Why does COVID-19 kill some people and spare others? Study finds certain patients – particularly men – have ‘autoantibodies’ that cause immune system proteins to attack the body’s own cells and tissues
- A new study found 10% of around 1,000 severely ill coronavirus patients have so-called autoantibodies
- They disable immune system proteins that prevent the virus from multiplying itself and also attack the body’s cells and tissues
- Researchers say the patients didn’t develop autoantibodies in response to the virus but had them before the pandemic began
- Of the 101 patients with autoantibodies, 94% were male, which may suggest why men are more likely to die from COVID-19 than women
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Researchers believe they are one step closer to understanding why the novel coronavirus kills some people and spares others.
In a new study, they found that some critically ill patients have antibodies that deactivate certain immune system proteins.
These antibodies, which are known autoantibodies, allow the virus to replicate and spread through the body, and also attack our cells and tissues.
What’s more, nearly all of the patients with these autoantibodies were men.
The international team, led by the Institut Imagine in Paris and Rockefeller University in New York City, says the findings suggest that doctors should screen patients for these autoantibodies so they can provide treatment to patients before they fall too ill.
A new study found some severely ill coronavirus patients have so-called autoantibodies, which allow the virus to replicating and spread throughout the body, and also attack the body’s cells and tissues. Pictured: Medics transfer a patient on a stretcher from an ambulance outside of Emergency at Coral Gables Hospital in Florida, July 2020
Nearly 10% of severely ill patients had autoantibodies (left) compared to those with mild or asymptomatic cases (center) and healthy controls (right)
Of the 101 patients with autoantibodies, 94% were male, which may suggest why men are more likely to die than women (above)
For the study, published in the journal Science, the team looked at nearly 1,000 patients with with life-threatening cases of COVID-19.
These patients were compared with more than 600 patients who had mild or asymptomatic cases and around 1,200 healthy controls.
Results showed nearly 10 percent of those with critical cases had autoantibodies that disable immune system proteins called interferons.
Interferons are signaling proteins released by infected cells and are named for their prowess to ‘interfere’ with the virus’s ability to multiply itself.
They are known as ‘call-to-arms’ immune cells because they control viral replication until more immune cells have time to arrive and attack the pathogen.
Autoantibodies block interferons and attack the body’s cells, tissues and organs.
None of the 663 people with asymptomatic or mild cases of COVID-19 had autoantibodies and just four of the healthy controls did.
However, the team said these critically ill patients didn’t make autoantibodies in response to being infected.
Rather, they always had them and the autoantibodies didn’t cause any problems until patients contracted the virus.
‘Before COVID, their condition was silent,’ lead author Paul Bastard, a PhD candidate at Instiut Imagine and a researcher at Rockefeller University, told Kaiser Health News.
‘Most of them hadn’t gotten sick before.’
The team also found that 94 percent of the 101 coronavirus patients who had autoantibodies were men.
Researchers say it may explain why, around the world, men have accounted for about 60 percent of deaths from COVID-19.
‘You see significantly more men dying in their 30s, not just in their 80s,’ Dr Sabra Klein, a professor of molecular microbiology and immunology at the Johns Hopkins Bloomberg School of Public Health, told Kaiser Health nNews.
Bastard, the lead author, says screening coronavirus patients might help predict which ones will become severely ill and allow doctors to treat them sooner.
‘This is one of the most important things we’ve learned about the immune system since the start of the pandemic,’ Dr Eric Topol, executive vice president for research at Scripps Research in San Diego, who was not involved in the study, told Kaiser Health News.
‘This is a breakthrough finding.’