New York, April 3 The SARS-CoV-2, the virus causing Covid-19, can infect cells of the heart's natural pacemaker that maintain the rhythmic beat, setting off a self-destruction process within the cells, according to a preclinical study.
The findings offer a possible explanation for the heart arrhythmias that are commonly observed in patients with Covid infection, said researchers at Weill Cornell Medicine, NewYork-Presbyterian and NYU Grossman School of Medicine.
In the study, reported in the journal Circulation Research, the team used an animal model as well as human stem cell-derived pacemaker cells to show that Covid can readily infect pacemaker cells and trigger a process called ferroptosis, in which the cells self-destruct but also produce reactive oxygen molecules that can impact nearby cells.
"This is a surprising and apparently unique vulnerability of these cells - we looked at a variety of other human cell types that can be infected by SARS-CoV-2, including even heart muscle cells, but found signs of ferroptosis only in the pacemaker cells," said Shuibing Chen, Professor at Weill.
Arrhythmias including too-quick (tachycardia) and too-slow (bradycardia) heart rhythms have been noted among many Covid patients, and multiple studies have linked these abnormal rhythms to worse Covid outcomes. How SARS-CoV-2 infection could cause such arrhythmias has been unclear, though.
In the new study, the researchers, examined golden hamsters - one of the only lab animals that reliably develops Covid-like signs from SARS-CoV-2 infection - and found evidence that following nasal exposure, the virus can infect the cells of the natural cardiac pacemaker unit, known as the sinoatrial node.
The team then used advanced stem cell techniques to induce human embryonic stem cells to mature into cells closely resembling sinoatrial node cells.
They found that these induced human pacemaker cells express the receptor ACE2 and other factors SARS-CoV-2 uses to get into cells and are readily infected by SARS-CoV-2. The researchers also observed large increases in inflammatory immune gene activity in the infected cells.
Further, they found that the pacemaker cells, in response to the stress of infection, showed clear signs of a cellular self-destruct process called ferroptosis, which involves accumulation of iron and the runaway production of cell-destroying reactive oxygen molecules.
Although in principle Covid patients could 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.
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