ArticlePloS one2015
Induction of microglia activation after infection with the non-neurotropic A/CA/04/2009 H1N1 influenza virus.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed.
- Low-replication influenza virus mediates high pathogenicity through an inflammation-driven lung-heart-brain axis in mice.Emerging microbes & infections · 2026Article
- Decoding the lung-brain axis in influenza: from pulmonary infection to central nervous system injury.Journal of neuroinflammation · 2026Review
- SARS-CoV-2 infection is associated with hypothalamic orexin suppression and persistent cortical NeuN attenuation.Journal of neuroinflammation · 2026Article
- Influenza A virus infection impairs neuronal activity in human iPSC-derived NGN2 neural co-cultures.Acta neuropathologica communications · 2026Article
- Persistent microglial activation following neonatal CMV infection mediates neurodegeneration.Science advances · 2026Article
- Exposure to manganese during juvenile development increases microglial activation in the hippocampus following systemic infection with A/California/04/2009 Influenza A H1N1 virus.Frontiers in toxicology · 2026Article
- Neurodegeneration in Parkinson's Disease: The Role of Environmental Toxins.Journal of central nervous system disease · 2026Review
- Influenza A infection accelerates disease-associated microglia formation during physiological aging.bioRxiv : the preprint server for biology · 2025Article
- Case Series: Reactivation of Herpetic Keratitis After COVID-19 mRNA Vaccination During Herpetic Prophylaxis.Vision (Basel, Switzerland) · 2025Article
- The Search for Disease Modification in Parkinson's Disease-A Review of the Literature.Life (Basel, Switzerland) · 2025Review
- Templating of monomeric alpha-synuclein results in inflammation and SNpc dopamine neuron death in a genetic mouse model of induced synucleinopathy.Scientific reports · 2025Article
- Review
- Environmental exposures and familial background alter the induction of neuropathology and inflammation after SARS-CoV-2 infection.NPJ Parkinson's disease · 2025Article
- Involvement of virus infections and antiviral agents in schizophrenia.Psychological medicine · 2025Review
- Shared interactions of six neurotropic viruses with 38 human proteins: a computational and literature-based exploration of viral interactions and hijacking of human proteins in neuropsychiatric disorders.Discover mental health · 2025Article
- Exploring the Link Between SARS-CoV-2 RT-PCR Cycle Threshold, Clinical Characteristics, and Laboratory Results in Hospitalized COVID-19 Patients With Neurological and Autoimmune Conditions.Medical journal of the Islamic Republic of Iran · 2025Article
- Underestimated virus impaired cognition-more evidence and more work to do.Frontiers in immunology · 2025Review
- Virally-initiated pain states: phenotypes, mechanisms, and future directions.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
- Is There such a Thing as Post-Viral Depression?: Implications for Precision Medicine.Biomolecules & therapeutics · 2024Review
- Respiratory infection with influenza A virus delays remyelination and alters oligodendrocyte metabolism.iScience · 2024Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Although influenza is primarily a respiratory disease, it has been shown, in some cases, to induce encephalitis, including people acutely infected with the pandemic A/California/04/2009 (CA/09) H1N1 virus. Based on previous studies showing that the highly pathogenic avian influenza (HPAI) A/Vietnam/1203/2004 H5N1 virus was neurotropic, induced CNS inflammation and a transient parkinsonism, we examined the neurotropic and inflammatory potential of the CA/09 H1N1 virus in mice. Following intranasal inoculation, we found no evidence for CA/09 H1N1 virus neurotropism in the enteric, peripheral or central nervous systems. We did, however, observe a robust increase in microglial activity in the brain characterized by an increase in the number of activated Iba-1-positive microglia in the substantia nigra (SN) and the hippocampus, despite the absence of virus in the brain. qPCR analysis in SN tissue showed that the induction of microgliosis was preceded by reduced gene expression of the neurotrophic factors bdnf, and gdnf and increases in the immune modulatory chemokine chemokine (C-C motif) ligand 4 (ccl4). We also noted changes in the expression of transforming growth factor-1 (tgfβ1) in the SN starting at 7 days post-infection (dpi) that was sustained through 21 dpi, coupled with increases in arginase-1 (arg1) and csf1, M2 markers for microglia. Given that neuroinflammation contributes to generation and progression of a number of neurodegenerative disorders, these findings have significant implications as they highlight the possibility that influenza and perhaps other non-neurotropic viruses can initiate inflammatory signals via microglia activation in the brain and contribute to, but not necessarily be the primary cause of, neurodegenerative disorders.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.