Covid-19 is characterized by cytokine storm. This is probably due to skweness of the disease response to TH2 profile. It is likely thought that TH2 downreegulates th1. What are the possible mechanisms?
A great question is the activity of the VDR (Vitamin D receptor). A competent immune response regulate between TH 1 and TH 2, so it is necessary in the body. It is a view point in regulation medicine. A possible fixation of the regulation can be created by VDR inhibition, and it seems so, that it is possible in Covid 19:
Article Shining Light on the COVID-19 Pandemic: A Vitamin D Receptor...
Also on researchgate, you can see this picture with the orange coloured Vitamin D hormon (Calcitriol). See picture with Yin/Yang and immune response behind the article: Article Vitamin D and the Immune System from the Nephrologist's Viewpoint
So it is possible, that the normal change between the two TH1 and TH2 cells can be blocked by inactivated VDR.
Very helpfull can be the analysation of Vit D 25 OH D3 together with the Calcitriol Vit D 1,25 OH D3, and a blocked VDR is normaly typical for a very high level of 1,25 OH D3 and very low 25 OH D3. Bad is, that the papers, who suggest a low 25 OH D3 is correlated with a bad outcome of the Sars cov 2 patients are without analysation from lab with 1,25 OH D3. So, I am very sure, that is very high in bad outcome of patients. In my Lab, I see very often extrem low 25 OH D3, often behind the Lab range, and a very high 1,25 OH D3,often over the normal range, especially in autoimmun patients, may be also in cytokin storm patients?
Best regards, J. A.