Hypercoagulability has emerged as a prominent consequence of COVID-19. This presents challenges not only in the clinic, but also in thrombosis research. Health and safety considerations, the status of the blood and plasma supply, the infection status of individual donors, and the mechanisms by which SARS-CoV-2 activates coagulation are all of concern. In this review, we discuss these topics from the basic research perspective. As in other respiratory illnesses, blood and plasma from COVID-19 positive patients carries minimal to no risk of infection to practitioners or researchers. There are currently no special regulatory mandates directing individual donors (for research purposes), blood centers/services or vendors (for blood products for research) to test blood/plasma for SARS-CoV-2 or antibodies. We discuss current theories about how SARS-CoV-2 leads to hyper-coagulant state in severe cases of COVID-19. Our current understanding of the mechanisms behind COVID-19 associated thromboembolic events have centered around three different pathways: (1) direct activation of platelets, enhancing coagulation; (2) direct infection and indirect activation (e.g. cytokine storm) of endothelial cells by SARS-CoV-2, shifting endothelium from an anti-thrombotic to a pro-thrombotic state; and (3) direct activation of complement pathways, promoting thrombin generation. Further investigation on how SARS-CoV-2 affects thrombosis in COVID-19 patients may bring novel anti-thrombotic therapies to combat the disease.