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In laboratory tests, a team from the German Center for Cardiovascular Research shows that the viruses can also penetrate heart cells and multiply there. Because they can clearly see the mechanisms, the researchers also conclude that there are two possible treatment methods. Heart problems are repeatedly found in patients suffering from Covid-19. As early as July, researchers at the University Medical Center Hamburg-Eppendorf (UKE) found out that the coronavirus can infect heart cells and multiply in them. A working group from the German Center for Cardiovascular Research has now shown how the infection takes place on cardiac muscle cells. Their results have been published in the journal Cardiovascular Research. To this end, heart muscle cells were first generated from stem cells that have not yet been assigned to a specific tissue type. These were then treated with isolated virus material from the first German corona patient who had returned to Germany from Wuhan, China, in March. The cells took up the virus, the virus RNA multiplied and the virus-typical spike protein was also formed.
In order to reproduce the heart more closely, the researchers built small clumps of cells from heart muscle cells, blood vessel cells and connective tissue cells. They also detected the spike protein in this. Sars-CoV2 could also multiply in real human heart tissue. Overall, however, the experiments suggested that heart cells are slightly less susceptible to the virus than other cell types. The rate of cell death triggered by the infection was therefore lower and it also took a little longer for the heart cells to die. The experts also observed the “heartbeat” of the twitching heart cells in the test tube. “The cells get really stressed when they are exposed to the virus. The so-called ‘beating rate’ only increases sharply and falls after three days because the cells die,” says Stefanie Dimmeler, who coordinated the experiments Communication from Goethe University Frankfurt cited.
Apparently the virus follows a slightly different mechanism in heart cells than in lung cells, for example. Heart muscle cells do not have the membrane protein TMPRSS2, which the coronavirus needs in lung cells in addition to the ACE2 receptor in order to penetrate the cells. In heart muscle cells it uses another protein, cathepsin.
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This already results in treatment options. Because active substances that inhibit this protein, so-called cathepsin inhibitors, successfully stopped the virus from multiplying in the heart muscle cells in the laboratory tests. The drug Remdesivir, which is already used for corona therapy, was also apparently able to prevent the pathogen from multiplying. It is still unclear whether this can also be used in acute therapy. “The heart muscle cells are normally well protected because the virus first has to penetrate the vascular barrier. In order to examine the virus infestation of the heart in the human body in the acute phase, we would have to take regular biopsies from the heart of sick people, which is almost impossible,” says Dimmeler . However, one could try to treat corona patients with problematic heart reactions with cathepsin inhibitors.