RT Journal Article
SR Electronic
T1 Molecular mimicry between Spike and human thrombopoietin may induce thrombocytopenia in COVID-19
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.08.10.455737
DO 10.1101/2021.08.10.455737
A1 Janelle Nunez-Castilla
A1 Vitalii Stebliankin
A1 Prabin Baral
A1 Christian A Balbin
A1 Masrur Sobhan
A1 Trevor Cickovski
A1 Ananda Mohan Mondal
A1 Giri Narasimhan
A1 Prem Chapagain
A1 Kalai Mathee
A1 Jessica Siltberg-Liberles
YR 2021
UL http://biorxiv.org/content/early/2021/08/11/2021.08.10.455737.abstract
AB Thrombocytopenia, characterized by reduced platelet count, increases mortality in COVID-19 patients. We performed a computational investigation of antibody-induced cross-reactivity due to molecular mimicry between SARS-CoV-2 Spike protein and human thrombopoietin, the regulator of platelet production, as a mechanism for thrombocytopenia in COVID-19 infections. The presence of a common sequence motif with similar structure and antibody-binding properties for these proteins strongly indicate shared molecular mimicry. Recent reports of antibodies in COVID-19 patients and pre-pandemic samples against epitopes containing the motif offer additional support for the cross-reactivity. Altogether, this suggests cross-reactivity between an antibody with affinity for Spike protein and a human protein. Consideration of cross-reactivity for SARS-CoV-2 is important for therapeutic intervention and when designing the next generation of COVID-19 vaccines to avoid potential autoimmune interference.One-Sentence Summary SARS-CoV-2 Spike protein may trigger the production of antibodies that can cross-react with human thrombopoietin.Competing Interest StatementThe authors have declared no competing interest.