SARS-CoV-2 targets plaque macrophages, and its entry is increased in cholesterol-loaded primary macrophages
By Elana Gotkine HealthDay Reporter
THURSDAY, Oct. 5, 2023 (HealthDay News) — Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) seems to infect coronary vessels, inducing plaque inflammation, according to a study published online Sept. 28 in Nature Cardiovascular Research.
Noting that patients with COVID-19 infection present an increased risk for ischemic cardiovascular complications up to one year after infection, Natalia Eberhardt, Ph.D., from New York University School of Medicine in New York City, and colleagues examined whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques.
The researchers reported that in coronary lesions taken at autopsy from severe COVID-19 cases, SARS-CoV-2 viral RNA was detectable and replicated. Plaque macrophages were targeted by SARS-CoV-2, and they exhibited stronger tropism for arterial lesions than adjacent perivascular fat, correlating with levels of macrophage infiltration. Increased SARS-CoV-2 entry was seen in cholesterol-loaded primary macrophages, which was partly dependent on neuropilin-1. A robust inflammatory response was induced by SARS-CoV-2 in cultured macrophages and human atherosclerotic vascular explants, with secretion of cytokines that trigger cardiovascular events.
“Our study highlights the hyperinflammatory response orchestrated by SARS-CoV-2-infected plaque macrophages and foam cells as a mechanistic link between infection of atherosclerotic coronary vessels and acute cardiovascular complications of COVID-19,” the authors write.
The laboratory of one author received research funding from several pharmaceutical companies.
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