The true prevalence would be much higher as the test only captures about 80 percent of COVID-related antibodies.
But why do some people get so sick from COVID-19, while others have few or no symptoms, and some don’t get infected at all?
“This is the puzzle we’re trying to solve,” says Professor Stuart Tange, an immunologist from the Garvan Institute of Medical Research who leads the Oceania Center for Human Genetic COVID efforts.
Rather than luck, the Union of Scientists believes the answer lies in our genes.
It’s investigating the DNA of people around the world who have experienced a severe and life-threatening case of COVID-19, have had an asymptomatic infection or may have been resistant to infection or disease.
“Our task is to find out why and how our genes affect our immunity to the coronavirus, and how and why immunity can also be affected by other non-genetic causes,” He says on his website.
In late 2020, the human COVID genetic effort made some major discoveries, revealing why some healthy people end up in intensive care units after contracting SARS-CoV2.
Around 15-20 percent of people With severe COVID, he develops antibodies that neutralize a key component of our immune system that prevents us from attacking the invading virus. Another 3.5 percent It was found that they had genetic mutations This impairs its immune response to some viruses, including SARS-CoV2.
Dr. Vanessa Bryant, an immunologist from WEHIThe oldest medical research institute in Australia. Bryant leads part of Australian Study First Few X (FFX) That investigates transmission of COVID-19 in homes.
“This could give us insight into new antiviral therapies and the different ways to shape and boost our immune system.”
While work on severe COVID continues, Tangye says the global consortium has now evolved to answer the most difficult questions.
“What has become clear is that there are a number of people who just don’t have symptoms, or are actually not infected, or are showing some kind of resistance,” he says.
“The next board is to identify genes that can basically give you a little bit of protection or a ‘force field’, or whatever you want to call it, that prevent you from getting infected, or prevent you from getting really sick if you do.”
This was a little more complicated, Tangi says, because healthy people who don’t have symptoms don’t show up at doctors’ offices.
“So you’re trying to get them out of the woodwork to go, you know, there are some people here who seem to have a great strength in resistance, and they’re not succumb to infection or disease, or even symptoms.”
last november, A study of UK healthcare workers During the first wave of the pandemic, some found that they were able to clear their bodies of the virus before producing COVID-19 antibodies.
It was assumed that exposure to other human coronaviruses – such as those that cause the common cold – helped them fight off infection.
“There can be elements of cross-reactivity,” Bryant says. “But the impact of that is still unknown and somewhat controversial, like, is it just providing an extra bump in our protection? We certainly don’t think it’s a major driver in protecting people from severe disease.”
At this point in the pandemic, it’s hard to say if people aren’t getting sick because of vaccines and boosters, a previous undiagnosed COVID infection, or something else.
says Professor John Christodoulou of the Murdoch Children’s Research Institute, who is also involved in the COVID Human Genetic effort.
Or it could be environmental factors like being too diligent about wearing a mask or being physically distant. Or it might just be blind luck.”
The human COVID genetic effort is also looking at whether – in extremely rare cases – some people carry a mutation that makes them resistant to severe SARS-CoV2 and COVID-19 infections.
Nearly 30 years ago, researchers discovered a genetic mutation that means about 1 percent of people of northern European descent are immune to HIV infection. This led scientists to develop drugs that block HIV.
Christodoulou hypothesizes that if there are mutations in the body’s ACE2 receptors — which are needed for the COVID-19 virus to enter our cells — they may prevent people from becoming infected.
“And that’s definitely one of the genes that people look at among that very small percentage of individuals who appear to be overexposed, those who have multiple family members with COVID, and yet remain COVID-free.”
But ACE2 receptors also regulate blood pressure and inflammation, and Bryant warns that the mutation may come with another health cost.
“But identifying these genetic changes really gives us a great opportunity to develop better drugs or refine our vaccine targets, and at the other end of the spectrum, identify people who are most at risk for serious disease.”
On Wednesday, Holmes and Alderton met with Tangye, and offered to contribute to the COVID study of the human genetic effort.
Tangye says it’s possible Alderton has had the virus but has not had symptoms. To find out, they will check his blood for antibodies and T cells specific to the virus and not in vaccines.
The study coordinator will then recruit Alderton and Holmes and, after taking a blood sample, sequence the entire DNA in their cells.
“We’ll see if there are any differences in some of the key genes in Tom, that might make a suggestion as to why he’s resistant or why he doesn’t get infected despite proximity and opportunity.”
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