ArticleJournal of translational medicine2019
Herpes simplex virus-1 (HSV-1) infection induces a potent but ineffective IFN-λ production in immune cells of AD and PD patients.
Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Profiling peripheral immune cells in Parkinson's disease: A scoping review.Journal of Parkinson's disease · 2026Review
- Comparative analysis of varicella-zoster virus and herpes simplex virus 1 interaction with epidermal terminal differentiation in primary human keratinocytes models of differentiation.bioRxiv : the preprint server for biology · 2026Article
- Evaluating long non-coding RNA signatures as biomarkers for inflammatory pathway regulation and rehabilitative outcomes in Parkinson's disease: toward a precision medicine approach.Frontiers in immunology · 2026Article
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- Elevated levels of CD56+ T Cells, CD16+ CD56+ T Cells, and CD56dim NK Cells in herpes simplex virus type 1 seropositive healthy individuals.Saudi medical journal · 2024Article
- The Quest for Immunity: Exploring Human Herpesviruses as Vaccine Vectors.International journal of molecular sciences · 2023Review
- Nicotinamide n-Oxide Attenuates HSV-1-Induced Microglial Inflammation through Sirtuin-1/NF-κB Signaling.International journal of molecular sciences · 2022Article
- The Analysis of Herpes Simplex Virus Type 1 (HSV-1)-Encoded MicroRNAs Targets: A Likely Relationship of Alzheimer's Disease and HSV-1 Infection.Cellular and molecular neurobiology · 2022Article
- Neuroinflammation in neurodegenerationFrontiers in immunology · 2022Review
- Chronic neuropsychiatric sequelae of SARS-CoV-2: Protocol and methods from the Alzheimer's Association Global Consortium.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- How an increase in the copy number of HSV-1 during latency can cause Alzheimer's disease: the viral and cellular dynamics according to the microcompetition model.Journal of neurovirology · 2021Article
- A Possible Role for HSV-1-Specific Humoral Response andVaccines · 2021Article
- Viral Involvement in Alzheimer's Disease.ACS chemical neuroscience · 2021Article
- Can Control Infections Slow Down the Progression of Alzheimer's Disease? Talking About the Role of Infections in Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe sequential activation of immediate early (IE), early (E) and late (L) genes is required to allow productive herpes simplex virus type 1 (HSV-1) infection. Several evidences suggest that, together with inflammation, an immunological response incapable to counteract HSV-1 reactivation plays a role in the pathogenesis of Alzheimer's (AD) and Parkinson's (PD) diseases. IFN-lambda (IFN-λ), a cytokine endowed with a robust antiviral activity, contains HSV-1 reactivation. HSV-1-induced IFN-λ, IL-10 and IL-1β as well as the expression of viral IE, E and L genes were analyzed in vitro in peripheral blood mononuclear cells (PBMC) of AD and PD patients as well as of healthy controls (HC).
methodsPBMC of AD, PD and HC were in vitro infected with one multiplicity of infection (1 MOI) HSV-1. IE, E, and L viral genes transcription as well as IFN-λ, IL-10 and IL-1β production were analyzed.
resultsIn HSV-1-infected cells of AD and PD patients compared to HC: (1) transcription of IE (ICP0, ICP27) genes was reduced whereas that of E (UL41, UL29) and L (UL48, LAT) genes was increased; (2) IFN-λ mRNA expression was increased. IL-1β was augmented and IL-10 was reduced in unstimulated cells of AD and PD compared to HC; HSV-1 infection significantly increased IL-10 production in HC alone.
conclusionsData herein show that a proinflammatory condition is present in AD and PD, in whom attempts to obstacle viral replication via an initial, possibly more potent IFN-λ-mediated control of IE viral genes is unsuccessful.
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