Immuno Senescence

COVID-19 immunopathology: From acute diseases to chronic sequelae

Innate cell‐mediated immunopathology in COVID‐19: Upon viral entry, there is a cascade of events that leads to inflammation, vascular damage, and blot. Tissue‐resident alveolar macrophages (AMs) and interstitial macrophages are among the first responders to SARS‐CoV‐2, which secret inflammatory cytokines including TNF, IL‐6, IL‐1β, and CCL2 that in addition to building up local inflammation but […]

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SARS-CoV-2 infection triggers several mechanisms that can accelerate aging

SARS-CoV-2 infection triggers several mechanisms that can accelerate aging: DNA Damage and Impaired Repair https://www.nature.com/articles/s41556-023-01097-w Cellular Senescence https://www.nature.com/articles/s41556-023-01097-w https://www.nature.com/articles/s43587-022-00170-7 Telomere Attrition https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1399676/full Epigenetic Age Acceleration https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1399676/full Immune System Dysregulation https://immunityageing.biomedcentral.com/articles/10.1186/s12979-023-00406-z Metabolic Disruption https://www.nature.com/articles/s41598-024-70612-2

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Targeting Senescent Cells and Spike Protein Debris

This video explains how SARS-CoV-2’s spike protein triggers cellular senescence, turning cells into non-functional states. The speaker describes how viral debris, including spike protein and syncytia, can be selectively removed through a slow, careful process, allowing the body to regenerate. The final step involves using binders and chelators to remove the liberated virus and debris

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Senescent Cells and Syncytia: The Lasting Impact of SARS-CoV-2

This video explains how SARS-CoV-2 can turn cells into “zombie cells” that enter a senescent state, unable to die, repair, or replicate. These cells fuse into syncytia, creating conglomerates that harbor spike proteins and the virus, leading to impaired oxygen exchange in the lungs. This phenomenon was found in 67% of lung pathology cases, contributing

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Spike Protein Impact: Widespread Damage from Virus and Vaccine

This video discusses the widespread effects of the SARS-CoV-2 virus and spike protein on the body, including how the vaccine’s spike protein production may cause more persistent and diverse organ damage. The conversation highlights the variability in COVID-19 symptoms and outcomes based on immunity and how the vaccine’s bio-distribution may lead to longer-lasting autoimmune responses

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Spike Protein Factories: Virus vs. Vaccine Entry Mechanisms

This video explains the entry mechanisms of SARS-CoV-2 and vaccines, comparing how the virus relies on receptors to enter cells, while vaccine-delivered lipid nanoparticles forcefully fuse with any cell, turning it into a spike protein factory. It highlights the concerning exosome shedding of spike proteins, which can spread to other cells like naturally occurring lipid

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SARS-CoV-2 protein induces the SASP phenotype

This video explains how spike proteins in infected cells cause irreversible damage, leading to the release of harmful cytokines like TNF-alpha and interleukin-6, which are prominent in long COVID. The speaker emphasizes the effectiveness of senolytics in selectively eliminating these damaged cells, with early tests showing a rapid release of spike proteins into the bloodstream

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Unraveling the enigma of long COVID: novel aspects in pathogenesis, diagnosis, and treatment protocols

“Unraveling the enigma of long COVID: novel aspects in pathogenesis, diagnosis, and treatment protocols” published in Inflammopharmacology is a comprehensive review exploring the complex nature of long COVID. https://link.springer.com/article/10.1007/s10787-024-01483-2  

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