ABSTRACT
Coronavirus disease 2019 (COVID-19) consists of a severe involvement of the lower respiratory tract leading to an acute respiratory syndrome. But there exist other infectious respiratory syndromes that have the same initial respiratory symptoms, show similar pattern in the size of the antigenic proteins and release comparable cytokines pathways, but with an unlike response magnitude. Here we propose that COVID-19 disease wrong response in the host immune system can be explained in the perspective of the antigen viral size. In COVID-19 sepsis, the < 70 kDa antigens activate the B-cell receptor (BCR), which modulates the shift in the pattern of T-helper 1 (Th1) to Th2 cytokines, increases the release of interleukin-10 (IL-10) and the up-regulation of the membrane form of tumor necrosis factor alpha (TNF-α), promoting the production of immunoglobulin G1 (IgG1)- and IgG3-neutralizing antibodies, but failing in IgG2a production and in developing long-lasting B-cell immune memory. The sustained infected cells lysis overfeeds high levels of viral proteins < 70 kDa, increases B-cell activation and, in the shift from a Th1 to a Th2 immune response, can trigger a cytokine storm. The continuous BCR activation increases IL-10 release that can lead to cytokine storm, apoptosis, and immune paralysis. Here, we propose a new vaccine design using the polymerization of viral antigens that could be ready in short time, would be cheap and easy to develop because it is based on classic technologies available in every country, is safe because it does not employ genetic material, and would able to promote long-lasting B-cell immune memory and IgG2a production.