Molecular mimicry between SARS-CoV-2 spike glycoprotein and mammalian proteomes: implications for the vaccine

Excerpt

The ethiopathology of the diseasome induced by the SARS-CoV-2 infection in the human host [1] is under intensive investigation. A likely mechanism is that the multitude of the diseases encompassed within COVID-19 derives from molecular mimicry phenomena between the virus and human proteins [2]. The rationale is that, following an infection, the immune responses raised against the pathogen can cross-react with human proteins that share peptide sequences (or structures) with the pathogen, in this way, leading to harmful autoimmune pathologies [3, 4]. Accordingly, lungs and airways dysfunctions associated with SARS-CoV-2 infection might be explained by the sharing of peptides between SARS-CoV-2 spike glycoprotein and alveolar lung surfactant proteins [2]. In support of this thesis, additional reports [5‐8] highlight molecular mimicry and cross-reactivity as capable of explaining the SARS-CoV diseases. Of special interest, cross-reactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2 has been also suggested [9]. …