- Pablo Ochoa
Since the emergence of COVID-19, scientists have been trying to understand why the infection affects people so differently.
Why do some get sick more severely than others? And why are different parts of the body affected for sometimes long periods, as in the case of a long-term Covid infection?
Currently, evidence is mounting that some of these cases may be related to the secretion of “spoof” antibodies known as “autoantibodies”.
It is well established that antibodies fight infection, but autoantibodies miss the target and attack the body’s own cells, tissues, or organs, not the foreign body.
But what is the role of autoantibodies in case of infection with Covid? And how does it lead to the deterioration of the patient’s condition?
When the body turns on itself!!
Even healthy people produce autoantibodies, but in quantities that do not cause serious damage to the immune system.
But in the case of infection with Covid-19, researchers at Yale University in the United States discovered that these autoantibodies harm the immune system and tissues in the brain, blood vessels and platelets, the liver, and the digestive system.
“In the case of Covid, the autoantibodies can target dozens of pathways of the immune system,” Aaron Ring, associate professor of immunology at Yale University, told the BBC.
In a recent study published in the medical journal Nature, a team of researchers under the supervision of Dr. Ring examined the blood samples of 194 patients who had contracted Covid to varying degrees of severity.
The researchers found a “significant increase” in autoantibody activity compared to the uninfected subjects. The greater the number of autoantibodies detected, the greater the severity of the patient’s disease.
“It’s a double-edged sword. Antibodies are a necessary weapon to fight infection, but some Covid-19 patients secrete antibodies that damage their own cells and tissues,” Ring says.
Obstructing the body to respond to Covid
Dr. Ring built his study on a previous study supervised by Jean-Laurent Casanova of The Rockefeller University in New York.
Dr. Casanova has been studying genetic variations that affect a person’s ability to fight infectious diseases for more than 20 years.
This study highlights the role of autoantibodies that attack some of the proteins that have the task of fighting viral infection and preventing the virus from reproducing inside the body (they are called type 1 interferons).
And in October 2020, the journal Science reported that Dr. Casanova’s team had discovered autoantibodies in about 10 percent of about a thousand severely infected Covid patients.
The team noted that about 95 percent of those who discovered their autoantibodies in that sample were men, which explains that the majority of severe cases of Covid disease occur in men.
Last month, the team revealed to the journal Science Immunology a study of 3,600 patients admitted to hospital with severe Covid-19.
The team of researchers found autoantibodies instead of the first type of interferon in the blood of 18 percent of the people who died from the disease.
The team detected these autoantibodies in more than 20 percent of patients with severe Covid-19 who are over the age of eighty, compared to 9.6 percent of those under the age of forty.
Dr. Casanova concluded that the research established with compelling evidence that “disability” caused by autoantibodies is “usually the reason why Covid-19 threatens the patient’s life.”
autoantibodiesAnd long-term covid
Other research studies have revealed a relationship between autoantibodies and long-term Covid disease, which persists even after the body has expelled the virus.
In a study published this month in the journal Nature Communications, researchers from Stanford University discovered that at least one in five people who were admitted to hospital with Covid-19 produced antibodies in the first week of hospitalization.
Blood samples were taken from about 50 patients, on different days, including the first day they were admitted to the hospital.
“Within a week of patients being admitted to hospital, about 20 percent of them produced antibodies that attacked their own tissues like never before,” said Paul Jay Utz, who leads the research team at Stanford University.
Dr. Otz believes that this explains the persistence of some symptoms for months even after treatment of the disease, in what is known as long-term Covid.
“If you get sick with COVID-19 and end up in a hospital, you probably won’t get rid of the symptoms even if you get rid of the cause,” Utz says.
In London, researchers from Imperial College University discovered autoantibodies in people with long-term Covid, while these antibodies were not detected in patients who recovered quickly from the virus, nor in people who did not contract the disease.
Danny Altman, who leads the research team at Imperial College, said they are working to explore the possibility of diagnosing long-term COVID-19 once newly secreted autoantibodies are found.
The research is still in its early stages, but a single result could be enough to help clinicians identify mechanisms and methods of treatment.
That’s not all
Despite exciting progress, scientists warn that the immune system’s response to Covid is complex, and that autoantibodies are not everything.
And researchers are working on another mechanism is the excessive immune response that occurs in some cases.
The secretion of a type of protein called cytokine can reach dangerous levels, causing damage to the cells of the body, known as cytokine storms.
And we still don’t know exactly what happens in our cells when the virus invades the body. It is the outcome of that battle that determines the severity of the disease and, in the end, its ability to kill its victim.