Why some people experience no symptoms from COVID while others fall severely ill and die may be due to five genomic factors, a study has found.
The genetic material studied came from patients in 208 intensive care units in the UK.
One of the biggest mysteries of COVID-19 has been why some people experience no symptoms from the illness, while others fall severely ill and die.
The answer may be in the genes, a new joint British and Australian study suggests.
Researchers from the University of Queensland, Monash University and the University of Edinburgh studied the genomes of 2244 critically ill patients with COVID-19 and compared the genetic makeup of these individuals to the genomes of a control group.
They found five genetic sequences more common in the critically-ill COVID group.
The genes that seemed to make patients more susceptible to COVID were those involved in inflammatory processes and the body’s response to invading viruses.
Lead author Kenneth Baillie and colleagues said knowing which genes play a role in COVID susceptibility could help scientists figure out which existing medications may be able to treat or slow down the illness.
“Our findings reveal that critical illness in COVID-19 is related to at least two biological mechanisms: innate antiviral defences, which are known to be important early in disease, and host-driven inflammatory lung injury, which is a key mechanism of late, life-threatening COVID-19,” he said.
“Both mechanisms may be amenable to targeted treatment with existing drugs.
“Large-scale randomised clinical trials will be essential before any change to clinical practice.”
He said many diseases were greater or less deadly depending on your genes, including the flu.
“Susceptibility to life-threatening infections and immune-mediated diseases are both strongly heritable,” he said.
“In particular, susceptibility to respiratory viruses such as influenza is heritable and known to be associated with specific genetic variants.”
The genes identified in the study were IFNAR2, OAS, DPP9, TYK2 and CCR2.
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