The severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) is a highly contagious virus that causes a severe respiratory disease known as Corona virus disease 2019 (COVID19). Indeed, COVID19 increases the risk of cardiovascular occlusive/thrombotic events and is linked to poor outcomes. The pathophysiological processes underlying COVID19-induced thrombosis are complex, and remain poorly understood. To this end, platelets play important roles in regulating our cardiovascular system, including via contributions to coagulation and inflammation. There is an ample of evidence that circulating platelets are activated in COVID19 patients, which is a primary driver of the thrombotic outcome observed in these patients. However, the comprehensive molecular basis of platelet activation in COVID19 disease remains elusive, which warrants more investigation. Hence, we employed gene co-expression network analysis combined with pathways enrichment analysis to further investigate the aforementioned issues. Our study revealed three important gene clusters/modules that were closely related to COVID19. Furthermore, enrichment analysis showed that these three modules were mostly related to platelet metabolism, protein translation, mitochondrial activity, and oxidative phosphorylation, as well as regulation of megakaryocyte differentiation, and apoptosis, suggesting a hyperactivation status of platelets in COVID19. We identified the three hub genes from each of three key modules according to their intramodular connectivity value ranking, namely: COPE, CDC37, CAPNS1, AURKAIP1, LAMTOR2, GABARAP MT-ND1, MT-ND5, and MTRNR2L12. Collectively, our results offer a new and interesting insight into platelet involvement in COVID19 disease at the molecular level, which might aid in defining new targets for treatment of COVID19induced thrombosis.