Several factors, such as age, pre-existing health conditions, and even genetic predispositions, play a significant role in determining the severity of a Covid-19 infection.
Updated On – 01:08 PM, Wed – 13 September 23
Representational Image.
London: A team of German scientists have discovered 28 new risk genes, pushing the total number to 51, that can increase the risk of severity in Covid-19 infections.
A great many criteria determine whether or not we get seriously ill from Covid-19. Besides our age and any previous or existing conditions, they also include genetic factors. Right from the start of the pandemic, scientists have been investigating the links between genetic factors and severe Covid-19.
“Knowing about genetic risk factors helps scientists to develop successful drugs and predict risks better,” said Dr. Kerstin Ludwig from the Institute of Human Genetics at the University Hospital Bonn.
According to the findings published in the journal Nature, the genes are linked to critical illness, hospitalisation and infection rates when individuals are infected with Covid. The increased number of genes will enable the scientists to map genes to pathways that are involved in viral entry, airway defence and immune system response.
To identify the 51 risk factors, the team, part of the Covid-19 Host Genetics Initiative (Covid-19 HGI), performed a meta-analysis of up to 219,692 cases and over 3 million controls.
Covid-19 HGI, launched as a large-scale international project at the start of the pandemic, aims to collate data from individual studies being set up all over the world and investigate it all together.
“The consortium has successfully identified 51 risk factors in all, 28 of which are new since the previous publication,” said Dr. Axel Schmidt, from the varsity.
Further investigation of how such susceptibility and severity gene map to different pathways would provide mechanistic insights into the human genetic architecture of Covid, the team said.
In a separate study, also published in the journal Nature, researchers from the University of California -San Francisco identified a mutation in one of the genes coding for human leukocyte antigen (HLA), that helped virus-killing T cells identify SARS-CoV-2 and launch a lighting attack.
The mutation — HLA-B*15:01 — is quite common, carried by about 10 per cent of the study’s population. It doesn’t prevent the virus from infecting cells but, rather, prevents people from developing any symptoms.
This may explain why some people never have common symptoms like a runny nose or sore throat, even after testing positive for the deadly virus.
