ArticleVeterinary pathology2022
Chronological brain lesions after SARS-CoV-2 infection in hACE2-transgenic mice.
Article in Veterinary pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05576714 (Investigation of Prognostic Biomarkers, Host Factors and Viral Factors for COVID-19 Associated Encephalopathy/Encephalitis and Multi-systemic Inflammatory Syndrome in Children), which is not on this map. Cited by 41 papers.
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The trial behind it
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Investigation of Prognostic Biomarkers, Host Factors and Viral Factors for COVID-19 Associated Encephalopathy/Encephalitis and Multi-systemic Inflammatory Syndrome in Children
Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- SARS-CoV-2 Effects on Respiratory and Neurological Systems: Morphological Findings and Gene Expression in K18-hACE2 Mice Model.Microorganisms · 2026Article
- A biosafe mouse model for SARS-CoV-2 infection that more realistically simulates COVID-19 symptoms.Signal transduction and targeted therapy · 2026Article
- Crosstalk betweenFrontiers in immunology · 2026Article
- Persistent neurological and behavioral alterations after SARS-CoV-2 infection in an optimized K18-hACE2 mouse model.Frontiers in microbiology · 2026Article
- Bivalent SARS-CoV-2 spike immunization with non-replicative antibiotic resistance-free DNA vaccine induces immunity to multiple virus variants.Scientific reports · 2025Article
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- Translating animal models of SARS-CoV-2 infection to vascular, neurological and gastrointestinal manifestations of COVID-19.Disease models & mechanisms · 2025Review
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- SARS-CoV-2 infection promotes lung thrombosis by inducing integrinβ3 expression in vascular endothelial cells.Scientific reports · 2025Article
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- Generation and characterization of a humanizedFrontiers in microbiology · 2025Article
- Long-term neurocognitive outcomes of SARS-CoV-2 infection in a hamster model.Frontiers in microbiology · 2025Article
- Utilizing HCoV-OC43 to better understand the neurological impact of COVID-19.Brain, behavior, & immunity - health · 2024Article
- Article
- Neuropathological lesions in intravenous BCG-stimulated K18-hACE2 mice challenged with SARS-CoV-2.Veterinary research · 2024Article
- Review
- Plitidepsin as an Immunomodulator against Respiratory Viral Infections.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Immunization with V987H-stabilized Spike glycoprotein protects K18-hACE2 mice and golden Syrian hamsters upon SARS-CoV-2 infection.Nature communications · 2024Article
- Immunisation efficacy of a stabilised SARS-CoV-2 spike glycoprotein in two geriatric animal models.NPJ vaccines · 2024Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes respiratory disease, but it can also affect other organs including the central nervous system. Several animal models have been developed to address different key questions related to Coronavirus Disease 2019 (COVID-19). Wild-type mice are minimally susceptible to certain SARS-CoV-2 lineages (beta and gamma variants), whereas hACE2-transgenic mice succumb to SARS-CoV-2 and develop a fatal neurological disease. In this article, we aimed to chronologically characterize SARS-CoV-2 neuroinvasion and neuropathology. Necropsies were performed at different time points, and the brain and olfactory mucosa were processed for histopathological analysis. SARS-CoV-2 virological assays including immunohistochemistry were performed along with a panel of antibodies to assess neuroinflammation. At 6 to 7 days post inoculation (dpi), brain lesions were characterized by nonsuppurative meningoencephalitis and diffuse astrogliosis and microgliosis. Vasculitis and thrombosis were also present and associated with occasional microhemorrhages and spongiosis. Moreover, there was vacuolar degeneration of virus-infected neurons. At 2 dpi, SARS-CoV-2 immunolabeling was only found in the olfactory mucosa, but at 4 dpi intraneuronal virus immunolabeling had already reached most of the brain areas. Maximal distribution of the virus was observed throughout the brain at 6 to 7 dpi except for the cerebellum, which was mostly spared. Our results suggest an early entry of the virus through the olfactory mucosa and a rapid interneuronal spread of the virus leading to acute encephalitis and neuronal damage in this mouse model.
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