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Infectious Diseases

Updated 25 August 2020

New research finds clues to why the elderly are more susceptible to Covid-19

A new study proposes that the reason why older people are more likely to get seriously ill and die from Covid-19 lies in the way our heart muscle cells change with age.

  • A study of heart cells found that Covid-friendly receptors become more prevalent as we age
  • This could be the reason why the elderly are more susceptible to severe coronavirus symptoms
  • Heart failure is one of the big fatality drivers in the pandemic

It's common knowledge that people over 70 are affected more severely by Covid-19.

Among 45 000 Chinese patients, the Covid-19 case fatality rate in those over 70 was found to be 10.2% – with the rate for cardiovascular disease at 10.5%, and hypertension at 6%.

What might be causing this? A new study published in the Journal of Molecular and Cellular Cardiology proposes that the answer lies in how our heart muscle cells change with age.

READ | Antiviral drugs tied to heart issue in Covid-19 patients 

The coronavirus bond

First, we need to look at how Covid-19 invades the body. What differentiates the new coronavirus from SARS is that SARS-CoV-2 has a type of spike protein which makes it easier to penetrate cells, bind to ACE2 receptors and replicate itself, while destroying resistance.

In severe cases, Covid-19 causes cytokine storms that may end up being fatal.

The researchers hypothesise that the virus may trigger heart problems in older patients as a result of ageing heart muscle cells (cardiomyocytes) being more susceptible to the invasion – due to the different ways that genes encode between DNA, RNA and proteins in these pathways. 

Increased receptors

They found that older cardiomyocytes have an increased number of receptors like ACE2, making the cells more sensitive to viral invasion.

"The expression of Ang-II synthetic enzyme ACE and cognate receptor gene AGTR1 together with BDKBR1 increased with age, the latter normally not expressed in myocytes until induced by inflammation and selectively activated by des-Arg9-bradykinin."

These are harmful amino acids that the researchers believe increase as the ACE2 receptors surface area decreases due to the viral spread.

READ MORE | Heart scans and Covid-19: What the latest science says

Losing battle

"Unlike most other cells, cardiomyocyte numbers remain stable, regenerating slowly. Although particularly vulnerable to viral infection, they have evolved intrinsic mechanisms to combat cytotoxic effects and viral replication mainly by generating type 1 interferon responses."

Unfortunately, the coronavirus fools these countermeasures by producing its own proteins that block these interferons, which becomes especially serious in older patients where virus-friendly receptors are more prevalent.

Need for more studies

More studies are, however, needed to assess whether the viral infection itself is directly damaging the heart muscle cells or if cardiac complications are caused by the cytokine storm.

Also, while older patients have more severe Covid-19 which is more likely to lead to death, scientists are still not sure whether they are more susceptible to infection than younger adults.

"Drugs to treat both acute and long-term effects of SARS-CoV-2 will need to focus on these three key stages of infection: preventing the virus entering cells, stopping viral replication and reducing resulting tissue damage, particularly in the hearts of aged individuals that are the most vulnerable members of society to Covid-19."

READ | Obesity ups odds for severe Covid-19, but age matters

Image credit: Getty Images