ArticleFrontiers in microbiology2024
Impact of age and sex on neuroinflammation following SARS-CoV-2 infection in a murine model.
Article in Frontiers in microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Infection of urban rodents by SARS-CoV-2 in COVID-19 healthcare facilities in Brazzaville, Republic of the Congo.One health outlook · 2026Article
- Differential Factors Associated With the Presence of Persistent Symptoms in Individuals Diagnosed With Long COVID: Protocol for a Longitudinal Matched Case-Control Study.JMIR research protocols · 2026Observational
- Neuroinflammation and Oxidative Stress in Parkinson's Disease, Alzheimer's Disease, and COVID-19: Microglia-Neutrophil Interaction.ACS omega · 2026Review
- Article
- The HDL-Mimetic Peptide 4F Mitigates Vascular and Cortical Amyloid Pathology and Associated Neuroinflammation in a Transgenic Mouse Model of Cerebral Amyloid Angiopathy and Alzheimer's Disease.Molecular neurobiology · 2025Article
- Exposure to COVID-19 virus-like particles modulates firing patterns of cortical neurons in the mouse brain.Communications biology · 2025Article
- SARS-CoV-2 (MA10) Infection Aggravates Cerebrovascular Pathology in Endothelial Nitric Oxide Synthase-Deficient Mice.Viruses · 2025Article
- Review
- Potential association between COVID-19 and neurological disorders: analysis of common genes and therapeutics.Frontiers in neurology · 2024Article
- A review of the roles of pathogens in Alzheimer's disease.Frontiers in neuroscience · 2024Review
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8 authors.
Funding
Abstract
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiological agent of COVID-19, is known to infect people of all ages and both sexes. Senior populations have the greatest risk of severe COVID-19, and sexual dimorphism in clinical outcomes has been reported. Neurological symptoms are widely observed in COVID-19 patients, with many survivors exhibiting persistent neurological and cognitive impairment. The present study aims to investigate the impact of age and sex on the neuroinflammatory response to SARS-CoV-2 infection using a mouse model. Wild-type C57BL/6J mice were intranasally inoculated with SARS-CoV-2 lineage B.1.351, a variant known to infect mice. Older male mice exhibited a significantly greater weight loss and higher viral loads in the lung at 3 days post infection. Notably, no viral RNA was detected in the brains of infected mice. Nevertheless, expression of IL-6, TNF-α, and CCL-2 in the lung and brain increased with viral infection. RNA-seq transcriptomic analysis of brains showed that SARS-CoV-2 infection caused significant changes in gene expression profiles, implicating innate immunity, defense response to virus, and cerebrovascular and neuronal functions. These findings demonstrate that SARS-CoV-2 infection triggers a neuroinflammatory response, despite the lack of detectable virus in the brain. Aberrant activation of innate immune response, disruption of blood-brain barrier and endothelial cell integrity, and suppression of neuronal activity and axonogenesis underlie the impact of SARS-CoV-2 infection on the brain. Understanding the role of these affected pathways in SARS-CoV-2 pathogenesis helps identify appropriate points of therapeutic interventions to alleviate neurological dysfunction observed during COVID-19.
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