RESEARCHERS have identified five genes that increase a person's chances of becoming critical ill or dying as a result of Covid.
The team, from Edinburgh University, made the discovery by comparing the DNA of 2,700 patients in 208 intensive care units across the UK, against samples from health volunteers.
They were able to pinpoint key differences in five genes which partly explain why some people develop life-threatening symptoms from the infection, while others are unaffected.
It could also offer clues as to why the virus wreaks such a devastating toll on certain families.
Last month, 74-year-old grandmother Gladys Lewis, from Wales, and her two sons aged 42 and 44, died within five days of one another.
In Northern Ireland, a mother, father, and son - who was in his 50s and worked for the health service in Belfast - also died in the space of two weeks between October and November.
And in one of the worst reported tragedies to date, an outbreak claimed the lives of seven members of the same family in the US state of New Jersey in the space of a few weeks in March.
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Dr Kenneth Baillie, the project’s chief investigator and an academic consultant in critical care medicine, said: "It certainly is the case that genetic effects run in families, so it's possible that that could explain these sorts of devastating events.
"It's also possible that there might be other, rarer gene mutations and we'll find them in the genomic sequencing, which is the next phase."
The findings echo previous research done in the 1980s which compared mortality from infectious diseases, cancer, and cardiovascular diseases among people who had been adopted.
It revealed that people whose biological parent had died young from an infectious disease were six times more likely to succumb to an infectious disease also - even if they had never met.
The same was not true of cancer or cardiovascular disease, where the adopted person's risk dovetailed with their adoptive parents - but not their biological mother or father.
While genes cannot influence exposure to pathogens such as respiratory viruses, they do affect how the body responds.
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Life threatening Covid is an inflammatory lung disease which occurs when the body's immune system overreacts to infection, attacking the host's own tissues.
The five genes identified by the Edinburgh University researchers are involved in two molecular processes: antiviral immunity and lung inflammation.
Having highlighted the genes, the team were then able to predict the effect of existing drug treatments on patients, because some genetic variants respond in a similar way to particular therapeutics.
For example, they showed that a reduction in the activity of one of the five genes -TYK2 - protects against Covid-19.
A class of anti-inflammatory drugs called JAK inhibitors, which includes the rheumatoid arthritis drug baricitinib, already produces this effect.
They also discovered that boosting the activity of another of the five genes - INFAR2 - is likely to create protection by mimicking the effect of protein molecules which are released by immune system cells to defend against viruses.
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However, experts caution that - to be effective - patients might need the treatment early in disease.
The researchers say that clinical trials should focus on drugs that target these specific antiviral and anti-inflammatory pathways.
Dr Baillie, who is also a senior research fellow at the Roslin Institute, thanked the patients and their families for taking part.
He added: “This is a stunning realisation of the promise of human genetics to help understand critical illness.
"Just like in sepsis and influenza, in Covid-19, damage to the lungs is caused by our own immune system, rather than the virus itself.
"Our genetic results provide a roadmap through the complexity of immune signals, showing the route to key drug targets.
“Our results immediately highlight which drugs should be at the top of the list for clinical testing. We can only test a few drugs at a time, so making the right choices will save thousands of lives."
The study is published in the journal, Nature.
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