From the Guidelines

Yes, viral infections can cause thrombosis (blood clots).

The evidence suggests that COVID-19, a viral infection, can lead to a hypercoagulable state, increasing the risk of thrombotic complications, including both microthrombosis and venous thromboembolism (VTE) 1.
Studies have shown that patients hospitalized with COVID-19 have a higher incidence of VTE compared to those with other underlying illnesses, and that anticoagulant thromboprophylaxis may reduce mortality in these patients 1.
The mechanisms underlying arterial thrombosis or thromboembolism in patients with COVID-19 are complex and involve multiple platelet-coagulation pathways, including coagulopathy, platelet activation and aggregation, and endothelial dysfunction 1.
Guidelines and recommendations have been published to facilitate clinical decision-making on the management of coagulopathy and thrombosis in critically ill patients with COVID-19, emphasizing the need for an individualized approach to patient management and prospective randomized clinical trials to address important anticoagulation issues in this population 1.

COVID-19 can lead to a hypercoagulable state, increasing the risk of thrombotic complications.
Anticoagulant thromboprophylaxis may reduce mortality in patients hospitalized with COVID-19.
The mechanisms underlying arterial thrombosis or thromboembolism in patients with COVID-19 are complex and multifactorial.
An individualized approach to patient management is recommended, taking into account the patient's specific risk factors and clinical presentation.

From the Research

Viral infections, including SARS-CoV-2, influenza, and other respiratory viruses, can lead to thrombotic complications 2, 3, 4, 5.
The pathophysiology of thrombosis in viral infections involves a hyperinflammatory response, platelet activation, and triggering of the coagulation cascade 2, 3.
Tissue factor (TF) expression is induced in various cell types during viral infection, contributing to disseminated intravascular coagulation and thrombosis 5, 6.
Extracellular vesicles (EVs) released by TF-expressing cells can also contribute to thrombosis, and elevated EVTF activity has been associated with mortality in severe viral infections 5.

The reported rate of venous thromboembolism (VTE) among critically ill patients infected with SARS-CoV-2 has been 21% to 69% 3.
The thrombotic risk appears to be significantly higher in patients with COVID-19 compared to those with influenza, but remains a concern in patients with influenza, particularly in those with severe disease or pneumonia 4.
Breakthrough VTE, or the acute development of VTE despite adequate chemoprophylaxis or treatment dose anticoagulation, has been shown to occur with severe infection 3.

The pathophysiology of thrombosis in viral infections is likely multifactorial, involving cell-mediated responses, endothelialitis, cytokine release syndrome, and dysregulation of fibrinolysis 3.
Anticoagulants, such as heparin, have emerged as potential therapeutic agents for addressing viral infection, inflammation, and thrombosis 3.
Early VTE prophylaxis should be provided to all admitted patients, and therapeutic anticoagulation therapy may be beneficial for critically ill patients 3.