A gene that may double the risk of lung failure and death from coronavirus has been found by scientists at the University of Oxford and could explain why people of South Asian ancestry have a greater danger of severe disease.
The researchers said the LZTFL1 gene changes the way the lungs respond to covid infection and is the most important genetic risk factor identified so far.
They noted that the gene interpretation is carried by nearly 60 per cent of people with South Asian background, compared with 15 per cent of those with European lineage.
The finding, published in the journal Nature Genetics on Thursday, could also incompletely explain the impact of COVID-19 in the Indian key. The experimenters used a combination of artificial intelligence (AI) and new molecular technology to pinpoint LZTFL1 as a gene responsible for the increased pitfalls.
LZTFL1 blocks a crucial defensive medium that cells lining the lungs typically use to defend themselves from the viral infection, they said. When these cells interact with SARS-CoV-2, which causes COVID-19, one of their defence strategies is to turn into lower specialised cells and come less welcoming to the contagion.
This process reduces the quantum on the face of cells of a crucial protein called ACE2, which the coronavirus uses to attach itself to the cells.
Still, for people with the LZTFL1 gene this process doesn’t work as well, and lung cells are left vulnerable to infection by the contagion.
The experimenters noted that it’s particularly important to offer vaccination to communities that are at lesser threat of serious COVID-19 infection as a consequence of carrying this inheritable predilection, as their increased threat should be cancelled out by immunisation.
Independent experts said the findings are veritably important but warrant farther disquisition.
“The discrepancy between the risk of serious disease and death in different ethnic groups has previously been attributed in part to socio-economic differences, but it was clear that this was not a complete explanation,” said Professor Frances Flinter, from Guy’s & St Thomas’ NHS Foundation Trust, UK.
“Evidence that LZTFL1 has emerged as a candidate causal gene, which is potentially responsible for some of the two-fold increased risk of respiratory failure from COVID-19 in some populations, provides a big step forward in our understanding of the variable susceptibility of some individuals to serious disease and death,” Flinter, who was not involved in the study, added.
Simon Biddie, from the University of Edinburgh, UK, said the study provides compelling evidence to suggest roles for LZFTL1 in severe COVID-19 that warrants urgent further investigation.
“The finding will need further experimental verification to provide direct evidence for regulation of LZTFL1, using for example genome engineering approaches,” Biddie, who was not a part of the study, added.
