so it seems to me you need to continue to look at how various diseases were studied prior to covid to determine how to deal with oxidative stress. take whatever disease you have...like hypertension...and start chugging away at the buzzwords used by Medcram..angiotensin II, 1,7 etc.
I suspect you will see a lot of NAC used in articles
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30937-5/fulltext
Our findings show the presence of viral elements within endothelial cells and an accumulation of inflammatory cells, with evidence of endothelial and inflammatory cell death. These findings suggest that SARS-CoV-2 infection facilitates the induction of endotheliitis in several organs as a direct consequence of viral involvement (as noted with presence of viral bodies) and of the host inflammatory response. In addition, induction of apoptosis and pyroptosis might have an important role in endothelial cell injury in patients with COVID-19. COVID-19-endotheliitis could explain the systemic impaired microcirculatory function in different vascular beds and their clinical sequelae in patients with COVID-19. This hypothesis provides a rationale for therapies to stabilise the endothelium while tackling viral replication, particularly with anti-inflammatory anti-cytokine drugs, ACE inhibitors, and statins.7, 8, 9, 10, 11 This strategy could be particularly relevant for vulnerable patients with pre-existing endothelial dysfunction, which is associated with male sex, smoking, hypertension, diabetes, obesity, and established cardiovascular disease, all of which are associated with adverse outcomes in COVID-19.
btw my relative who succumbed to the cytokine storm had no known underlying issues and did not have thalessemia.
So who knows why the flu wrecked the body in that case
Young, Fit, Athlete but not Super Athlete. Dead in about 4 days from pneumonia/sepsis