From COVID-19 to clot: the involvement of the complement system

In December 2019, the world observed an unexpected outbreak of an emerging disease named coronavirus (COVID-19) that was first reported in Wuhan city of Hubei province of China. Recent literature has shown the association between COVID-19 infection and derangement in the coagulation profile. In this paper, we are discussing thrombo-genesis, especially the role of the complement system in the immune response against COVID-19 and the pathogenesis associated with tissue inflammation and thrombosis. This role can stipulate a groundwork for further investigation of the pathophysiologic importance of complement in COVID-19, and could propose targets for specific intervention. In addition, we delineated current treatments for thrombosis and the potential therapies by using agents to block the terminal complement pathway. Low molecular weight heparin for all (unless contraindicated) hospitalized COVID-19 patients can be lifesaving. Agents that inhibit the terminal events of the complement cascade might be crucial for ensuring an efficient treatment, decrease clots and permit early discharge in relation to COVID-19. Communicated by Ramaswamy H. Sarma

Automated summary

This paper discusses the role of the complement system and the associated pathogenesis in COVID-19. The complement system could potentially be a target for treatment and further investigation. Low molecular weight heparin may be life-saving for hospitalized COVID-19 patients. Agents that inhibit the complement cascade could play a crucial role in COVID-19 treatment.