Potential Autoimmunity Resulting from Molecular Mimicry between SARS-CoV-2 Spike and Human Proteins

Area of Science:

• Immunology
• Virology
• Computational Biology

Background:

• Molecular mimicry between viral and host proteins can trigger autoimmune diseases.
• Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) causes COVID-19, a disease with diverse clinical manifestations.
• Autoimmunity may explain the varied symptoms and complications observed in COVID-19 patients.

Purpose of the Study:

• To computationally investigate molecular mimicry between SARS-CoV-2 Spike protein and human epitopes.
• To identify potential autoimmune triggers contributing to COVID-19 pathogenesis.
• To understand the implications of molecular mimicry for COVID-19 complications and therapeutic development.

Main Methods:

• Utilized computational methods to analyze SARS-CoV-2 Spike protein sequences.
• Identified shared motifs between viral antigens and human protein epitopes.
• Evaluated the potential for antibody cross-reactivity and autoimmune responses.

Main Results:

• Discovered molecular mimicry hotspots within the SARS-CoV-2 Spike protein.
• Identified a TQLPP motif shared with thrombopoietin, suggesting a link to thrombocytopenia in COVID-19.
• Found an ELDKY motif shared with human proteins like PRKG1 and tropomyosin, potentially causing clotting disorders and cardiac issues.

Conclusions:

• Molecular mimicry between SARS-CoV-2 and host proteins offers a potential explanation for COVID-19's diverse complications.
• Cross-reacting antibodies targeting thrombopoietin, PRKG1, and tropomyosin may underlie thrombocytopenia, clotting disorders, and cardiac disease in COVID-19.
• Considering autoimmune potential is crucial for developing effective and safe therapeutic interventions for COVID-19.