An autoimmune-like antibody response is linked with severe COVID-19
Do COVID-19 patients suffer from their own immune response?
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Many immunologists, like myself, took the first days of the pandemic to believe that patients with strong anticuerposis were illness-free early on.
We've been misled.
I've come to understand that the image is even tougher for many months in researching COVID-19 as most scientists.
A recent research conducted by my colleagues and myself has added more proof that it may be so critical in certain patients to avoid dysregulated immune systems as to manage the virus itself.
Under the guidance of Dr. Ignacio Sanz, Head of rheumatology of Emory, I am an immunologist at the University of Emory.
Our specialty is immune dysregulation.
The COVID 19 pandemic has been harshly turned into a pyrrhical force of the immune system to battle infection.
In the case of patients with serious COVID-19 infections, there has been indications that, apart from combating the virus, the inflammatory mechanism used to combat the SARS-CoV-2 virus could be responsible for damage.
Clinical studies identified so-called cytokine storms in which an overwhelming quantity in COVID-recovered children was generated by the immune system and by antibodies causing unsafe blood clots and by inflammation of different organ systems, including blood vessels.
They were both early signals that certain patients might have been targeted from a healing to a damaging reaction to the virus SARS-CoV-2, which triggers COVID-19.
Fast thought and courageous actions taken by front-line doctors have contributed, early in the infection of patients in hospital, to the usage of steroid pharmaceutical drugs that dampen immune reaction.
This way life has been preserved.
Although it is not obvious yet what the damping components of the immune system doctors are.
Understanding the essence of COVID-19 immune dysregulation could help classify people that are most successful with these therapies.
More targeted and powerful ways to modulate the existing immune system reserved for autoimmune disorders might also be justified.
The proper anticorps require time
Mighty arms are antibodies.
The contagious agent such as viruses and bacteria are bound to the white blood cells or B cells to keep them from infecting your healthy cells.
These aggregates release intense inflammatory reactions and function as home beacons that can effectively attack the pathogens in your immune system.
They will also kill in some conditions.
Antibodies have the ability to contribute to major organ destruction and to a continuing period of immunity self-targeting whether a B cell develops antibodies that invade one's cells.
We term this self-destruction a cardiovascular disorder.
B cells undertake a preparation phase to deter autoimmune disasters and to maintain an optimal reaction to the invasive pathogen.
Those that respond to the virus strengthen their antibodies and develop, which means strong antibodies that disable the invader.
B cells are killed and are aimed at the tissue.
But it needs time to develop.
The distinction in life and death may be attributed to two weeks of cell B "training" during a serious infection.
Faster reaction of antimicrobials is possible.
To close this distance, an alternate B-cyan activation mechanism – called extrafollicular activation – produces quick-acting antibodies, which tend to overcome several of the established protection checklists which are accompanying a more accurate response.
Extrafollicular reactions evolve rapidly, are quickly formed and die down as the more targeted reactions arrive on the scene.
Unless they don't.
Cardiovascular reactions in COVID-19
Our laboratory showed that extrafollicular immune system reaction in people with Autoimmune Disorders such as lupus was a frequent feature of this form of responses between 2015 and 2018.
Chronically aggressive extrafollicular responses are recorded in patients with this condition, contributing to elevated levels of self-targeted anticorps and organ damage such as the lungs, heart , and kidneys.
A major measure of lupus disease seriousness and now COVID-19 could be the presences of particular forms of B cels produced by extrafollicular responses in the blood.
In a recent paper, my colleagues and I established extrafollicular B cell signatures, close to those found in active lupus in cases with extreme COVID-19.
In the early stages of infection response, we have seen that the fast-track mechanism of antibody synthesis is rapidly triggered by patients with serious disease.
These patients develop large amounts of viral antibodies that can neutralize the virus, some of them.
However, others that we've seen appear suspiciously close to in inflammatory diseases like lupus as well as these shielding antibodies.
Ultimately, patients with such auto-immune-style B cell reactions are not healthy enough, with high systemic organ insufficiency and death.
Immune reaction temperature in COVID-19
Let me be clear: it's not an allergic disease, COVID-19.
The inflammatory autoimmune reactions observed by my team will simply represent a "natural" reaction to a viral infection which is already out of control.
However it does not imply that it's not risky, even though this sort of answer is "natural."
This extended extrafollicular reactions have proved to help the seriousness of autoimmune disorders, both by developing targeted antimycosis and by inflammating tissue such as the lung and the kidney.
This indicates that these early immune reactions to a viral infection such as COVID-19 are tense with the later targeted antibody reaction; that is, the body's quick development of antibodies to the virus runs the risk of targeted not the virus but the tissues and bodies of the patient itself.
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Immunologists like me need more details.
Why can only those patients use such intense B cell reactions?
Are anticuerpos that are triggered by this reaction especially susceptible to organ assault and destruction?
Does persistent automatic reaction lead to "lingering" COVID-19 cases even after washing of this viral infection??
In view of these complexities, the medical community must understand how steroid therapy (or even more effective autoimmune-focused therapies) dampening immune responses is a vital tool in the battle against COVID-9 in the right patients.
Doctors and specialists would try to build on the principle of managing your virus reaction as important as the regulation of the virus itself in certain COVID-19 situations.
This essay is written by a nonprofit website named The Dialogue, which spreads thoughts by academics.
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