The standard method for detecting infection with SARS-CoV-2 leading to COVID-19 disease involves a genotypic (PCR) test for the virus on nasopharyngeal swabs, but it is unpleasant, requires specific training, and can have poor sensitivity [1–7]. What would be desirable is a rapid and phenotypic test on the host that indicates the presence, and if possible the severity, of clotting pathologies, which is one of the consequences of infection. Presently, the standard method for this is based on CT chest scans for pneumonia, which have high sensitivity but lower specificity (see [7–10] and below), but this is neither cheap nor universally available.
A poor prognosis for recovery, is linked to various comorbidities, of which Type 2 Diabetes Mellitus (T2DM) is probably the most frequently mentioned comorbidity. It is widely recognised [11–21] that extensive blood clotting has a major role in the pathophysiology of COVID-19 disease severity and progression, yet so can excessive bleeding [22, 23]. The solution to this apparent paradox lies in the recognition  that these phases are separated in time: the later bleeding is mediated by the earlier clotting-induced depletion of fibrinogen and of von Willebrand factor (VWF). This first phase of hypercoagulability is accompanied by partial fibrinolysis of the formed clots, and an extent of D-dimer formation that is predictive of clinical outcomes . These features, together with the accompanying decrease in platelets (thrombocytopaenia), leads to the subsequent bleeding. Thus it is suggested that the application of suitably monitored levels of anti-clotting agents in the earlier phase provides for a much better outcome [13, 24].
As well as the extent of clotting, including states similar to the life-threatening disseminated intravascular coagulation (DIC) , a second issue pertains to its nature. Some years ago, we discovered that in the presence of microbial cell wall components [26, 27], and in a variety of chronic, inflammatory diseases [28–30] (including sepsis ), blood fibrinogen can clot into an anomalous, amyloid form . These forms are easily detected by a fluorogenic stain such as thioflavin T, or the so-called Amytracker stains . In all cases, however, these experiments were performed in vitro using relevant plasma, with clotting being induced by the addition of thrombin. In our preliminary experiments this was also the case for plasma from COVID-19 patients, but the signals were so massive that they were essentially off the scale. However, as we report here, the plasma of COVID-19 patients carries a massive load of preformed amyloid clots (with no thrombin being added), and this therefore provides a rapid and convenient test for COVID-19. As the presence of T2DM is a well-known co-morbidity, that significantly decreases survival and a positive outcome for COVID-19 patients, we included such a group in our sample cohort too.