Table 1.

Comparison of COVID-19 immunothrombosis with HIT and VITT.

	COVID-19 Pneumonia	HIT	VITT
Thrombosis Mechanism	RNAaemia Embolism from pulmonary vein territory?	Platelet Degranulation at sites of thrombosis linked to vessel wall thrombosis or injury	Platelet degranulation at venous territory which drain microbial basins triggered by PF4 microbial interactions
Age	Older- Male		Younger Female
PF4 Autoantibodies	8% Reported low level and may not directly activate platelets Platelet activation by other immune complexes	High titre	Very common high titre
Anion scaffold for PF4	None	Heparin (acting in the vasculature and in marginal zone B cells in spleen)	Double stranded DNA (acting in lymph nodes leading to breakage of tolerance)
Location of Thrombosis	Arterial Predominant Venous reported	Venous and arterial	Venous
Other Autoantibodies	Multiple but pathogenic role debatable	No	No
Initiating Event	Multiple mechanisms including RNA activation of coagulation	-Vascular wall insult with heparin PF4 interaction	1) Endovascular PF4 binding of microbes 2) Extravascular DNA-PF4 interaction at sites of “needle stick injury”
Adjuvant	RNA	Heparin-PF4 large complexes	Viral DNA-PF4 complexes No evidence self DNA-PF4 complexes?
Primary Vascular Territory	Intravascular Lung Primary Secondary Systemic thrombosis –arterial and venous	Intravascular at sites of clot –typically DVT but also arterial	Cavernous sinsus or portal venous thrombosis Would not occur with inhaled DNA vaccines?