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Source: COVID-19-Autoimmune Diseases   Sep 26, 2021  2 years ago
WARNING! Various Studies Confirm That COVID-19 Increases Risk Of Developing Autoimmune Diseases Including New Types Of Autoimmune Conditions!
WARNING! Various Studies Confirm That COVID-19 Increases Risk Of Developing Autoimmune Diseases Including New Types Of Autoimmune Conditions!
Source: COVID-19-Autoimmune Diseases   Sep 26, 2021  2 years ago
COVID-19 And Autoimmune Diseases: Various new studies are showing that an infection with the SARS-CoV-2 can also trigger a variety of autoimmune conditions and diseases including some never seen before.

In the first study by researchers from Stanford University School of Medicine-USA, the study team found that in severe hospitalized COVID-19 patients, the immune system is tricked into producing so-called autoantibodies that have the potential to eventually attack healthy tissue and cause inflammatory diseases.
The study team found autoantibodies in blood samples from roughly 50% of 147 COVID-19 patients they studied, but in fewer than 15% of 41 healthy volunteers. For 48 COVID-19 patients, the researchers had blood samples taken over different days, including the day of hospital admission, allowing them to track the development of the autoantibodies.
Lead author, Dr Paul Utz of Stanford University told Thailand Medical News, "Within a week, about 20% of these patients had developed new antibodies to their own tissues that weren't there the day they were admitted."
Dr Utz said, "We haven't studied any patients long enough to know whether these autoantibodies are still there a year or two but the chances of developing an autoimmune disease was extremely high.”
The study findings were published in the peer reviewed journal: Nature Communications.
To date, COVID-19 is associated with a wide range of clinical manifestations, including autoimmune features and autoantibody production.
The study team developed three protein arrays to measure IgG autoantibodies associated with connective tissue diseases, anti-cytokine antibodies, and anti-viral antibody responses in serum from 147 hospitalized COVID-19 patients.
Alarmingly autoantibodies are identified in approximately 50% of patients but in less than 15% of healthy controls. When present, autoantibodies largely target autoantigens associated with rare disorders such as myositis, systemic sclerosis and overlap syndromes. A subset of autoantibodies targeting traditional autoantigens or cytokines developed de novo following SARS-CoV-2 infection.
Autoantibodies track with longitudinal development of IgG antibodies recognizing SARS-CoV-2 structural proteins and a subset of non-structural proteins, but not proteins from influenza, seasonal coronaviruses or other pathogenic viruses.
The study team concluded that SARS-CoV-2 causes development of new-onset IgG autoantibodies in a significant proportion of hospitalized COVID-19 patients and are positively correlated with immune responses to SARS-CoV-2 proteins.
In the second study by Australian researchers from RMIT University, Launceston General Hospital, University of Tasmania and Monash University, utilizing computer-based prediction programs to identify regions of SARS-CoV-2 proteins that antibodies are likely to recognize and bind to and comparing them to all human proteins in the body,  a number of potential similarities were found and the study team was able to map the potential for SARS-CoV-2 infection to trigger autoantibody formation and existing or new autoimmune disease s, affecting different parts of the body.
The study findings were published in the peer reviewed journal: Frontiers In Bioinformatics.
Extrapulmonary involvement in COVID-19 includes autoimmune-like diseases such as Guillain-Barré syndrome and Kawasaki disease, as well as the presence of various autoantibodies including those associated with autoimmune diseases such a systemic lupus erythematosus (e.g. ANA, anti-La). Multiple strains of SARS-CoV-2 have emerged globally, some of which are found to be associated with increased transmissibility and severe disease.
The study team performed an unbiased comprehensive mapping of the potential for cross-reactivity with self-antigens across multiple SARS-CoV-2 proteins and compared identified immunogenic regions across multiples strains.
Utilizing the Immune Epitope Database (IEDB) B cell epitope prediction tool, regions predicted as antibody epitopes with high prediction scores were selected. Epitope sequences were then blasted to eight other global strains to identify mutations within these regions.
Of the 15 sequences compared, eight had a mutation in at least one other global strain. Predicted epitopes were then compared to human proteins using the NCBI blast tool. In contrast to studies focusing on short sequences of peptide identity, the study team had taken an immunological approach to selection criteria for further analysis and had identified 136 alignments of 6–23 amino acids (aa) in 129 human proteins that are immunologically likely to be cross-reactive with SARS-CoV-2.
Additionally, to identify regions with significant potential to interfere with host cell function-or promote immunopathology, the team identified epitope regions more likely to be accessible to pathogenic autoantibodies in the host, selected using a novel combination of sequence similarity, and modelling protein and alignment localization with a focus on extracellular regions.
The study findings identified 11 new predicted B-cell epitopes in host proteins, potentially capable of explaining key aspects of COVID-19 extrapulmonary pathology, and which were missed in other in silico studies which used direct identity rather than immunologically related functional criteria.
Another study by researchers from the University of Birmingham also found that many patients with COVID-19 produce immune responses against their body’s own tissues or organs.
The study findings were published in the peer reviewed journal Clinical & Experimental Immunology.
