Viruses are not all the same. Nor are the damage they can create to the cells of the human organism superimposable, even when perhaps they are not the first “target” of the infection. It is the scientific morality that emerges from a particularly sophisticated research, which appeared on Immunology and conducted by a group of researchers from the University of Queensland, including John Fraser e Arutha Kulasinghe.
The study, conducted on the hearts of people who died following Covid-19 and the consequent molecular analysis of myocardial cells, shows that the Sars-CoV-2 virus would not limit itself to creating a sort of inflammatory and coagulative “decompensation”, as it can happen even after infection with influenza viruses, but it would be able to trigger real modifications of cellular DNA, with damage that persist over time and that could help explain the onset of Long-Covid.
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Specific tests on heart cells
The starting point of the experts was the objective greater impact on the heart of Covid compared to the flu and the other viroses of the season. The scholars have examined the cardiac tissues collected during autopsies of patients who died from Covid (seven), flu (two) and other causes (six), precisely to directly evaluate what happens in the heart tissue following the infection. viral.
Virus-induced damage and failure to repair
While they did not identify viral particles in the heart samples they examined, they saw a number of Sars-CoV-2 virus-induced cellular DNA damage and failure. In particular, according to what the researchers write, “DNA damage and repair mechanisms promote genomic instability and are related to chronic diseases such as diabetes, cancer, atherosclerosis and neurodegenerative disorders”.
A key to long-Covid?
Compared to other respiratory viruses, therefore, Sars-CoV-2 would attack the heart differently. Generally, in fact, the problems related to influenza viruses are mainly linked to the excessive inflammatory response that characterizes the infection.
In the case of Covid-19, however, the virus itself would somehow attack the cardiac cellular DNA, with potential repercussions from a distance. In practice, it would be a sort of direct attack and not a reflex action linked to the organism’s abnormal response to the viral stimulus.
No, it’s not like the flu
This observation can help to understand the possible mechanisms at the origin of the long-Covid that occurs in some people and above all offer possible indications for future therapies. At the moment, however, the numbers of patients studied do not allow to risk definitive evaluations: it is necessary to understand what happens on numerically larger samples. What is certain is that, as the authors themselves point out, Covid is not “just like the flu”.
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Thus Covid has an impact on the heart
The Sars-CoV-2 virus, in addition to a direct action on the endothelial cells present on the innermost wall of blood vessels, can promote an inflammatory response with alteration in the coagulation control mechanisms. All of this causes an increased risk of thrombosis and embolismsboth in the arteries and in the veins.
The inflammation induced by the virus and probably the presence of the virus itself can in fact alter the balance of coagulation processes, with a consequent greater risk of heart attack and phenomena such as pulmonary embolisms.
But that’s not all: compared to the classic seasonal flu, Covid-19 induces documented myocardial damage in some patients with an increase in tissue death markers, such as CPKMB or troponin. The potential mechanisms that explain cardiac involvement are linked to various phenomena: they range from the classic inflammatory storm with consequent release of cytokines, up to the lack of “satisfaction” of cardiac requests linked to the increase in myocardial demand, up to the direct diffusion of virus in the myocardium. In addition, of course, to the increased risk of clotting problems.
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