Not just immune system. There is one more reason why you can get severe covid infection. Read here

Apart from weak immunity, there is another factor that determines whether COVID can cause severe infection and that is dysfunctional endothelium, in more simple words, the vascular system, a recent study cited. Many clinical symptoms, such as the destruction of blood vessels in the lungs and acute respiratory distress syndrome, pointed to an impact on the endothelium, it also said.

'In our study, we investigated which immune cells are activated in severe cases and in what way the endothelium, in other words, the blood vessels, and their activation play a role in the disease progress,' explained Prof. Christine Falk, Scientist at the Hanover Medical School (MHH) and the German Center for Infection Research (DZIF). The study has been published in the 'Signal Transduction and Targeted Therapy Journal'.

What is endothelium and how COVID can impact it? 

The endothelium is a thin layer of cells that line blood vessels, forming a barrier between blood flow and the surrounding tissues. 

COVID infection can cause strong activation of the immune system and endothelial cells in the lungs, resulting in the release of various soluble plasma proteins. Severe COVID-19 cases are associated with a dysfunction of the endothelium, wherein the barrier between the alveoli (tiny air sacs inside your lungs) and the surrounding vessels is no longer intact.

How severe is the damage? 

During the study, the researchers saw that there are seven plasma proteins that are associated with the severe form of the disease. They can cause serious inflammation that can permanently damage the endothelial barrier. 

Furthermore, recovery from severe COVID-19 cases seems to be related to the regeneration of this endothelial barrier.

Currently, investigations are on to find whether endothelial inflammation with the overreaction of the T-lymphocytes (that play a central role in adaptive immune response) can cause lasting damage, to what extent the regeneration of the lung is impaired and the nervous system is affected. 

Which immune cells were detected in the COVID-19 ICU patients? 

The study showed excessive activation of T-lymphocytes and natural killer cells as well as the development of memory T-cells and strong proliferation of plasmablasts, cells that can produce large amounts of antibodies.

Furthermore, COVID patients who are in the ICU had high titres of spike-and nucleocapsid-specific antibodies. And the immune cell phenotype of these patients mainly changed over time and was less related to the progressive severity of the disease.

The progression of COVID-19, on the other hand, was closely linked to increased levels of various soluble plasma proteins, namely certain inflammatory mediators and especially endothelial factors.

"We were able to demonstrate that ICU patients with COVID-19 can be divided into different groups based on their plasma protein profile, which is associated with disease severity", explained lead author Louisa Ruhl, a PhD doctoral student at MHH.

How do the activated immune cells act on the endothelial cells?

Christine Falk's team now wants to investigate which elements of the immune system lead to activation and damage of the endothelium and whether the strong activation of the immune system also leads to the development of virus-specific T-lymphocytes that can recognise and destroy infected cells and thus contribute to overreaction.

The study has shown that there are also shifts in the immune cell repertoire in recovered ICU patients with COVID-19. This could be related to the development of Long-COVID cases.

(With inputs from agencies)