Study shows age is a major risk factor for dying from COVID-19 infection

According to a study published recently in the Journal of Molecular and Cellular Cardiology, genes that play a significant role in enabling SARS-CoV-2 to penetrate the heart cells become more active as people age.

Study shows age is a major risk factor for dying from COVID-19 infection
Man wearing a face mask. Image Credit: shameersrk.

This discovery might help explain why age is a significant risk factor for dying from COVID-19 infection; in particular, individuals aged over 70 years have the highest risk. The study could also help explain why the disease can lead to heart complications, such as inflammation of the heart and heart failure, in severe cases of COVID-19 infection.

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. 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.

Anthony Davenport, Professor, Department of Medicine, University of Cambridge

Professor Davenport headed an international research team from the University of Cambridge, Maastricht University, KU Leuven, and Karolinska Institute to study the connection between heart failure and COVID-19.

The team analyzed cells, called cardiomyocytes, to observe their level of susceptibility to COVID-19 infection. The heart muscle contains cardiomyocytes that contract and relax, allowing the heart to pump blood across the body. When these cells are damaged, the heart muscles lose their ability to perform, which leads to heart failure.

The virus should initially penetrate the cell to cause damage. The coronavirus called SARS-CoV-2 has a spherical shape, with “spike” proteins present on its surface through which it enters the cells. These spike proteins attach to a protein receptor, called ACE2, found on the surface of specific cells.

In addition, the virus is capable of hijacking other enzymes and proteins, such as Cathepsins B and L and TMPRSS2 to gain entry.

The team compared cardiomyocytes obtained from five young males, aged between 19 and 25 years, and from five older males, aged between 63 and 78 years. They observed that the genes that give instructions to the body to make these proteins were all considerably more active in cardiomyocytes from the older persons. This indicates that there might be an increase in the corresponding proteins found in the 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. 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.”

Dr Emma Robinson, Maastricht University and KU Leuven

Existing drugs can inhibit some proteins encoded by the genes. For instance, the camostat—an anti-inflammatory drug—blocks TMPRSS2 and has been demonstrated to inhibit the entry of SARS-CoV-2 in cells cultured in the laboratory.

The research also suggests novel targets for drugs that can potentially be developed—for example, compounds that inhibit the virus from binding to ACE2 may be useful in protecting the heart.

The more we learn about the virus and its ability to hijack our cells, the better placed we are to block it, either with existing drugs or by developing new treatments.”

Anthony Davenport, Professor, Department of Medicine, University of Cambridge

Journal reference:

Robinson, E. L., et al. (2020) Genes encoding ACE2, TMPRSS2 and related proteins mediating SARS-CoV-2 viral entry are upregulated with age in human cardiomyocytes. Journal of Molecular and Cellular Cardiology.


The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of AZoLifeSciences.
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