Pattern of molecular mimicry between spike protein of SARS CoV2 and human thrombopoietin in beta, delta and omicron variants: a basic pathophysiological process of COVID-19 related thrombocytopenia.

Thrombocytopenia is a possible problem in COVID-19. Hemorrhagic problem might be a result of thrombocytopenia in COVID-19. Due to the emergence of thrombocytopenia in COVID-19, the pathophysiology of thrombocytopenia in COVID-19 is currently a important topic in blood research. An important possible pathogenesis is the molecular mimicry. In variants of COVID-19, the change in spike might occur and the effect on molecular mimicry, which might further imply for association with thrombocytopenia. Specific study on this phenomenon can help better understand on the pathogenesis process of thrombocytopenia. In this study, the authors assessed the magnitude of molecular mimicry between the spike protein of SARS CoV2 and human thrombopoietin in wild type and important variants of COVID-19. In this work, the authors used a molecular similarity analysis to assess the impact of mutations in delta and delta plus variations. Each variant has a decreased similarity score and the omicron variant has the least similarity score. In this study, the decreased similarity score in the variant can imply decreased mimicry phenomenon. Hence, it can imply that there will be decreased COVID-19 thrombocytopenia problem in the variant. AJBR