More than 10 per cent of young and healthy people who develop severe Covid-19 have misguided antibodies that attack not the virus, but the immune system itself, according to a study published in journal ‘Science’. Another 3.5 per cent, at least, carry a specific kind of genetic mutation, causing early death of the Covid afflicted patients, as per the study.
In both groups, the upshot is basically the same: The patients lack type I interferon, a set of 17 proteins crucial for protecting cells and the body from viruses. “Whether the proteins have been neutralized by so-called auto-antibodies, or were not produced in sufficient amounts in the first place due to a faulty gene, their missing-in-action appears to be a common theme among a subgroup of Covid19 sufferers whose disease has thus far been a mystery,” said the researchers.
The findings help explain why some people develop a disease much more severe than others in their age group--including, for example, individuals who required admission to the ICU despite being in their 20s and free of underlying conditions. They may also provide the first molecular explanation for why more men than women die from the disease.
“These findings provide compelling evidence that the disruption of type I interferon is often the cause of life-threatening Covid-19,” said Jean-Laurent Casanova, head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at The Rockefeller University and a Howard Hughes Medical Institute investigator. “
The study participants included various nationalities from Asia, Europe, Latin America, and the Middle East. “Covid-19 may now be the best understood acute infectious disease in terms of having a molecular and genetic explanation for nearly 15% of critical cases across diverse ancestries,” Casanova said.
In one study, the researchers genetically analyzed blood samples from more than 650 patients who had been hospitalized for life-threatening pneumonia due to SARS-CoV-2, 14 percent of whom had died. They also included samples from another group of over 530 people with asymptomatic or benign infection. They initially searched for differences between the two groups across 13 genes known to be critical for the body’s defense against the influenza virus. These genes govern type I interferons.
It soon became obvious that a significant number of people with severe disease carried rare variants in these 13 genes, and more than 3 percent of them were in fact missing a functioning gene.
