Researchers uncover cause of irregular heartbeat in Covid patients: The Tribune India

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New York, April 3

SARS-CoV-2, the virus that causes Covid-19, can infect natural pacemaker cells that maintain heartbeat, triggering a process of self-destruction within the cells, a preclinical study has found.

The findings offer a possible explanation for cardiac arrhythmias commonly seen in Covid-infected patients, researchers from Weill Cornell Medicine, NewYork-Presbyterian and NYU Grossman School of Medicine said.

In the study reported in the journal Circulation Research, the team used an animal model as well as pacemaker cells derived from human stem cells to show that Covid can easily infect pacemaker cells and trigger a process called ferroptosis, in which cells self-destruct but also produce reactive oxygen molecules that can impact neighboring cells.

“This is a surprising and seemingly unique vulnerability of these cells – we have looked at a variety of other human cell types that can be infected with SARS-CoV-2, including even heart muscle cells, but we found signs of ferroptosis only in pacemaker cells,” said Shuibing Chen, a professor at Weill.

Arrhythmias, including heartbeats that are too fast (tachycardia) and too slow (bradycardia), have been noted in many Covid patients, and several studies have linked these abnormal rhythms to worse Covid outcomes. However, how SARS-CoV-2 infection might cause such arrhythmias is unclear.

In the new study, researchers examined golden hamsters – one of the only laboratory animals that reliably develop Covid-like signs from SARS-CoV-2 infection – and found evidence that after nasal exposure, the virus can infect nature cells. pacemaker unit, known as the sinoatrial node.

The team then used advanced stem cell techniques to induce the maturation of human embryonic stem cells into cells that closely resemble cells in the sinoatrial node.

They found that these induced human pacemaker cells express the ACE2 receptor and other factors that SARS-CoV-2 uses to enter cells and are easily infected by SARS-CoV-2. The researchers also observed large increases in the activity of inflammatory immune genes in the infected cells.

Furthermore, they found that pacemaker cells, in response to the stress of infection, showed clear signs of a cellular self-destruction process called ferroptosis, which involves iron accumulation and runaway production of iron molecules. cell-killing reactive oxygen.

Although Covid patients can be treated with ferroptosis inhibitors specifically to protect sinoatrial node cells, antiviral drugs that block the effects of SARS-CoV-2 infection in all cell types would be preferable, the researchers said. IANS

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