptides (Aβ) and are responsible for the inflammatory response and neurodegeneration that lead to loss of memory. Recent data suggest that Aβ possess antimicrobial and anti-viral activity in vitro . Here, we have used cocultures of neuroglioma (H4) and glioblastoma (U118-MG) cells as a minimal in vitro model to investigate whether Aβ is produced by neuroglioma cells and whether this could result in protective anti-viral activity against HSV-1 infection. Results showed that H4 cells secreted Aβ 42 in response to HSV-1 challenge and that U118-MG cells could rapidly internalize Aβ 42 . Production of pro-inflammatory cytokines TNF α and IL-1β by H4 and U118-MG cells occurred under basal conditions but infection of the cells with HSV-1 did not significantly upregulate production. Both cell lines produced low levels of IFN α . However, extraneous Aβ 42 induced strong production of these cytokines. A combination of Aβ 42 and HSV-1 induced production of pro-inflammatory cytokines TNF α and IL-1β, and IFN α in the cell lines. The reported anti-viral protection of Aβ 42 was revealed in transfer experiments involving conditioned medium (CM) of HSV-1-infected H4 cells. CM conferred Aβ-dependent protection against HSV-1 replication in de novo cultures of H4 cells challenged with HSV-1. Type 1 interferons did not play a role in these assays. Our data established that H4 neuroglioma cells produced Aβ 42 in response to HSV-1 infection thus inhibiting secondary replication. This mechanism may play a role in the etiology of AD.
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Another study demonstrated Aβ42 was produced by a neuroglioma (H4) cell line in response to HSV-1.
“Another study demonstrated Aβ42 was produced by a neuroglioma (H4) cell line in response to HSV-1 [113].”
From What would it take to prove that a chronic infection is a causal agent in Alzheimer’s disease? (2025) · cites this paper as [113]
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- Authors
- Bourgade, K., Le Page, A., Bocti, C., Witkowski, J. M., Dupuis, G., Frost, E. H., & Fülöp, T.
- Affiliations
- Université de Sherbrooke (CA)
- Research Center on Aging, Graduate Program in Immunology, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, QC, Canada
- Gdańsk Medical University (PL)
- Department of Medicine, Research Center on Aging, Graduate Program in Immunology, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, QC, Canada
- Venue
- Journal of Alzheimer’s Disease
- Publisher
- SAGE Publications
- Published
- 2016-01-19
- Volume
- 50
- Issue
- 4
- Pages
- 1227-1241
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2293235256
- Cited by
- 161
- References
- 83
- Citations by year
- 2026: 9 · 2025: 18 · 2024: 4 · 2023: 13 · 2022: 23 · 2021: 28 · 2020: 18 · 2019: 18 · 2018: 18 · 2017: 8 · 2016: 4
- FWCI
- 12.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (106634)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Epidemiology › Herpesvirus Infections and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta 42, herpes simplex virus type 1
- MeSH terms
- Herpes Simplex, Humans, Neuroglia, Neurons, Peptide Fragments, Tumor Necrosis Factor-alpha, Virus Replication, Amyloid beta-Peptides, Interferon-alpha, Culture Media, Conditioned, Herpesvirus 1, Human, Coculture Techniques, Cell Line, Tumor, Interleukin-1beta, Amyloid Precursor Protein Secretases
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