Coronavirus: Are genes the Best Medicine?

Day 1: China informs the World Health Organisation (WHO) of an outbreak of a mystery ‘pneumonia’. Day 32: the UK announces its first case of coronavirus. Day 72: the WHO declares the disease a pandemic. 72 days for the world to change forever. But could the susceptibility to and severity of coronavirus be influenced by your genetics?

Symptoms of COVID-19 vary and are dependent on several risk factors, such as age and underlying health conditions. Genetics has already played a pivotal role in understanding, tracking, and treating the virus, but more recently, researchers have been studying whether the genetics are another risk factor in making someone more or less likely to develop symptoms, and how severe the symptoms are.

Genes are sections of DNA which act as an instruction manual for the body, used to create and maintain every biological process, including the immune system. There is a copy of these genes in almost every single cell in the body. Sometimes, when these cells (with the genes inside them) divide and replicate to make new cells, they accidentally change the gene sequence. In humans, 99.9% of our genetic information is the same in everyone, and the remaining 0.1% is caused by changes in the gene sequence. This 0.1% is what determines differences between us. If any changes occur in a gene which impacts the immune response, this can put someone at a higher risk of developing viruses, and experience worse symptoms.

The first hint that genetics may play a role in symptom susceptibility and severity comes from twin studies. In these studies, researchers compare how often certain traits occur in identical twins, who share 100% of their DNA, compared to non-identical twins, who only share 50% of their DNA (the same amount as in normal siblings). The aim is to see whether genetics or the environment have more of an influence on those traits. One study found that, in identical twins, if one twin contracted coronavirus and had severe symptoms, the other twin was more likely to develop the virus with the same severity of symptoms, compared to non-identical twins. Therefore, the researchers concluded that genetics is one of the underlying reasons behind symptom severity, others being age, underlying health conditions, environment, and lifestyle.

So, as the risk of developing severe covid symptoms is partly due to genetics, which genes are actually involved?

In a study carried out in the UK, researchers looked at the genes of 2,244 patients in intensive care with COVID-19. They scanned the genome (all the genetic information) of the patients, to see if there were any changes in any genes, which could explain why these patients experience more severe symptoms.

This study revealed changes to several genes, which may link to symptom severity, including:

  • Tyrosine Kinase 2 (TYK2) gene: This gene plays a role in immunity and inflammation, by regulating immune cells. Changes to this gene can cause the gene to work too hard, which causes a much higher inflammatory response than necessary. This can cause damaging inflammation of the lungs.
  • Dipeptidyl peptidase 9 (DPP9) gene: This gene also plays a role in the inflammatory response to a virus. Again, changes to the gene may cause a much higher inflammatory response, which can cause damage to the lungs.
  • Oligoadenylate synthetase (OAS) gene: This gene triggers a part of the immune response which destroys a virus’ RNA (their version of genetic material), so that the virus cannot replicate and multiply itself inside of the body. If there is a change in this gene, it may not work as well, which means the virus is able to replicate itself much more easily inside the body and cause more harm.
  • Interferon alpha and beta receptor subunit 2 (IFNAR2) gene: This gene is linked to a group of proteins, collectively called an interferon. When a cell is invaded by a virus, it releases interferons to neighbouring cells which then increase their own anti-viral defences, to better fight off a virus. Changes in this gene may cause too little interferon to be produced, meaning the virus is able to invade surrounding cells and replicate more quickly and easily. The researchers found that changes to this gene accounted for 15% of severe covid symptoms.

These findings are vital in understanding the mechanism of the disease and why some patients experience much more severe symptoms than others. This understanding can help in the development of new, or re-purposing of old medicine to treat the disease. Anti-inflammatory drugs, used to treat conditions such as rheumatoid arthritis, can be repurposed to treat damaging lung inflammation, potentially caused because of changes in the TYK2 and DPP9 genes. Also, due to the research on the IFNAR2 gene, scientists have investigated whether giving interferons to patients will help fight the virus. Although these drugs, amongst others, are in the very early stages of testing on COVID-19 patients and still requires large-scale clinical trials to determine safety and effectiveness, none of this would have been possible without the help of genetics.

Overall, research into the genetics of COVID-19 has shown that changes to several genes may be an underlying reason for the variability in coronavirus symptoms in patients. These findings have not only aided in our understanding of the mechanism of the disease but also in potential treatments for those suffering from severe covid. However, there are still many other factors involved which increase your risk of development and severity of COVID-19, and therefore, genes alone don’t ensure that someone won’t suffer severe symptoms. So, continue to follow government guidelines, wash your hands, and stay safe.

 

References

https://covid.joinzoe.com/post/genetics-covid

https://www.bbc.co.uk/news/health-54832563

https://www.nature.com/articles/s41586-020-03065-y

https://ukricvse.services.ukri.org/en/article/cad0009/

https://www.phgfoundation.org/blog/further-genetic-clues-to-severe-covid-19

 

Disclaimer

The information in this blog is for information and entertainment purposes only. I am not a medical professional, so I have never and will never give medical advice in this blog. You should always speak to a healthcare professional about your unique health needs. My opinions are entirely my own and do not reflect the organisations or people I work for. I only discuss published literature in this blog which are referenced with links.


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