Hijacking Coagulation Using Platelets

One-third of COVID-19 patients in ICUs develop thrombotic complications leading to high morbidity

- Dr Rajani Kanth Vangala

In the one year since SARS-CoV-2 (COVID-19) arrived on the scene, the virus has precipitated nothing short of a serious global health crisis. One of the virus’s less-obvious dimensions has been its impact on the human cardiovascular system.

Over the past year, COVID-19 has been associated with several critical cardiovascular complications. So much so that even patients with no history of cardiovascular disease seem to be at risk of developing cardiovascular complications as a result of COVID-19. Indeed, patients with severe COVID-19 infection commonly experience thrombotic disorders with elevated D-dimer, sepsis, disseminated intravascular coagulation (DIC) with high mortality rates.

Several large-scale studies have shown that 18.8%-36.2% of COVID-19 patients show thrombocytopenia at the time of admission into hospital and in cumulative, 31% of ICU patients experience thrombotic complications. Even though there is overwhelming evidence of a hypercoagulable state in COVID-19 patients, the molecular events and underlying mechanisms still remain largely a mystery.

The role of platelets

It is well known that platelets play an important role in thrombosis and hemostasis. During infection, activated platelets adhere to the sub-endothelium and their hyperactivity can result in thrombus formation, leading to arterial ischemia and pulmonary embolisms. Many viral infections, such as hepatitis C (HCV), Ebola, human immunodeficiency virus (HIV), dengue virus (DV) and influenza, directly lead to the activation of platelets triggering uncontrolled coagulation cascades, resulting in lung injury. We know that SARS-CoV-2 uses a spike protein to bind to ACE2 receptors on the host cell for entry and multiplication, but we have little insight into how this influences platelets.