COVID-19 infection was first reported in 2019 and was shortly declared a pandemic. Without ample time for targeted research into therapy, various existing drugs were tried with limited success and vaccines speedily emerged. Although with serious consequences in some instances, vaccination brought relief as a public health measure. Before long, breakthrough infections were recorded postvaccination and protection waned with time. With new cases still being recorded, it has become necessary to try more agents with the potential for therapeutic benefits. In viral infections, it is the immune consequences that kill and not the viruses. Therefore in treatment, it is either the body is protected from the infection or the immune consequences. The phase of infection is preclinical and may go unnoticed. Once symptoms appear it is the immune consequences that the body is left to grapple with. That may be why antiviral agents when symptoms appear is too little too late. Victims of COVID-19 infection die from the perturbation of the clotting and fibrinolytic pathways resulting in ineffective oxygenation of the tissues from extensive microthrombi. Therefore, anything that would lyse the microthrombi and allow tissue perfusion should hold the aces. This is where Nattokinase, a fibrinolytic serine protease comes in. It counters Plasminogen Activator Inhibitor-1 which levels mirror disease severity and gives tissue plasminogen activator freedom to lyse the fibrin that clogs the vasculature. This is at the center of the disease pathophysiology and saves the infected individual.