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Covid, this is how the virus damages the heart

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It was already known that Covid also affected the heart. But now it is also understood how the virus manages to interact directly and indirectly with the cells of the heart: this is confirmed by the first results of the “Cardio-CoV” study, carried out by the Monzino Cardiology Center in collaboration with the National Institute of Infectious Diseases Spallanzani ” of Rome, just published on Cardiovascular Research, scientific journal of the European Society of Cardiology (ESC). The study was entirely funded by the Lombardy Region.

Covid-19, the aftermath it can leave on the heart

The researchers, coordinated by Maurizio Pesce, head of the Monzino Cardiovascular Tissue Engineering Research Unit, confirmed that stromal cells, one of the most common cell types in the heart, can be directly attacked by the virus, becoming in turn a vehicle for infection. The greater or lesser replication capacity of the virus in these cells is closely related to the expression levels of the cellular ACE2 receptor. At the same time, regardless of ACE2 levels, stromal cells can react to the invasion of Covid-19 by activating an important inflammatory response. This dual effect resulting from the interaction between viruses and stromal cells can explain the variability of the heart damage found and the cardiac complications that are observed in the most serious cases of Covid-19.

Covid: the consequences on the heart

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“Since the onset of the pandemic, Sars-CoV-2 has shown the power to trigger serious heart problems, such as arrhythmias and heart failure, in some cases persistent even after the virus has recovered – explains Pesce – for this reason we are focused on the interaction between the virus and the heart, with the aim of increasing the current knowledge underlying the clinical manifestations, and identifying new therapies capable of protecting it. In particular, we focused on the stromal cells of the heart which have long been and thoroughly studied in the Monzino laboratories. The main feature of these cells is that they are protagonists of the inflammatory response underlying fibrosis and heart failure, observed in many Covid-19 patients. We isolated these cells, we exposed them to the new Coronavirus in vitro and we analyzed them with proteomics and transcriptomics procedures. Our observations confirmed that the virus actually enters cells through the ACE2 receptor and that therefore it can undergo replication and spread to the heart. In parallel, we observed that the same cells can also evolve towards a pro-inflammatory fate that would result in the deposition of fibrotic tissue, observed in many COVID-19 patients. Finally, we showed that the degree of SARS-CoV-2 infection depends on the expression levels of the ACE2 receptor, i.e. the more ACE2 is present, the greater the infection. Evolution in an inflammatory sense, on the other hand, seems independent of the levels of expression of the receptor ”.

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“The knowledge acquired thanks to this project allows us to insert an important piece in the panorama of the pathogenetic mechanisms underlying the various clinical manifestations of COVID-19, many of which are still largely unknown. Showing that a particular type of heart cell, the stromal cells, can be an important one reservoir viral, i.e. a source of virus production in COVID-19 patients, we have indicated the heart as an additional direct target of the virus that may need specific early antiviral treatments, both to prevent its spread and to limit the expansion of the fibrotic tissue, one of the biggest obstacles to proper cardiac function ”he adds Alessandra Amendola, Biologist Manager at the Spallanzani Virology Laboratory who collaborated in the Cardio-CoV project.

“At the level of better clinical management of COVID-19 patients – concludes Maurizio Pesce – our results support the use of the anti-inflammatories already used in the current anti-COVID-19 protocols to minimize the inflammatory response in the heart, and allow to exclude that there is an interaction between anti-hypertensive treatments and the severity of the infection, at least at the heart level, contrary to what was thought at the beginning of the pandemic. In fact, we have found confirmation that these drugs do not impact on the basal levels of ACE2 expression in patients’ cells. The Cardio-COV study will now develop around two objectives: to define the molecular mechanism that causes ACE2 expression in stromal cells to identify a drug capable of inhibiting viral replication in the heart, and to analyze the inflammatory evolution of the cardiac stroma. to identify new molecular targets, to which to aim in order to prevent their progression “.

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