Research on CD147 may be very helpful in the long run. I am a retired physician and am aware of studies showing that aspirin will slow down progression of emphysema. Perhaps the stimulation of fibroblasts is due to local micro-clotting attracting fibroblasts by way of signals from platelets aggregating at these sites.
So my first question is: Does aspirin, Plavix, heparin, or other anti-platelet/anticoagulant-class medications used in hospitalized COVID-19 patients reduce the chance of pulmonary fibrosis?
My second question is: Do the new endothelial cell protective agents such as Flavicin and Salifen have benefit in such patients?
Lastly, there is a relatively inexpensive medication/(extract) named Pynogenol used in preventing recurrent venous thrombosis in patients with lower extremity venous insufficiency and more to the point, good studies showing it is protective in diabetic retinal micro-vascular disease. If I were a patient suffering from progressive COVID-induced pulmonary fibrosis, I would certainly look into these types of options.
Stopping pulmonary fibrosis is certainly worthwhile. In hepatic fibrosis there is regeneration of tissue if the cause is removed- the structure may not be perfect, but the function is pretty good.
Reversal of pulmonary fibrosis is usually not seen; Kaplan-Meier nomograms for pulmonary function with age show a consistent decline. For instance, quitting smoking does not restore the lung function to the baseline for age, but the slope of the decline may become parallel to the "normal" for age. As in myocarditis, the damage from pulmonary fibrosis should be seen as permanent.
It would be good to put the mice through another study comparing proper early treatment to untreated Covid infection to mRNA injection.
Spike protein is a nasty devil. A new preprint that just showed up today speaks to the fact that spike induces hemagluttination, and that IVM both stops this, and even reverses it after the fact.
Title: SARS-CoV-2 Spike Protein Induces Hemagglutination: Implications for COVID-19 Morbidities and Therapeutics and for Vaccine Adverse Effects
Conclusions: Spike protein from four lineages of SARS-CoV-2 induced HA in human RBCs, which supports other indications that spike protein-induced RBC clumping, as well as viral attachments to other blood cells and endothelial cells, may be key to the morbidities of COVID-19. IVM, a macrocyclic lactone indicated to bind strongly to multiple glycan sites on SARS-CoV-2 spike protein, blocked HA when added to RBCs prior to spike protein and reversed HA when added afterwards......
The paper also mentions CD147; "For endothelial cells of blood vessel linings, for example, the disparity between 28,000 SA-tipped CD147 receptors and 175 ACE2 receptors per cell21 51 provides a supporting indication of the role of glycans in widespread endothelial damage reported in COVID-19 patients" Note that SA = terminal sialic acid moieties.
Research on CD147 may be very helpful in the long run. I am a retired physician and am aware of studies showing that aspirin will slow down progression of emphysema. Perhaps the stimulation of fibroblasts is due to local micro-clotting attracting fibroblasts by way of signals from platelets aggregating at these sites.
So my first question is: Does aspirin, Plavix, heparin, or other anti-platelet/anticoagulant-class medications used in hospitalized COVID-19 patients reduce the chance of pulmonary fibrosis?
My second question is: Do the new endothelial cell protective agents such as Flavicin and Salifen have benefit in such patients?
Lastly, there is a relatively inexpensive medication/(extract) named Pynogenol used in preventing recurrent venous thrombosis in patients with lower extremity venous insufficiency and more to the point, good studies showing it is protective in diabetic retinal micro-vascular disease. If I were a patient suffering from progressive COVID-induced pulmonary fibrosis, I would certainly look into these types of options.
Stopping pulmonary fibrosis is certainly worthwhile. In hepatic fibrosis there is regeneration of tissue if the cause is removed- the structure may not be perfect, but the function is pretty good.
Reversal of pulmonary fibrosis is usually not seen; Kaplan-Meier nomograms for pulmonary function with age show a consistent decline. For instance, quitting smoking does not restore the lung function to the baseline for age, but the slope of the decline may become parallel to the "normal" for age. As in myocarditis, the damage from pulmonary fibrosis should be seen as permanent.
It would be good to put the mice through another study comparing proper early treatment to untreated Covid infection to mRNA injection.
Conveyed with excellence. Big Thank You / Kudos.
Damn that spike protein.
Spike protein is a nasty devil. A new preprint that just showed up today speaks to the fact that spike induces hemagluttination, and that IVM both stops this, and even reverses it after the fact.
https://www.biorxiv.org/content/10.1101/2022.11.24.517882v1.full.pdf+html
Title: SARS-CoV-2 Spike Protein Induces Hemagglutination: Implications for COVID-19 Morbidities and Therapeutics and for Vaccine Adverse Effects
Conclusions: Spike protein from four lineages of SARS-CoV-2 induced HA in human RBCs, which supports other indications that spike protein-induced RBC clumping, as well as viral attachments to other blood cells and endothelial cells, may be key to the morbidities of COVID-19. IVM, a macrocyclic lactone indicated to bind strongly to multiple glycan sites on SARS-CoV-2 spike protein, blocked HA when added to RBCs prior to spike protein and reversed HA when added afterwards......
The paper also mentions CD147; "For endothelial cells of blood vessel linings, for example, the disparity between 28,000 SA-tipped CD147 receptors and 175 ACE2 receptors per cell21 51 provides a supporting indication of the role of glycans in widespread endothelial damage reported in COVID-19 patients" Note that SA = terminal sialic acid moieties.