We knew heart damage was common among patients hospitalized with COVID-19, but now how or why. Today, researchers announced the results from studies that have found the spike protein from the coronavirus 2 virus can lead to heart muscle injury through the inflammatory process.
The spike protein is found on the surface of SARS-CoV-2, the virus that causes COVID-19. The spike protein facilitates virus entry into healthy cells, which is the first step in infection. Zhiqiang Lin, Ph.D., lead author of the study and an assistant professor at the Masonic Medical Research Institute in Utica, New York, explained the role of the spike protein.
“It’s already known from the clinical side that COVID-19 infection can induce heart injury, however, what we don’t know is the mechanistic details of how this occurs. What we suspect is that the spike protein has unknown pathological roles. Our data show that the spike protein from SARS-CoV-2 causes heart muscle damage. That’s why it’s important to get vaccinated and prevent this disease.”
Spike proteins latch onto receptors known as angiotensin-converting enzyme 2 (ACE2) on target cells. ACE2 is an important enzyme controlling blood pressure. SARS-CoV-2 infection may impair ACE2 function, which in turn leads to blood pressure increase and, thereby, injures the heart.
To investigate the impact of the SARS-CoV-2 spike protein on the heart, researchers cloned the SARS-CoV-2 spike protein and a NL63 spike protein into the AAV9 viral vector. The AAV9 viral vector was delivered into lab mice to activate the spike protein in the heart muscle cells. They found that the AAV9-mediated the SARS-CoV-2 spike protein, and not the NL63 spike protein, caused heart dysfunction, hypertrophic remodeling (enlargement) and cardiac inflammation.
In lab testing of heart cells cultured in dishes, researchers also observed that the SARS-CoV-2 spike protein made heart muscle cells much larger compared to cells without either spike protein.