Scientists from Weill Cornell Medicine and elsewhere found the SARS-CoV-2 virus can infect specialized pacemaker cells that maintain the heart’s rhythmic beat, setting off a self-destruction process within the cells.
The findings offer a possible explanation for the heart arrhythmias that are commonly observed in patients with SARS-CoV-2 infection.
The research is published in Circulation Research and was conducted by Shuibing Chen et al.
Arrhythmias including too-quick (tachycardia) and too-slow (bradycardia) heart rhythms have been noted among many COVID-19 patients, and multiple studies have linked these abnormal rhythms to worse COVID-19 outcomes.
How SARS-CoV-2 infection could cause such arrhythmias has been unclear, though.
In the study, the researchers showed that SARS-CoV-2 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.
They found evidence that following nasal exposure the virus can infect the cells of the natural cardiac pacemaker unit, known as the sinoatrial node.
The researchers also observed large increases in inflammatory immune gene activity in the infected cells.
The team’s most surprising finding, however, was that the pacemaker cells, in response to the stress of infection, showed clear signs of ferroptosis, which involves accumulation of iron and the runaway production of cell-destroying reactive oxygen molecules.
The scientists were able to reverse these signs in the cells using compounds that are known to bind iron and inhibit ferroptosis.
They suggest that although in principle COVID-19 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 plan to continue to use their cell and animal models to investigate sinoatrial node damage in COVID-19 – and beyond.
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