COVID-19 has been associated with a variety of unexpected symptoms, both at the time of infection and for many months afterwards. It is not fully understand what causes these symptoms, but one of the possibilities is that COVID-19 is triggering an autoimmune process where the immune system is misdirected to attack itself.
Also after COVID-19, a number of patients have developed a range of different autoimmune diseases. This includes Guillain-Barré syndrome, a disorder in which the immune system attacks nerves, often resulting in tingling and weakness in arms and legs.
There are also reports of autoimmune responses that don’t clearly correspond to any known autoimmune disease. This suggests COVID-19 disease may trigger new autoimmune illnesses.
The details and mechanisms of exactly how and how often this occurs is still emerging with virus induced autoantibodies playing a key role.
The human immune system is tightly regulated. Within it, immune cells known as B and T lymphocytes – the soldiers of the immune system are normally able to distinguish between itself versus external targets.
It has been found that when the immune system becomes confused, B and T cells may start to target our own bodies, which we call autoimmunity.
Past studies have showed that viral infection can sometimes trigger this confusion, resulting in autoimmune diseases.
Viruses can trigger autoimmunity by two key mechanisms ie “molecular mimicry” and “bystander activation”.
So called molecular mimicry occurs when the part of the virus the B or T cells recognize looks similar to a normal protein in our body. The B or T cell then sees both the viral and the self-protein as something to attack and eliminate. Viral infections can also cause organ damage and cell death directly. When our cells die and burst, they release self-proteins. These would normally stay hidden and wouldn’t trigger an immune reaction.
On the other hand bystander activation occurs when B and T cells accidentally get in contact with self-proteins, confusing the immune system, which otherwise is trained to ignore self-proteins.
To date there are multiple reports of antibodies which recognize self-proteins, also known as autoantibodies, emerging in individuals with severe COVID-19.
Alarmingly some of these autoantibodies that emerge in individuals with severe COVID recognize autoantibodies associated with well-known autoimmune diseases, including:
-systemic lupus erythematosus (SLE), which affects joints, skin, blood cells as well as organs such as the brain, lungs and kidneys
-rheumatoid arthritis, affecting the joints
-Guillain-Barré syndrome, mentioned above
-immune thrombocytopenia, which attacks blood platelets, resulting in excessive bruising and bleeding
-autoimmune haemolytic anaemia, which attacks red blood cells which can result in breathlessness, tiredness, headaches and chest pain.
In various clinical reports that describe the onset of these diseases after COVID-19, the autoimmune symptoms start during or after the respiratory symptoms.
However it’s unclear whether the patients were already predisposed to these diseases, or the infection unmasked an autoimmune process that had already begun. Or perhaps the infection triggered completely new autoimmunity. The triggers may even vary for different people.
SARS-CoV-2 infections may also trigger new autoimmune responses and, potentially, new autoimmune diseases. This has already occurred with a condition called multi-system inflammatory syndrome in children (MIS-C).
Initially described as a Kawasaki-like disease associated with COVID-19, MISC-C causes additional symptoms in children and adolescents with the condition. This includes rashes, shock, excessive bleeding, heart problems, and severe gastrointestinal symptoms.
Interestingly autoantibodies measured in children diagnosed with MIS-C have a large variety of targets. Many have no association to known autoimmune diseases, and instead are associated with the heart and surrounding tissue, as well as the gastrointestinal tract.
Alarmingly this indicates a potential mechanism for new autoimmune conditions that affect these organs.
The Australian researchers from the second study mentioned above, identified regions of SARS-CoV-2 proteins that antibodies are likely to recognise and bind to. They then compared them to all human proteins in the body, to identify potential similarities.In doing so they were able to map the potential for SARS-CoV-2 infection to trigger autoantibody formation and existing or new autoimmune diseases, affecting different parts of the body.
Many of the human proteins the COVID-19-Autoimmune Diseases study team identified were associated with other diseases, including multiple sclerosis, SLE and rheumatoid arthritis. Other human proteins they identified were associated with diseases of the heart and vascular system, airways, as well as epilepsy, all of which have been reported in COVID-19 patients.
Ultimately, understanding the mechanisms, the immune system targets, and those who are at risk, may offer targeted treatments for autoimmune illnesses after COVID-19.
To date most reports of autoimmune disease after COVID-19 studied small patient numbers or are case reports. Large studies reviewing the evidence are needed, especially covering multiple autoimmune diseases.
One study, for example, five cases of Guillain-Barré Syndrome were reported out of 1,000-1,200 cases of COVID-19 admitted to the hospital. Although this indicates a small incidence in the autoimmune disease after COVID, it doesn’t tell us what is occurring worldwide.
Study reports of the percentage of people positive for autoantibodies to specific targets range from 5% to a massive 50% in COVID-19 positive cases.
Autoantibodies are not only being patients with severe COVID cases but also in those with mild symptoms and even in those who were asymptomatic!
Autoimmune diseases and conditions are also expected to constitute a large proportion of Long COVID issues now and more so in the future.
For more on Autoimmune Diseases and COVID-19, keep on logging to Thailand Medical News.  


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