Genes that play an important role in allowing SARS-CoV-2, the virus responsible for COVID-19, to invade heart cells become more active with age, says a new study that joins the growing research into decoding why the elderly are most susceptible to the deadly respiratory disease.
The findings, published in the Journal of Molecular and Cellular Cardiology, could help explain why age is a major risk factor for dying from COVID-19 complications, 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.
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"When this novel coronavirus first emerged, we expected it to be primarily a respiratory illness, as the virus usually takes hold first in the lungs," said lead researcher Anthony Davenport, professor at University of Cambridge.
"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."
The researchers examined cells known as cardiomyocytes to see how susceptible they were to infection by the coronavirus.
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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 significantly more active in cardiomyocytes from the older males.
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.
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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 significantly 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.
"As we age, the cells of our heart muscles produce more of the proteins needed by the coronavirus to break into our cells," said Emma Robinson from Maastricht University and KU Leuven.