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  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Impact Of Age And Sex On Neuroinflammation Following Sars-cov-2 Infection In A Murine Model.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Impact Of Age And Sex On Neuroinflammation Following Sars-cov-2 Infection In A Murine Model.

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Impact of age and sex on neuroinflammation following SARS-CoV-2 infection in a murine model.

Venkatramana D Krishna1, Allison Chang2, Holly Korthas3

  • 1Department of Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota, Saint Paul, MN, United States.

Frontiers in Microbiology
|July 30, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

COVID-19 infection triggers brain inflammation in mice, even without detectable virus in the brain. Older male mice showed more severe lung symptoms, indicating age and sex impact neuroinflammation during SARS-CoV-2 infection.

Keywords:
COVID-19SARS-CoV-2brainmouse model

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Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • COVID-19, caused by SARS-CoV-2, affects all ages and sexes, with older individuals at higher risk for severe disease.
  • Neurological symptoms and persistent cognitive impairment are common in COVID-19 patients.
  • Sexual dimorphism in clinical outcomes suggests sex-based differences in disease progression.

Purpose of the Study:

  • To investigate the impact of age and sex on the neuroinflammatory response to SARS-CoV-2 infection.
  • To utilize a mouse model to explore age- and sex-dependent neurological effects of the virus.
  • To identify molecular pathways involved in SARS-CoV-2-induced neuroinflammation.

Main Methods:

  • Intranasal inoculation of wild-type C57BL/6J mice with SARS-CoV-2 lineage B.1.351.
neuroinflammation
transcriptomics
  • Assessment of weight loss, viral load in lungs, and brain viral RNA detection at 3 days post-infection.
  • Analysis of gene expression (IL-6, TNF-α, CCL-2) in lung and brain tissues.
  • RNA-sequencing (RNA-seq) transcriptomic analysis of brain tissue to identify affected pathways.

    • Main Results:

    • Older male mice exhibited greater weight loss and higher lung viral loads compared to other groups.
    • No SARS-CoV-2 RNA was detected in the brains of infected mice.
    • Increased expression of IL-6, TNF-α, and CCL-2 was observed in both lung and brain tissues.
    • Transcriptomic analysis revealed significant changes in brain gene expression related to innate immunity, viral defense, cerebrovascular function, and neuronal activity.

    Conclusions:

    • SARS-CoV-2 infection induces a neuroinflammatory response in the brain, independent of direct viral presence.
    • Key mechanisms include aberrant innate immune activation, compromised blood-brain barrier integrity, and suppressed neuronal function.
    • These findings highlight potential therapeutic targets for mitigating neurological dysfunction in COVID-19 patients.