Coronavirus-associated molecular mimicry through homology to a SARS-CoV-2 peptide could be leading to susceptibility in patients with HLA-A*02:01 and HLA-A*24:02 serotypes

Abstract

Relationship of COVID-19 and immunity is complex and can involve autoimmune reactions through molecular mimicry. We investigated autoimmunity related pathological mechanisms involving molecular mimicry that are common to certain coronaviruses, including SARS-CoV-2, by means of a selected peptide sequence (CFLGYFCTCYFGLFC). Accordingly, coronavirus-associated sequences that are homologous to that 15mer sequence in the SARS-CoV-2 proteome are attained first. Then, homologous human and coronavirus sequences are obtained, wherein the coronavirus sequences are homologous to the 15mer SARS-CoV-2 peptide. All the identified query-subject sequences contained at least 7 residue matches in the aligned regions. Finally, parts of those coronavirus and host sequences, which are predicted to have high affinity to the same human leukocyte antigen (HLA) alleles as that of the SARS-CoV-2 sequence, are selected among the query and subject epitope-pairs that were both (predicted to be) strongly binding to the same HLA alleles. The proteins or the protein regions with those predicted epitopes include, but not limited to, immunoglobulin heavy chain junction regions, phospholipid phosphatase-related protein type 2, slit homolog 2 protein, and CRB1 isoform I precursor. These proteins are potentially associated with certain pathologies, but especially the possible CRB1 related coronavirus pathogenicity could be furthered by autoimmunity risk in HLA*A24:02 serotypes. Overall, results imply autoimmunity risk in COVID-19 patients with HLA*A02:01 and HLA*A24:02 serotypes in general, through molecular mimicry. This is also common to other coronaviruses than SARS-CoV-2. These results are indicative at the current stage, they need to be validated. Yet, they can pave the way to autoimmunity treatment options to be used in COVID-19 and its associated diseases.

Severe rhabdomyolysis temporally associated with SARS-CoV-2 vaccine in an adolescent: a case report

“…However, adjuvants like aluminium are not present in BNT162b2_ V. Post-vaccination autoimmune phenomena other than ASIA have been documented in connection to a variety of vaccinations with report of rhabdomyolysis secondary to H1N1 influenza vaccination (14); molecular mimicry has been suggested as a potential explanation (15). Of note, genetic similarity has been established between the SARS-CoV-2 spike glycoprotein, a core element of the BNT162b2_V, and several human proteins (16). As ofyet, no clear peptide sharing between the SARS-CoV-2 spike protein and skeletal muscle-related proteins has been identified, reactions to vaccines resulting in eosinophilic myocarditis have been reported following hepatitis, meningococcal and some combination vaccines however (17).…”