Some of the healthy Australians who develop the most serious coronavirus symptoms are missing a crucial set of proteins which helps protect the body from viruses, new groundbreaking research reveals.
And in about 10 per cent of these cases, the body is actively fighting with COVID-19 to help shut down those protections.
Patients who lack the type I interferon genetic mutation – a set of 13 proteins crucial for protecting cells from viruses – were more associated with severe infections, according to the two papers published in Science.
The discovery also helps explain why some people were more susceptible to life-threatening cases than others in their age group.
Professor John Christodoulou, co-leading the Australian arm of the COVID Human Genetic Effort, said the two papers provide a potential explanation for severe infections seen in up to 15 per cent of cases.
“The way SARS-CoV-2 affects people differently has been puzzling,” he said.
“The virus can cause a symptom-free infection and go away quietly, or it can kill in a few days.”
In addition to the people who produce misguided antibodies which attack their own cells rather than the coronavirus, another 3.5 per cent carry genetic mutations which will impair their immune response.
And the new research also helps explain why more men die than women.
“Also 10 per cent of individuals with severe COVID-19 infection had auto-antibodies to type I interferon, neutralising the early protective effect of innate immunity,” professor Christodoulou said.
“Importantly, 95 per cent of these individuals were men, which might explain at least some of the sex differences we see in COVID-19 infection, which tends to affect males more severely.”
Professor Jean-Laurent Casanova, head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at America’s Rockefeller University, says the good news is that now doctors should be able to address it.
“These findings provide compelling evidence that the disruption of type I interferon is often the cause of life-threatening COVID-19,” he said.
“And at least in theory, such interferon problems could be treated with existing medications and interventions.”