COVID-19 MAY BE INDUCING PROGRESSIVE, IRREVESIBLE PROGERIA IN A CLINICAL SUBSET
March 26, 2021
In looking for a link to upregulated MMPs with other findings, it is critical that MMPs are upregulated in all Progeria disease. Defective/deficient CSA and CSB proteins are the hallmark of Cockayne Syndrome, a Progeria Disease. This defect causes nucleotide excision repair (NER). Damaged DNA is unable to repair itself. This is directly related to NAD+ deficiency, COVID may dysregulate NAD+.
Most concerning is that everything involved with Cockayne Syndrome is occurring in Long COVID patients. From Cachexia to neurodegeneration, hearing loss, new onset type 2 diabetes and now eye problems are occurring.
Investigation into CSA, CSB and NAD+ levels of Long COVID patients is urgently needed.
This explains why some are "hit" with Long COVID symptoms months after experiencing the acute phase of the disease. It takes that amount of time for the body to cellulary age to the point where symptoms appear. Mitochondrial dysfunction is also a significant factor in Cockayne Syndrome.
I believe a bioweapon has been released, either accidentally or intentionally, that makes the body progressively unable to repair itself. This must be recognized and openly discussed IMMEDIATELY as its spread is rapidly accelerating. It is entirely possible that even asymptomatic infection leads to death.
Differential expression of metalloproteinase and tissue inhibitor of metalloproteinase genes in aged human fibroblasts
Preclinical research shows that COVID-19 infection may dysregulate NAD+ synthesis
Mitochondrial deficiency in Cockayne syndrome
Dysmyelination not demyelination causes neurological symptoms in preweaned mice in a murine model of Cockayne syndrome