![]() Coagulopathy has become a key indicator of mortality in infected subjects ( 2). For example, a significant deadly expression of the infection is the development of disseminated intravascular coagulopathy. We believe the answer is probable, since some of the systemic disease clinical manifestations of COVID-19 cannot be explained solely by the binding of SARS-CoV-2 spike proteins with cell membranes of tissues that exhibit angiotensin-converting enzyme 2 (ACE2). We will begin with the first question of whether cross-reactivity can be involved in the multi-system response of COVID-19 infection. First, does cross-reactivity play a role in the multi-system disorders associated with SARS-CoV-2 infection? Second, how does cross-reactivity contribute to the pathophysiology of SARS-CoV-2–induced autoimmunity? Third, are there any concerns for autoimmune development with either infection or vaccination with SARS-CoV-2? There are three important questions regarding the role of cross-reactivity with SARS-CoV-2. An insufficiently vetted vaccine might mean trading freedom from COVID-19 to an autoimmune assault in the future. In this mechanism, antibodies formed against SARS-CoV-2 would also bind to human tissue proteins leading to autoimmune reactivity. Cross-reactivity occurs when amino acid sequence homology exists between a pathogen and self-tissue proteins ( 1). While, naturally, the search for a successful vaccine and efficient treatment protocols are paramount, immunologists who focus on autoimmunity have been concerned whether the infection or even a newly developed vaccine itself can trigger autoimmunity via cross-reactivity. The COVID-19 pandemic has placed an immediate call to action for medical researchers to investigate how SARS-CoV-2 can impact the worldwide human population. Thus, our results can establish the potential risk for autoimmunity and multi-system disorders with COVID-19 that may come from cross-reactivity between our own human tissues and this dreaded virus, and thus ensure that the badly-needed vaccines and treatments being developed for it are truly safe to use against this disease.Ĭoronavirus disease (COVID-19) has become one of the greatest global public health concerns of our century. The human monoclonal antibodies used in this study are almost identical with these approved antibodies. Very recently, human monoclonal antibodies were approved for use on patients with COVID-19. This extensive immune cross-reactivity between SARS-CoV-2 antibodies and different antigen groups may play a role in the multi-system disease process of COVID-19, influence the severity of the disease, precipitate the onset of autoimmunity in susceptible subgroups, and potentially exacerbate autoimmunity in subjects that have pre-existing autoimmune diseases. We also did selective epitope mapping using BLAST and showed similarities and homology between spike, nucleoprotein, and many other SARS-CoV-2 proteins with the human tissue antigens mitochondria M2, F-actin and TPO. We found that SARS-CoV-2 antibodies had reactions with 28 out of 55 tissue antigens, representing a diversity of tissue groups that included barrier proteins, gastrointestinal, thyroid and neural tissues, and more. We applied both human monoclonal anti-SARS-Cov-2 antibodies (spike protein, nucleoprotein) and rabbit polyclonal anti-SARS-Cov-2 antibodies (envelope protein, membrane protein) to 55 different tissue antigens. We sought to determine whether immune reactivity occurs between anti-SARS-CoV-2 protein antibodies and human tissue antigens, and whether molecular mimicry between COVID-19 viral proteins and human tissues could be the cause. 5Department of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.4Department of Neurology, Harvard Medical School, Boston, MA, United States.3Regenera Medical, Los Angeles, CA, United States.2Department of Preventive Medicine, Loma Linda University School of Medicine, Loma Linda, CA, United States.1Department of Immunology, Immunosciences Laboratory, Inc., Los Angeles, CA, United States.Aristo Vojdani 1,2*, Elroy Vojdani 3 and Datis Kharrazian 2,4,5
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