Hospitalized patients with Covid-19 are much more likely to harbor autoantibodies —Antibodies directed at your own tissues or against substances that your immune cells secrete into your blood — than people who have not had the disease.
The information, which is published in
Nature Communications, is especially relevant because autoantibodies can be precursors of an autoimmune disease full-fledged, such as multiple sclerosis or rheumatoid arthritis, in which it is the immune system itself that causes the pathology.
And, as PJ Utz, a researcher at the
Stanford University (USA) and director of the study, the fact of having suffered a serious Covid, as if to end up in the hospital, can make
be out of harm’s way even after recovering. ‘
The researchers looked for autoantibodies in blood samples drawn during March and April 2020 out of 147 patients with Covid-19 and used blood samples taken from other donors before the pandemic as controls.
The analyzes of these samples identified and measured the levels of antibodies directed to the virus; autoantibodies; and antibodies directed against cytokines, proteins secreted by immune cells to communicate with each other and coordinate your overall strategy.
In this way, they saw that more than 60% of all hospitalized patients with Covid-19 were carriers of antitokine antibodies, compared to 15% of healthy controls.
According to the researchers, this could be the result of a immune system overload caused by a persistent and virulent infection. Faced with a powerful immune response to deal with the virus, explains Utz, the abundance of cytokines (substances produced to deal with the ‘invader’) can divert the erroneous production of antibodies that attack them.
If any of these antibodies block the ability of a cytokine to bind to its appropriate receptor, the immune cell of the desired receptor may not be activated. That, in turn, could give the virus more time to replicate and lead to a much worse outcome.
Fortunately, the researchers were able to track back the development of autoantibodies in about 50 patients due to the availability of blood samples drawn on different days, including the one they were admitted for the first time.
“One week after registering at the hospital, approximately 20% of these patients had developed new antibodies against their own tissues that were not there on the day they were admitted,” he says. Utz-. In many cases, these autoantibody levels were similar to those who would be seen in a diagnosed autoimmune disease.
In some cases, the presence of these newly detected autoantibodies may reflect an increase, driven by the immune response, of antibodies that had been hidden, he explains. Utz.
Could it be that inflammatory shock in the systems of patients with severe COVID-19 it would cause an increase in the levels of previously undetectable, and perhaps harmless, autoantibodies that these individuals may have been carrying prior to infection.
In other cases, the generation of autoantibodies could be caused by exposure to viral materials that resemble our own proteins, he explains. Utz.
“It is possible that, in the course of a SARS-CoV-2 infection poorly controlled, in which the virus remains too long while an intensifying immune response continues to break the viral particles into pieces, the immune system sees fragments of the virus that I hadn’t seen before. If any of these viral pieces look too much like one of our own proteins, this could trigger the production of autoantibodies. ‘
The find strengthens the case for vaccination, he warns.
Vaccines contain only one protein, the so-called SARS-CoV-2 spike protein, or the genetic instructions for making it. With vaccination, the immune system is never exposed to the many new viral proteins generated during infection and potentially confused by their presence.
Furthermore, vaccination is less inflammatory than a real infection, he adds Utz, so the immune system is less likely to get confused and make antibodies to its own signaling proteins or to the body’s own tissues.
‘Patients who, in response to vaccination, rapidly develop adequate antibody responses to the protein of pico viral they should be less likely to develop autoantibodies, “he says.
In fact, a recent study published in
Nature showed that, unlike SARS-CoV-2 infection, the Covid-19 vaccine produced by Pfizer does not trigger any detectable generation of autoantibodies between recipients.
And, this researcher warns, although the majority of people who contract Covid outgrow it and feel fine, “you have to consider that you cannot know in advance that, if we get infected, we will have a mild Covid, unless we are vaccinated.
Because, as has already been proven, the most serious cases can complicate the rest of our lives because the «virus can trigger autoimmunity».
According to Utz, “we still cannot say that severe Covid-19 will cause an autoimmune disease; we have not studied any patients long enough to know if these autoantibodies stay a year or two later». But, he concludes, “I would not want to take that risk.”
This team will continue to study blood samples from people infected with SARS-CoV-2 who are asymptomatic or who have had mild symptoms of Covid-19 in order to determine if the massive hyperarousal The immune system, which does not occur in mildly symptomatic or asymptomatic people, is what causes problems, or if the mere molecular similarity of the SARS-CoV-2 proteins is sufficient to trigger the generation of autoantibodies.