CNN
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About 20% of people infected with COVID-19 knew they had it for the first time because they were diagnosed with it during a routine screening test. They had no symptoms. Some people have been diagnosed with long-term COVID-19 after being unable to get rid of the aftereffects for months after being infected.
There are myriad factors that determine how people live after being infected with COVID-19. This also includes viral load. Where the virus first entered the body – nose, possibly mouth, eyes. their age and underlying health. The genetic characteristics of the mutants that infect them, to name a few.
New research is exploring another side of the puzzle of how people experience this infection: genes.
a study A paper published Wednesday in the journal Nature showed that people with common alterations in genes that encode specific immune system molecules on the surface of cells called human leukocyte antigens (HLA) are more likely to be asymptomatically infected with the novel coronavirus.
Another study, recently posted online as a preprint ahead of peer review and publication, found that people with specific alterations in the gene near FOXP4, which encodes a protein active in the lungs and immune system, appeared to be more likely to develop long-term coronavirus.
HLA is used to determine if an organ is suitable for a patient needing a transplant, so the bell could ring. These molecules protrude from the surface of certain white blood cells, as well as cells in many other tissues of the body.
“I think of them like arms sticking out and hands at the ends of the arms,” says study author Jill Hollenbach, PhD, professor of neurology at the Weill Institute for Neurosciences at the University of California, San Francisco.
Hollenbach says the job of HLA molecules is to present fragments of proteins to the immune system so that they can recognize them if they encounter them again.
Imagine in a cell that takes in the virus that causes Covid-19, part of the virus breaks down inside the cell, and some of its protein fragments migrate to the surface, where HLA molecules grab and hold the fragments so that T cells can recognize them, she says.
T cells are immune cells that help the body recognize and remember proteins. They build the immune system’s memory so that it can react if it finds the pathogen again.
So the HLA molecule sticks out like an arm, “and what you’re holding in your hand is this… a small peptide fragment of a protein from the virus,” Hollenbach said.
There are three general groups of HLA: HLA-A, HLA-B and HLA-DR. Within these groups there are hundreds of variations of these molecules. Each looks so specifically for certain types of protein fragments and retains them in a particular way that T cells can see it and learn how to make antibodies against them, Hollenbach says.
For this study, Hollenbach started with people whose HLA types were identified toward a large registry of potential bone marrow donors called “Be The Match.” She called for more than 29,000 people to participate in a smartphone-based study in which people report positive test results and record their symptoms. The first “discovery” group consisted of more than 1,400 people who had not been vaccinated and reported testing positive for COVID-19. Of these, 136 reported no symptoms related to infection.
The researchers then took a closer look at this group to see if there were similarities in the genes that encode HLA molecules. And there were similarities. People in this group were more likely to carry genes encoding a specific type of her HLA molecule called HLA-B*15:01.
People with two copies of the gene were eight times more likely to remain asymptomatic than those without these mutations.
Next, Hollenbach wanted to know how that particular type of HLA molecule prevented people from developing symptoms.
HLA-B*15:01 was found to recognize parts of other SARS virus types associated with common seasonal respiratory infections. A fragment of the protein it recognizes is shared with the virus that causes Covid-19. Therefore, people with these HLA molecules likely already had immunity to SARS-CoV2 and were able to clear the virus before they had symptoms, Hollenbach said.
About 20% of people infected with the new coronavirus have no symptoms. About 20% of them carry the HLA variant, Hollenbach said. So this is not the only explanation why people may have silent infections, the researchers note, and that carrying HLA-B*15:01 is no guarantee that a person will not develop symptoms.
“There are undoubtedly other genetic and non-genetic factors that are important, but we don’t know what they are at this time,” Hollenbach said. “In this case, we know that this particular genetic factor is strongly associated with asymptomatic infection.”
Genes may also help explain why people end up on the other side of COVID-19, coping with symptoms that develop into protracted, prolonged COVID-19.
For more than three years, an international group of scientists has been searching for genes that may be associated with severe COVID-19.
researcher edited data Results were extracted from 24 studies involving approximately 6,500 people and compared with more than 1 million others used as controls.
The long-running investigation into the novel coronavirus stems from that effort, led by scientists at the Karolinska Institutet in Stockholm.
An analysis of 11 of these studies, which involved sequencing every gene in a person’s body and then comparing the genomes of large numbers of people, found that people with long-term Covid-19 likely shared DNA around a gene called FOXP4. This gene is thought to be involved in the immune response of cells in the small air sacs of the lung. These cells also appear to help repair lung damage.
“This particular genetic variation is interesting because it provides insight into some of the underlying mechanisms associated with long-lasting novel coronavirus and suggests the existence of a genetic predisposition. However, this information alone cannot be relied upon to identify individuals at risk,” said Dr. Hugo Zeberg, an evolutionary geneticist at Karolinska University and lead author of the study.
Genes are probably just part of why someone is prolonging COVID-19, according to Zeberg, and there are probably many genes involved.
The study, published as a preprint ahead of peer review, found that people with this version of the gene around FOXP4 were about 60% more likely to develop long-term coronavirus than those without the variant.
Zeberg said their group plans to collect more cases and add them to the study, which they hope will point to other genes that may be involved.
“We hope our results will inspire others in the scientific community to investigate these links further,” he said.
