Constant contact with viruses can trigger our body to respond with an autoimmune disease.
Find out more in this blog by Dr.
Gloria Sabater.

The most prominent pathogenic viruses that have been proposed in the triggering and initiation of autoimmune diseases include: parvovirus B19, Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes-6 virus, HTLV-1, hepatitis A and C viruses, and rubella virus.
These viruses have been implicated in the onset of chronic inflammatory or autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, Sjogren’s syndrome, primary biliary cholangitis, multiple sclerosis, polymysitis, uveitis, Henoch-Schonlein purpura, systemic juvenile idiopathic arthritis, systemic sclerosis thyroiditis, and autoimmune hepatitis.

Although the exact etiology of autoimmune diseases is still unknown.
There are several factors that are thought to contribute to the onset of an autoimmune disease.
These include genetic predisposition, environmental triggers such as bacterial infections, including the gut microbiota, viral fungi and parasitic infections, as well as physical and environmental agents, hormonal factors and immune system dysregulation.

Suggested mechanisms of autoimmunity induction include molecular mimicry, i.e., there are multiple mechanisms by which infection by a pathogen can lead to autoimmunity.
The pathogen can contribute elements that are sufficiently similar in amino acid sequence or structure to the self-antigen.
So the pathogen acts as a self-‘mimicry’.
An infection can lead to the activation of antigen-presenting cells which, in turn, can activate pre-primed autoreactive T cells.
This leads to the production of pro-inflammatory mediators, which in turn can lead to tissue damage.

Constant contact with viruses can trigger our body to respond with an autoimmune disease.
Find out more in this blog by Dr.
Gloria Sabater.

The most prominent pathogenic viruses that have been proposed in the triggering and initiation of autoimmune diseases include: parvovirus B19, Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes-6 virus, HTLV-1, hepatitis A and C viruses, and rubella virus.
These viruses have been implicated in the onset of chronic inflammatory or autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, Sjogren’s syndrome, primary biliary cholangitis, multiple sclerosis, polymysitis, uveitis, Henoch-Schonlein purpura, systemic juvenile idiopathic arthritis, systemic sclerosis thyroiditis, and autoimmune hepatitis.

Although the exact etiology of autoimmune diseases is still unknown.
There are several factors that are thought to contribute to the onset of an autoimmune disease.
These include genetic predisposition, environmental triggers such as bacterial infections, including the gut microbiota, viral fungi and parasitic infections, as well as physical and environmental agents, hormonal factors and immune system dysregulation.

Suggested mechanisms of autoimmunity induction include molecular mimicry, i.e., there are multiple mechanisms by which infection by a pathogen can lead to autoimmunity.
The pathogen can contribute elements that are sufficiently similar in amino acid sequence or structure to the self-antigen.
So the pathogen acts as a self-‘mimicry’.
An infection can lead to the activation of antigen-presenting cells which, in turn, can activate pre-primed autoreactive T cells.
This leads to the production of pro-inflammatory mediators, which in turn can lead to tissue damage.

WHAT ABOUT CORONAVIRUSES

Corona viruses represent an important group of viruses that mainly affect humans through zoonotic transmission.
In the last two decades, this is the third case of the appearance of a new coronavirus, after the severe acute respiratory syndrome (SARS) in 2003 and the Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012.

In December 2019, a new outbreak of a new strain of coronavirus infection emerged in Wuhan, China, SARS-CoV-2 or Covid-19.
The disease, which was declared a pandemic in early March 2020, is characterized by fever, dry cough, myalgia or extreme fatigue, can be asymptomatic or with minimal constitutional symptoms similar to those of the flu that lead to a favorable outcome in many cases.

However, some of the patients trigger severe pneumonia with sepsis leading to acute respiratory distress syndrome (ARDS) with respiratory failure requiring mechanical ventilation.
And it is sometimes accompanied by hyperferritinemia and involvement of multiple organs, including hematological, gastrointestinal, neurological and cardiovascular complications that lead to death.
ARDS described in up to 20% of Covid-19 cases is reminiscent of cytokine release syndrome-induced ARDS and secondary hemophagocytic lymphohistiocytosis (sHLH) seen in patients with SARS-CoV and MERS-CoV, as well as in leukemia patients receiving T-cell therapy. These cases with Covid-19 are those that develop through excessive cytokine release and uncontrolled immune activation, multi-organ failure with a serious prognosis.

SARS-CoV-2 infection could trigger or mimic a form of organ-specific autoimmunity in genetically predisposed patients.

Covid-19 and Autoimmunity: The Role of Molecular Mimicry

Despite the current wave of intensive research around the world, the etiopathology of diseases induced by SARS-CoV-2 infection is the central question that remains obscure.
One likely explanation is that the heterogeneity and multitude of disorders induced by the current pandemic stem from phenomena of molecular mimicry between the virus and human proteins.

The scientific basis is that, after infection, the immune responses generated against SARS-CoV-2 can cross-react with human proteins that share peptide sequences with the virus, resulting in autoimmune pathological sequelae.

In addition, in the clinical context exposed above, it is noteworthy to report that Sars CoV-2 shares 6 minimum immune determinants with the Kawasaki antigen , as well as possible cross-reactions and the consequent Kawasaki autoimmune disease in predisposed subjects.

Even more impressive seems the distribution of heptapeptides between the human proteome and the viral spike glycoprotein.
The clinical scenario that emerges is disturbing.
In fact, the list of reported proteins, when modified, configures almost all the diseases that have been described in association with SARS-CoV-2.

The Covid-19 vaccine and the limitations of molecular mimicry

The extent of molecular mimicry between SARS-CoV-2 and the human proteome should be carefully analyzed as a preliminary mandatory step for any vaccine formulation.

In fact, due to the similarity between the pathogen and the host peptide, a possible consequence of vaccination could consist of specific autoimmune reactions that affect autoantigens, such as the alveolar surfactant protein already analyzed.

Only peptide sequences that belong exclusively to the virus can represent the basis of safe and specific vaccination protocols.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289100/

https://immunityageing.biomedcentral.com/articles/10.1186/s12979-020-00185-x