- Pablo Uchoa
- BBC World
Since the emergence of the new coronavirus, scientists have been trying to understand what makes each person’s response to this disease so different.
Why are some people sicker than others? Why does it affect different organs of the body and may last for a long time and become a long-term new crown?
Now, more and more evidence shows that some processes may be related to the production of autoantibodies called “rogue” antibodies.
Antibodies usually fight infections, but autoantibodies mistakenly target their own cells, tissues, or organs.
But what role do they play in the new coronavirus? Can they make the disease worse?
When the body works on its own
Even healthy people can produce autoantibodies, but they are generally not large enough to cause major damage to the immune system.
However, Yale University researchers said that in patients with new coronary disease, they not only damage the immune system, but also damage healthy tissues in the brain, blood vessels, platelets, liver, and gastrointestinal tract.
Aaron Ring, assistant professor of immunobiology at Yale University School of Medicine, told the BBC that autoantibodies can target “dozens of immune pathways” in a new coronavirus infection.
In a study recently published in the journal Nature, his team performed blood screening on 194 patients infected with the virus of varying degrees and found that their autoantibody activity was compared with those of uninfected people. obviously increase”.
The more autoantibodies detected, the greater the severity of the disease experienced by the patient.
“This is a double-edged sword. Antibodies are the key to fighting infection, but some patients with COVID-19 also produce antibodies that destroy their own cells and tissues,” he said.
Block the immune response to the new coronavirus
Dr. Lin’s research is based on the work led by Jean-Laurent Casanova (Jean-Laurent Casanova) of Rockefeller University in New York.
For more than 20 years, Dr. Casanova’s laboratory has been studying genetic mutations that affect a person’s ability to resist infection.
Their research emphasizes the role of autoantibodies, which attack proteins (called type 1 interferons) that are responsible for fighting viral infections and preventing viral replication.
In October 2020, Dr. Casanova’s team stated in the journal Science that they had found about 10% of autoantibodies in nearly 1,000 patients with severe new crown disease.
A key detail is: Nearly 95% of these patients are men, which may explain why men account for the majority of patients with severe COVID-19.
Last month, they reported the findings of a larger study in the journal Science Immunology, studying 3,600 patients with COVID-19 who were admitted to the hospital due to severe illness.
Among them, 18% died of this disease, and the researchers found autoantibodies against type 1 interferon in their blood.
More than 20% of patients with severe new coronary disease over 80 years old have these autoantibodies, and the proportion of patients under 40 years old is 9.6%.
Dr. Casanova said that these findings provide “convincing evidence” that the “interference” caused by rogue antibodies “is often the cause of life-threatening new crowns.”
Autoantibodies, autoimmune diseases and long-term COVID-19
Other studies are discovering the link between autoantibodies and COVID-19-related diseases, even after the virus is cleared from the body, the link continues.
In a study published this month in the journal Nature Communications, researchers at Stanford University found that at least one-fifth of people admitted to the hospital for COVID-19 developed autoantibodies within the first week of admission.
About 50 patients took blood samples on different days, including the day they were first admitted to the hospital.
PJ Utz, professor of immunology and rheumatology at Stanford Medical School and principal investigator, said: “Within a week after admission, about 20% of patients developed new antibodies to their own tissues, and these antibodies were not at the time of admission. exist.”
Professor Utz said that this can also explain why some symptoms persist for several months after the disease is cleared. This condition is called the long-term new crown.
“If you are sick and hospitalized due to the new crown, even after recovering, you may not be out of danger.”
In the United Kingdom, researchers at Imperial College London have found autoantibodies in patients who have been infected with the new coronavirus for a long time. These antibodies are not present in people who have recovered quickly or who have not detected the disease.
The head of the research team, Professor Danny Altmann, told the BBC that the team is trying to determine whether the long-term new crown can be diagnosed by identifying the autoantibodies that have been produced recently.
This research is still in its infancy, but it may produce a test that is simple enough to be used in surgeons.
He said: “We very much hope that it will not only develop in the direction of diagnosis, but also in the direction of treatment. We hope that this will highlight specific mechanisms and treatment methods.”
For experts, these findings also provide reasons for vaccination.
Professor Utz said that in poorly controlled viral infections, the virus will stay for a long time, and the ever-increasing immune response will continue to break down virus particles into fragments and disrupt the immune system.
But the vaccine only contains a spike protein or genetic instructions to produce the spike protein, so the immune system will not be affected by the frenzied activity of autoantibodies.
Not all
Although the progress in this field is exciting, scientists warn that the immune response to the new crown is complex, and the production of autoantibodies is not all.
Another mechanism being studied is an overactive immune response in some cases.
The amount of a protein called cytokine can reach dangerous levels and cause damage to the body’s own cells-this is the so-called cytokine storm.
We still don’t know exactly what happens in our cells when the virus enters the body-it is the result of the fight between the virus and the cell that determines the severity of the disease and ultimately determines whether it is fatal.