In a new study, researchers found genes that play an important role in allowing SARS-CoV-2 to invade heart cells to become more active with age.
The findings could help explain why age is a major risk factor for dying from COVID-19, with people over 70 years at greatest risk, and why the disease can cause heart complications in severe cases, including heart failure and inflammation of the heart.
The research was conducted by a team at the University of Cambridge and elsewhere.
When this novel coronavirus first emerged, scientists expected it to be primarily a respiratory illness, as the virus usually takes hold first in the lungs.
But as the pandemic has progressed, we’ve seen more and more COVID-19 patients—particularly older patients—affected by heart problems.
This suggests that the virus is capable of invading and damaging heart cells and that something changes as we age to make this possible.
In the study, the team examined the link between COVID-19 and heart failure. They examined cells known as cardiomyocytes to see how susceptible they were to infection by the coronavirus.
Cardiomyocytes make up the heart muscle and are able to contract and relax, enabling the heart to pump blood around the body.
Damage to these cells can affect the ability of the heart muscles to perform, leading to heart failure
To cause damage, the virus must first enter the cell. SARS-CoV-2 is a coronavirus—spherical in shape with ‘spike’ proteins on its surface, which it uses to gain entry.
The spike protein binds to ACE2, a protein receptor found on the surface of certain cells. The virus is also able to hijack other proteins and enzymes, including TMPRSS2 and Cathepsins B and L to gain entry.
The researchers compared cardiomyocytes from five young (19-25-year-old) males and five older (63-78 year old) males and found that the genes that give the body instructions to make these proteins were all much more active in cardiomyocytes from the older males.
This suggests that there is likely to be an increase in the corresponding proteins in aged cardiomyocytes.
The team says as people age, the cells of the heart muscles produce more of the proteins needed by the coronavirus to break into the cells.
This makes these cells more vulnerable to damage by the virus and could be one reason why age is a major risk factor in patients infected with SARS-CoV-2.
Some of the proteins encoded by the genes can be inhibited by existing medicines.
For example, the anti-inflammatory drug camostat inhibits TMPRSS2 and has been shown to block SARS-CoV-2 entry in cells grown in the laboratory.
The study also suggests new targets for medicines that could be developed such as compounds blocking the binding of the virus to ACE2 that may be beneficial in protecting the heart.
One author of the study is Professor Anthony Davenport from the Department of Medicine.
The study is published in the Journal of Molecular and Cellular Cardiology.
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