Figure 2.

Molecular mimicry is characterized by the presence of epitopes on SARS-CoV-2 spike glycoprotein that cross-react with host antigens leading to the activation of cellular and humoral autoreactivity, due to the similarity to self-epitopes. Bystander activation implies the activation of a non-specific and over-reactive antiviral immune response. This phenomenon leads to the liberation of self-antigens from the damaged tissue and the release of cytokines from the antigen presenting cells (APCs). Self-antigen is then taken up by APCs and presented to T cells. This way, APCs activate autoreactive T cells, exacerbating the tissue destruction. A persistent viral infection can lead to the phenomenon of epitope spreading. In fact, the perpetuation of tissue damage can promote the release of new self-antigens that may activate more autoreactive T cells when taken up by APCs [83].