Oxford University researchers have discovered the gene that doubles the risk of COVID-19-related respiratory failure.
According to a publication by Oxford University, sixty percent of persons of South Asian heritage have a high-risk genetic signature. This inclusion helps Oxford researchers to explain why some UK populations have observed an increase in mortality, as well as the impact of COVID-19 on the Indian subcontinent.
Previous research found a region of DNA on chromosome 3 that increased the chance of COVID death in persons under 65. Scientists, on the other hand, had no idea how this genetic signal increased risk or what genetic modification was responsible.
Professors James Davies and Jim Hughes of the University of Oxford’s MRC Weatherall Institute of Molecular Medicine led a team that employed cutting-edge technology to figure out which gene was generating the impact and how it was doing so in a research published in Nature Genetics.
Study co-lead Jim Hughes, Professor of Gene Regulation explained why it was initially so difficult for the Oxford research team to identify genes affected by the indirect switch.
‘The reason this has proved so difficult to work out, is that the previously identified genetic signal affects the “dark matter” of the genome. We found that the increased risk is not because of a difference in gene coding for a protein, but because of a difference in the DNA that makes a switch to turn a gene on. It’s much harder to detect the gene which is affected by this kind of indirect switch effect.’ Study co-lead Jim Hughes, Professor of Gene Regulation stated.
How Oxford Researchers Uncover Gene that Doubles Risk of Death from COVID-19
The researchers used an artificial intelligence program to analyze massive amounts of genetic data from hundreds of different types of cells from all over the body, demonstrating that the genetic signal is likely to harm lung cells. The researchers could then zoom down on the DNA at the genetic signal using a very precise technique they had only recently devised. This research looks at how billions of DNA letters fold up to fit inside a cell to determine which gene was being controlled by the sequence that increased the risk of severe COVID-19.
Laboratory work lead from the Hughes research group, Dr Damien Downes made a comment on how this thoughful method provided data to uncover gene that doubles risk of death from COVID-19.
‘Surprisingly, as several other genes were suspected, the data showed that a relatively unstudied gene called LZTFL1 causes the effect.’ Dr Damien Downes commented.
Associate Professor of Genomics at Oxford University’s Radcliffe Department of Medicine, Professor James Davies said, “The genetic factor we have found explains why some people get very seriously ill after coronavirus infection. It shows that the way in which the lung responds to the infection is critical. This is important because most treatments have focussed on changing the way in which the immune system reacts to the virus.’
How Does the Gene Affect Vaccination?
The researchers discovered that the higher-risk form of the gene hinders the cells that line the airways and lungs from adequately reacting to the virus. However, because it has no effect on the immune system, the researchers believe that people who possess this variant of the gene will respond properly to vaccinations.
Drugs and other therapies that target the mechanism that prevents the lung lining from changing into less specialized cells, according to the researchers, might lead to novel treatments tailored to patients who are most prone to develop severe symptoms.
Sixty percent of persons of South Asian heritage have this higher-risk variant of the gene, compared to only 15 percent of those of European ancestry, which may explain why the former group has higher death rates and hospitalizations. The study also discovered that 2% of persons with Afro-Caribbean heritage had the higher risk genotype, suggesting that this genetic component does not fully explain why black and minority ethnic populations had higher death rates.