ArticleFrontiers in cellular neuroscience2021
Long-Term Consequence of Non-neurotropic H3N2 Influenza A Virus Infection for the Progression of Alzheimer's Disease Symptoms.
Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Decoding the lung-brain axis in influenza: from pulmonary infection to central nervous system injury.Journal of neuroinflammation · 2026Review
- Convergence of neuroinflammation across major neurotropic viral exposomes in AD and ADRD.Journal of neuroinflammation · 2026Review
- CGRP reception potentiates anxiety in an influenza A derived immune engram.bioRxiv : the preprint server for biology · 2026Article
- Article
- Association between influenza A virus and SARS-CoV-2 infections and mood disorders.Brain, behavior, & immunity - health · 2026Article
- Potential Non-Specific Benefits of Seasonal Influenza Vaccination: Evidence, Knowledge Gaps, and Future Directions.Vaccines · 2026Review
- Neurodegeneration in Parkinson's Disease: The Role of Environmental Toxins.Journal of central nervous system disease · 2026Review
- Exploring the role of infectious pathogens in Alzheimer's disease neuroinflammation.Frontiers in cellular and infection microbiology · 2026Review
- Gut dysbiosis leads to cognitive decline through CNTF-mediated activation of microglia in mice.BMC biology · 2025Article
- HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025Review
- Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection.Nature medicine · 2025Article
- Viruses and neurodegeneration: a growing concern.Journal of translational medicine · 2025Review
- Neuroinvasive and neurovirulent potential of SARS-CoV-2 in the acute and post-acute phase of intranasally inoculated ferrets.PloS one · 2025Article
- Influenza A Virus PB1-F2 Induces Affective Disorder by Interfering Synaptic Plasticity in Hippocampal Dentate Gyrus.Molecular neurobiology · 2024Article
- The potential therapeutic role of itaconate and mesaconate on the detrimental effects of LPS-induced neuroinflammation in the brain.Journal of neuroinflammation · 2024Article
- Changes in the Expression of Proteins Associated with Neurodegeneration in the Brains of Mice after Infection with Influenza A Virus with Wild Type and Truncated NS1.International journal of molecular sciences · 2024Article
- The effects of urolithin A on poly I:C-induced microglial activation.Frontiers in cellular neuroscience · 2024Article
- Systemic perturbations in amino acids/amino acid derivatives and tryptophan pathway metabolites associated with murine influenza A virus infection.Virology journal · 2023Article
- Transcriptomic Profiling of Influenza A Virus-Infected Mouse Lung at Recovery Stage Using RNA Sequencing.Viruses · 2023Article
- Biological agents and the aging brain: glial inflammation and neurotoxic signaling.Frontiers in aging · 2023Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza viruses until today are a leading cause of worldwide severe pandemics and represent a major threat to human and animal health. Although the primary target of influenza viruses is the lung, infection may manifest with acute and even chronic neurological complications (e.g., status epilepticus, encephalopathies, and encephalitis) potentially increasing the long-term risk for neurodegenerative diseases. We previously described that a peripheral influenza A virus (IAV) infection caused by non-neurotropic H3N2 (maHK68) variant leads to long-term neuroinflammation and synapse loss together with impaired memory formation in young adult mice. Processes of neuroinflammation have been associated with neurodegenerative diseases such as Alzheimer's disease (AD) and prolonged or excessive innate immune responses are considered a risk factor for AD. Here, the role of purely peripheral IAV infection for the development and progression of AD in a transgenic mouse model (APP/PS1) was investigated. At 2 months of age, mice were infected with H3N2 IAV and the detailed analysis of microglia morphology revealed neuroinflammation in the hippocampus already of 6 months old non-infected APP/PS1 mice together with impaired spatial learning, however, microglia activation, amyloid-β plaques load and cognitive impairments were even more pronounced in APP/PS1 mice upon H3N2 infection. Moreover, CA1 hippocampal dendritic spine density was reduced even at 120 dpi compared to wild-type and also to non-infected APP/PS1 mice, whereas neuronal cells number was not altered. These findings demonstrate that non-neurotropic H3N2 IAV infection as a peripheral immune stimulation may exacerbate AD symptoms possibly by triggering microglial hyperactivation.
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