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SARS-CoV-2 Orf6 Triggers MTCH1-Dependent Mitochondrial Dysfunction and Necroptosis in Human Neurons | Research Square
SARS-CoV-2 Orf6 Triggers MTCH1-Dependent Mitochondrial Dysfunction and Necroptosis in Human Neurons | Research Square

A new preprint study shows that the SARS-CoV-2 protein ORF6 directly kills human neurons. Not by accident, but through necroptosis - a kind of cell death where neurons burst and fuel inflammation. This may underlie the long-term brain symptoms of Long COVID.

·researchsquare.com·
SARS-CoV-2 Orf6 Triggers MTCH1-Dependent Mitochondrial Dysfunction and Necroptosis in Human Neurons | Research Square
COVID and the brain: researchers zero in on how damage occurs
COVID and the brain: researchers zero in on how damage occurs

SARS-CoV-2 preferentially infects astrocytes, which support neuron function, potentially leading to symptoms like fatigue and confusion.

SARS-CoV-2 can also infect pericytes, leading to restricted blood flow and small-vessel strokes.

·nature.com·
COVID and the brain: researchers zero in on how damage occurs
Pioneering discovery and therapeutics at the brain-vascular-immune interface
Pioneering discovery and therapeutics at the brain-vascular-immune interface

A new paper in Cell, “Pioneering discovery and therapeutics at the brain-vascular-immune interface,” describes COVID-19 as a neurological disease alongside multiple sclerosis, Alzheimer’s, stroke and traumatic brain injury.

“COVID-19 can accelerate progression of dementia and induce BBB disruption and inflammatory blood clots causally linked with neuroinflammation and neuronal loss.8 In neurodevelopmental disorders, prematurity and perinatal hypoxia that trigger brain hemorrhage and BBB disruption are risk factors for cerebral palsy, intellectual disability, and autism. Collectively, these risk factors highlight the interconnected vascular and immune triggers of neurological diseases.”

·cell.com·
Pioneering discovery and therapeutics at the brain-vascular-immune interface