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The coronavirus would have the ability to chop fibers of the heart and remove DNA from cells

The new coronavirus seems to cut the fibers of the heart into small pieces and with great precision. At least that’s what happened by infecting heart cells in a laboratory, a new study reveals.

Fibers of the heart muscle affected by the coronavirus.

A healthy heart muscle (left), made from adult stem cells, has long fibers that allow it to contract. A SARS-CoV-2 infection causes these fibers to break into small pieces (right), which can prevent the heart from maintaining rhythm

This cutting of muscle fibers, which could permanently damage heart cells, is already terrifying for a laboratory experiment; However, researchers have found evidence that a similar process could be happening in the hearts of COVID-19 patients. It should be noted that this new finding, which has been published in the prepress database bioRXiv last month, it has not yet been peer-reviewed or proven to actually happen in people.

“What we’re seeing here is completely abnormal,” says study co-author Todd McDevitt, a senior researcher at Gladstone Institute in San Francisco, referring to the fact that no other disease is known to be capable of affecting heart cells in that way.

The new finding could explain how COVID-19 inflicts damage to the heart. Previous studies have found signs of abnormalities in this organ in infected patients, including inflammation of muscle tissue, even in relatively mild cases.

For the study, the researchers used special stem cells and created three types of heart cells, known respectively as cardiomyocytes, cardiac fibroblasts, and endothelial cells. In Petri dishes, these cells were exposed to SARS-CoV-2, the virus that causes COVID-19. Of these three cell types, the virus was able to infect and make copies of itself only within cardiomyocytes, or muscle cells of the heart.

The new study was presented by Bruce Conklin (left), Melanie Ott (center), and Todd McDevitt (right)

Cardiomyocytes contain muscle fibers that are made of units called sarcomeres, essential for the contractions that allow the heartbeat. These sarcomeres usually line up in the same direction to form long filaments. But something strange was revealed on the lab plate: the filaments were cut into small fragments.

“The alterations discovered in the sarcomeres would make it impossible for the muscles of the heart cells to generate an appropriate heart rhythm, with the regular succession of systoles and diastoles,” explains Dr. Bruce Conklin, another of the study authors.

But discoveries in the laboratory don’t always translate to real life. So the researchers analyzed tissue samples from three patients who died of COVID-19. Then they saw that the sarcomere filaments were disordered or rearranged – in a pattern similar to, but not exactly the same, as seen in Petri dishes.

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More studies are still needed to conclude that the changes in sarcomeres seen in heart cells are permanent. The authors note that scientists need to carry out a special process to see them, something that is not usually practiced, which would explain why this finding may have gone unnoticed in autopsies until now.

“I hope our work motivates doctors to review samples from their patients and look for these characteristics,” McDevitt longs.

Erased DNA

The researchers also observed another strange fact in the laboratory experiments. For some heart cells, the DNA within the nucleus seemed to have disappeared. “This could mean that cells are essentially disabled and unable to perform their normal functions,” say the authors.

Once scientists understand how SARS-CoV-2 damages heart cells, they could use drugs to mitigate these effects. For example, if the virus uses enzymes to cut sarcomeres, it would be possible to find a drug that blocked this enzyme. (Although the authors clarify that it is not yet clear if it is the virus that directly cuts the sarcomeres or if it unleashes cells to cut the fibers through another mechanism).

“It will be important to identify a protective therapy, one that safeguards the heart from the damage that we are seeing in our models. Even if we cannot prevent the virus from infecting cells, we can give the patient drugs that prevent these negative consequences when the disease is present, “McDevitt concludes.

Source: Live Science


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