August 13, 2021
I couldn't get the endotheliopathy of Long COVID being the same as Acute COVID out of my mind. So, I have done some more work on it. This is what I now believe.
Due to the presence of NETs in COVID, and the presence of NETs in Long COVID, I believe Telomere Dysfunction, either existing or de novo, is at the core of the endotheliopathy being observed. Please see the attached paper.
Regarding Long COVID, telomere length does not affect lifespan - unless ARTIFICIALLY SHORTENED. What does aging in this artificially shortened telomere world look like? Aplastic anemia, organ fibrosis, atrophy of the small intestine and the spleen, skin and hair lesions. This does not resemble normal aging, which is why it has escaped diagnosis, until now.
(N-Acetyl-L-Cysteine, a common anti-oxidant, can inhibit mTOR.) Second, according to calculations, molecular damage, especially mtDNA mutations and telomere shortening, cannot reach deadly threshold during animal lifetime. This damage can only become life-limiting, when artificially accelerated.
Post COVID-19 fibrosis, an emerging complicationof SARS-CoV-2 infection
Novel autoantibody adds fuel to COVID-19 'firestorm' of inflammation, blood clots
Telomere dysfunction promotes small vessel vasculitis via the LL37-NETs-dependent mechanism