Platelet dysfunction caused by differentially expressed genes as key pathogenic mechanisms in COVID-19.

At the end of 2019, the novel coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) became prevalent worldwide, which brought a heavy medical burden and tremendous economic losses to the world population. In addition to the common clinical respiratory symptoms such as fever, cough and headache, patients with COVID-19 often have hematological diseases, especially platelet dysfunction. Platelet dysfunction usually leads to multiple organ dysfunction, which is closely related to patient severity or mortality. In addition, studies have confirmed significant changes in the gene expression profile of circulating platelets under SARS-CoV-2 infection, which will further lead to changes in platelet function. At the same time, studies have shown that platelets may absorb SARS-COV-2 mRNA independently of ACE2, which further emphasizes the importance of the stability of platelet function in defense against SARS-CoV-2 infection. This study reviewed the relationship between COVID-19 and platelet and SARS-CoV-2 damage to the circulatory system, and further analyzed the significantly differentially expressed mRNA in platelets after infection with SARS-CoV-2 on the basis of previous studies. The top eight hub genes were identified as NLRP3, MT-CO1, CD86, ICAM1, MT-CYB, CASP8, CXCL8 and CXCR4. Subsequently, the effects of SARS-CoV-2 infection on platelet transcript abnormalities and platelet dysfunction were further explored on the basis of 8 hub genes. Finally, the treatment measures of complications caused by platelet dysfunction in patients with COVID-19 were discussed in detail, so as to provide reference for the prevention, diagnosis and treatment of COVID-19.