Thus coronaviruses induce cells to commit suicide

It's called apoptosis, and it's a physiological programmed death mechanism for cells. When a coronavirus infection is in place, however, things seem to change

(photo: PIRO4D / Pixabay) Sars-Cov-2, Sars-Cov-1, Mers-Cov: they are all coronaviruses, and all highly pathogenic, that is, capable of generating significant damage to the organisms they infect. We saw it about ten years ago with the SARS and MERS epidemics, and every day we deal with the pathogenicity of Sars-cov-2, the virus responsible for Covid-19. That these microorganisms are capable of deteriorating, sometimes even irreparably, the tissues of the respiratory system has been known for some time, but until now it was unknown how this damage occurred. A group of scientists from the University of Hong Kong managed to shed light on the issue: coronaviruses induce a programmed cell death mechanism, apoptosis, effectively causing them to commit suicide. The findings, which identify a potential target for future coronavirus infection drugs, were published in the open-access journal Science Advances.

Apoptosis, when cells decide to die

Apoptosis, from the Greek apóptosis, a term that indicates the fall of flower petals: thus, in biology, we refer to the refined mechanism of death programmed cell. In fact, in the presence of certain stimuli, the cells that make up an organism can decide, precisely to preserve it in its entirety, to activate some molecular mechanisms that eventually lead to the breakdown of the cell itself, and therefore to its death. A real suicide, which however does not cause damage to the body, on the contrary, it allows it to live. But not always everything goes as it should and even apoptosis can cause significant damage: this is what happens to the cells of the respiratory system when the body is infected with a highly pathogenic virus. It all starts as a defense mechanism: since the virus inside the cell creates a lot of damage, the cell, to escape it, opts for programmed death. The more pathogenic (and contagious) a virus is, the more cells will decide to die, causing extensive damage to the respiratory tissues, which only worsens the severity of the viral infection. If for some viruses this mechanism is already known (it also happens with the flu), for coronaviruses it had not yet been investigated in detail.

The study

To fill this gap, the Hong Kong University researchers, led by Hin Chu, studied what happens to respiratory tissues after Mers-Cov infection in vitro, in human lung cells and in mice. In particular, they observed that, following infection by the coronavirus, an increase in the mRna molecules that encode for a specific protein, called Perk, is recorded in the epithelial cells of the bronchi, responsible for inducing the molecular mechanism of apoptosis. The molecules of mRna, inside the cell, in fact, function as messengers carrying instructions: in this case the message contained is that of proceeding to cell death. To understand if this was actually the mechanism responsible for the damage due to viral infections, the researchers tried to block the Perk protein: not only in this way was the propagation of Mers-Cov between cells reduced, but it also significantly decreased the cellular apoptosis due to infection and, consequently, tissue damage. And Sars-Cov-2? In the case of this virus, as in Sars-Cov-1, the same mechanism dependent on the Perk protein was not found, but in any case, by blocking apoptosis, the researchers managed to limit cell damage and viral infection. In conclusion, it would seem that Mers-CoV, Sars-Cov-1 and Sars-Cov-2 use different molecular paths to lead the infected cell to suicide: what they have in common, however, is precisely that they can induce most of the damage. through apoptosis. It is hoped that, by understanding these basic mechanisms, drugs aimed at specifically blocking them and thus limiting the serious effects of coronavirus infection could be developed in the future.


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