SARS-CoV-2 Spike and Human Proteins

The emergence and rapid outbreak of a novel coronavirus, namely, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in China in 2019, caused a global pandemic, which is popularly known as the coronavirus disease 2019 pandemic (COVID-19).

Some of the common symptoms of COVID-19 include cough, fever, loss of taste/smell, and shortness of breath. Additionally, many individuals infected with SARS-CoV-2 remain asymptomatic.

However, some COVID-19 patients experience more severe complications including thrombosis, myocarditis, and thrombocytopenia.

Scientists identified molecular mimicry hotspots in the S region. They revealed the presence of molecular mimics with a high autoimmune potential in clusters within the S protein of SARS-CoV-2. Researchers observed that some clusters contained many molecular mimics whose motifs are found in human proteins. Molecular mimics present in the α-helices exhibited higher structural similarity based on the normal conformation of the helix. Additionally, molecular mimics in coil regions showed marked similarities.

Researchers reported that a TQLPP motif (coil region) in the Spike and thrombopoietin protein shares similar antibody binding properties. The finding of the study related to the TQLPP motif indicated significant potential for cross-reactivity between Spike and hTPO due to molecular mimicry, and this may affect platelet production and cause thrombocytopenia. In silico studies also predicted cross-reactivity with other TQLPP-containing proteins (e.g., NEK10), which requires in vivo validation.

The current study has also shed light on cross-reactivity facilitated through the ELDKY (α-helices) motif between the S domain and PRKG1, TPM1, and TPM3. Researchers stated that PRKG1 is connected with cardiac complications and blood clotting disorders.

The authors reported two epitopes, namely, the TQLPP motif and ELDKY motif, to be associated with molecular mimicry in SARS-CoV-2. This computational study provides insights into the autoimmune potential of SARS-CoV-2 (pathogen) for therapeutic intervention or vaccine design, to avoid any autoimmune interference.

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