ArticlePloS one2014
Neuroinvasion of the highly pathogenic influenza virus H7N1 is caused by disruption of the blood brain barrier in an avian model.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Decoding the lung-brain axis in influenza: from pulmonary infection to central nervous system injury.Journal of neuroinflammation · 2026Review
- Natural infections of highly pathogenic avian influenza virus H5N1 in wild birds between 2020 and 2023 in the UK: a retrospective study with focus on microscopic lesions, viral distribution and neurotropism.Veterinary research · 2025Article
- High fever, low GCS, and high lactate: independent risk factors for progression of influenza-associated encephalopathy to acute necrotizing encephalopathy in children.BMC infectious diseases · 2025Article
- Article
- Influenza H7N9 virus disrupts the monolayer human brain microvascular endothelial cells barrier in vitro.Virology journal · 2023Article
- Type II Grass Carp Reovirus Rapidly Invades Grass Carp (Viruses · 2023Article
- Article
- The Effects of Viruses on Insulin Sensitivity and Blood-Brain Barrier Function.International journal of molecular sciences · 2023Review
- A Breakdown of Immune Tolerance in the Cerebellum.Brain sciences · 2022Review
- Neuroinflammation in neurodegenerationFrontiers in immunology · 2022Review
- Altered gene expression in human brain microvascular endothelial cells in response to the infection of influenza H1N1 virus.Animal diseases · 2022Article
- Severe acute respiratory syndrome coronavirus 2 infection reaches the human nervous system: How?Journal of neuroscience research · 2021Review
- The Novel Coronavirus Infection (COVID-19) and Nervous System Involvement: Mechanisms of Neurological Disorders, Clinical Manifestations, and the Organization of Neurological Care.Neuroscience and behavioral physiology · 2021Article
- The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier.Neurobiology of disease · 2020Article
- Neurological Damage by Coronaviruses: A Catastrophe in the Queue!Frontiers in immunology · 2020Review
- Neonatal influenza virus infection affects myelination in influenza-recovered mouse brain.Journal of veterinary science · 2018Article
- CNS infection and immune privilege.Nature reviews. Neuroscience · 2018Review
- H5N1 Influenza a Virus Replicates Productively in Pancreatic Cells and Induces Apoptosis and Pro-Inflammatory Cytokine Response.Frontiers in cellular and infection microbiology · 2018Article
- The Olfactory Bulb: An Immunosensory Effector Organ during Neurotropic Viral Infections.ACS chemical neuroscience · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) causes central nervous system (CNS) lesions in avian and mammalian species, including humans. However, the mechanism used by IAV to invade the brain has not been determined. In the current work, we used chickens infected with a highly pathogenic avian influenza (HPAI) virus as a model to elucidate the mechanism of entry of IAV into the brain. The permeability of the BBB was evaluated in fifteen-day-old H7N1-infected and non-infected chickens using three different methods: (i) detecting Evans blue (EB) extravasation into the brain, (ii) determining the leakage of the serum protein immunoglobulin Y (IgY) into the brain and (iii) assessing the stability of the tight-junction (TJ) proteins zonula occludens-1 and claudin-1 in the chicken brain at 6, 12, 18, 24, 36 and 48 hours post-inoculation (hpi). The onset of the induced viremia was evaluated by quantitative real time RT-PCR (RT-qPCR) at the same time points. Viral RNA was detected from 18 hpi onward in blood samples, whereas IAV antigen was detected at 24 hpi in brain tissue samples. EB and IgY extravasation and loss of integrity of the TJs associated with the presence of viral antigen was first observed at 36 and 48 hpi in the telencephalic pallium and cerebellum. Our data suggest that the mechanism of entry of the H7N1 HPAI into the brain includes infection of the endothelial cells at early stages (24 hpi) with subsequent disruption of the TJs of the BBB and leakage of virus and serum proteins into the adjacent neuroparenchyma.
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