How the SARS-Cov-2 coronavirus attacks the heart
Numerous studies have already shown that severe COVID-19 courses associated with organ damage are. Also heart complications are among the possible consequences of a coronavirus infection. A German research team has now been able to track the virus’ journey into the heart and show how the pathogen does it heart attacks.
researchers of Ruhr-University Bochum a Dr. Nazha Hamdani found out how in a recent study Coronavirus SARS-CoV-2 infects human heart muscle cells and that this infection of the heart is primarily promoted by inflammation and oxidative stress. The results were recently published in the “International Journal of Cardiology” presents.
Heart damage in coronavirus infections
Especially in those affected with underlying diseases such as obesity, Diabetes and high blood pressure heart complications occur in severe cases of COVID-19. But so far it has remained unclear how exactly the corona virus damages the heart.
Using state-of-the-art technology, the working group at Bochum University Hospital has now analyzed heart tissue structures from patients who had contracted COVID-19 and some of whom died as a result of the infection.
SARS-Cov-2 can directly attack heart muscle cells
One of the team’s first fundamental findings is that the virus is indeed capable of directly affecting heart muscle cells. SARS-Cov-2 was detected directly in the heart muscle cells of those affected.
“Our observations show that the virus puts pressure on the heart muscle, attacking and weakening the force of contraction, i.e. the pumping function of the heart”explains research director Hamdani.
How does the corona virus get to the heart?
A key question that arises from this is how the virus gets to the heart and enters the organ. The researchers discovered a possible mechanism associated with heart muscle cell dysfunction in those affected with severe SARS-Cov-2 infections.
This leads to activation of certain enzymes that break down proteins. The process is called in technical jargon as proteolytic activity designated.
Overall, the findings indicate that SARS-Cov-2 enters cells via activation of the spike protein by enzymes responsible for breaking down proteins, and that entry into cells depends on these breaking enzymes.
Heart cells are stimulated to commit suicide by SARS-Cov-2
Special proteins are involved in the process that are responsible for the cellular suicide (apoptosis) are responsible. “The results imply that apoptosis contributes to the deterioration in cardiac contractility observed in Sars-Cov-2 patients”explained Dr. Hamdani.
As the research team was able to show in a further step of the study, the processes described above were significantly aggravated when they took place in an environment that oxidative stress and inflammatory reactions is.
This seems to be the reason why heart damage in the course of a coronavirus infection is particularly common people with underlying diseases appear.
Responsible for the deterioration are so-called Neutrophile. These are primary cell types that play an essential role during inflammatory reactions and migrate rapidly from the bloodstream to damaged tissue.
SARS-Cov-2 can spread through the heart in several ways
In addition, the team was able to demonstrate that SAR-Cov-2 also contains the protein Neuropilin-1 (NRP-1) as a portal of entry into the cells. Consequently, according to Hamdani, are equal to the corona virus several mechanisms available to spread in the heart.
“Sars-Cov-2 is able to spread in the infected heart in a receptor-dependent and receptor-independent manner”summed up Dr. Hamdani. (vb)
Author and source information
This text corresponds to the specifications of medical specialist literature, medical guidelines and current studies and has been checked by medical professionals.
Author:
Graduate editor (FH) Volker Blasek
Sources:
- Ruhr-Universität Bochum: How the corona virus attacks the heart (published: 06/29/2022), news.rub.de
- Melina Tangos, Heidi Budde, Nazha Hamdani et al.: Sars-Cov-2 infects human cardiomyocytes promoted by inflammation and oxidative stress; in: International Journal of Cardiology (2022), internationaljournalofcardiology.com
Important NOTE:
This article contains general advice only and should not be used for self-diagnosis or treatment. He can not substitute a visit at the doctor.
