Figure 12.

Summary of our findings. Our data indicate that COVID-19 is a highly heterogeneous disease with multiple etiologies (A) Correspond to a representation of the alveolar sacs. (B) Amplification of the alveolar area to denote the organization of the lung in healthy conditions. (C) Correspond to the lung organization in COVID-19 conditions, including enhanced coagulation (intravascular and parenchymal), fibroblast proliferation, loss of epithelial, ciliated, and SMC, as well as endothelial cells from the alveoli. Several questions remain about the immune response, including the lack of immune organization around lesions (as indicated in phenotype 1), the strong B cell response in the lung that could not control the infection, and associated damage. The lack of viral mRNA in the lung and the abundance of protein M inside the blood vessels suggest replication in other tissues. The presence or absence of hemorrhagic events and the formation of fibrin webs inside the blood vessels. All these different phenotypes provide several opportunities to reduce or prevent the devastating consequences of COVID-19.