Mice study claims to have found long COVID’s ‘real’ perpetrator Premium

A new study has found that rather than being part of the effect, fibrin is the driver of long COVID symptoms, potentially heralding a breakthrough treatment.

In scientific circles, the SARS-CoV-2 virus is well-known as a vasculopathic agent: a damager of blood vessels.

The dominant respiratory symptoms associated with COVID-19 are largely due to clotting and inflammation in the blood vessels of the lungs (rather than the direct involvement of the airways). Its more severe complications, including neurological ones like stroke, are rooted in vasculopathy as well.

Persistent thrombo-inflammation is an important mechanism in a complex web of factors that leads to the myriad symptoms of post-acute sequelae of SARS-CoV2 infection — a.k.a. long COVID. This condition continues to affect millions of people worldwide even after high population immunity and the significantly lower incidence of severe COVID-19.

This is why blood thinners have played a significant role in managing the complications due to COVID-19. Sadly, researchers have found that these complications aren’t correlated with the severity of initial COVID-19, meaning a person can have these complications after mild or even asymptomatic COVID-19 infection.

Large knowledge gaps exist regarding the mechanisms underlying the blood’s difficulties with clotting (coagulopathy), their consequences, and treatment options for the resulting inflammation and neuropathology.

A study published in Nature on August 28 provided a new perspective on this scenario and has seeded hope of a breakthrough in managing these cases.

The study was concerned with fibrinogen and fibrin, two components of blood that play important roles in clotting. Fibrinogen is a soluble protein that is formed in the liver and subsequently converted to the insoluble fibrin.