The virus needs porphyrins for its survival (probably for its replication), so it attacks the hemoglobin (the protein that carries oxygen in the blood), in particular, the OFR10 and OFR3 proteins attack the beta chain, and orph1ab subtracts the porphyrin. The concepts seem a bit abstruse for a layman, but simply speaking, this translates into less oxygen available to the body, with consequent accumulation of carbon dioxide. Thus, the lung cells enter into a state of distress and become the site of the cytokine storm – that is, an enormous immune response – responsible for the acute inflammation that characterizes COVID-19 pneumonia.
The value of hemoglobin in the blood can be an important parameter to assess the SARS- CoV-2 infection: in men, the average value of Hb (hemoglobin) is higher than in women. This would explain the higher incidence of COVID-19 pneumonia in men compared to women, the lower incidence, and the better prognosis in children and pregnant women, where Hb values are lower due to an increased need for iron, which makes less available the "nutrition" of the virus. In elderly or middle-aged patients with diabetes, pneumonia from COVID-19 has a higher incidence, therefore linked to increased Hb glycated in the blood, and therefore there is more "nourishment" for the virus.
The viral damage, therefore, is systemic, i.e., it affects the blood and is not confined to the lung alone. This would also explain the birth of healthy babies from COVID-19 positive mothers. Because in fetal Hb – stay with me, we will now use some technical concepts – two gamma chains replace the two beta chains, a difference is the presence of a residual serine, instead of a histidine present in the same position of the beta chain, probably responsible for the binding with viral proteins, which could mimic the action of 2,3bifosfoglycerate.