ABSTRACT
SARS-CoV-2, a new virus that appeared in Wuhan, China, in 2019 has approximately an 80% genomic match to the Severe Acute Respiratory Symptom (SARS) virus, which is known to come from a bat virus. Symptoms of Kawasaki disease in general and incomplete Kawasaki disease have been seen in a subset of pediatric patients having a current or previous infection of SARS-CoV-2. A viral infection, such as a SARS-CoV-2 virus infection, could result in extensive antigen-antibody immune complexes that cannot be quickly cleared in a subset of patients and thus create a type III hypersensitivity immune reaction and cause Kawasaki disease or Kawasaki disease symptoms (also known as multisystem inflammatory syndrome) in a subset of patients. Extensive binding of antibodies to viral antigens can create antigen-antibody immune complexes, which, if not eliminated in certain individuals having dysfunctional complement systems, can start inflammatory type III hypersensitivity symptoms, including protease releases that can disrupt epithelium, mesothelium, and endothelium basement membranes, and induce pervasive inflammation throughout the body. This could continue after SARS-CoV-2 infections end if the first wave of protease attacks on basement membranes created new secondary autoantibodies and new uncleared antigen-antibody immune complexes.
Subject(s)
Coronavirus Infections/complications , Coronavirus Infections/virology , Mucocutaneous Lymph Node Syndrome/etiology , Mucocutaneous Lymph Node Syndrome/virology , Pneumonia, Viral/complications , Pneumonia, Viral/virology , Antigen-Antibody Complex , Basement Membrane/immunology , Basement Membrane/pathology , COVID-19 , Child , Humans , Immune Complex Diseases/immunology , Mucocutaneous Lymph Node Syndrome/diagnosis , Pandemics , Peptide Hydrolases/chemistry , Skin/pathology , Systemic Inflammatory Response Syndrome/therapySubject(s)
Antibody-Dependent Enhancement , Antigen-Antibody Complex/biosynthesis , Betacoronavirus/pathogenicity , Coronavirus Infections/therapy , Immune Complex Diseases/immunology , Pneumonia, Viral/therapy , Severe Acute Respiratory Syndrome/therapy , Antibodies, Viral/biosynthesis , Antigen-Antibody Complex/drug effects , Betacoronavirus/immunology , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/immunology , Coronavirus Infections/virology , Humans , Immune Complex Diseases/complications , Immune Complex Diseases/drug therapy , Immune Complex Diseases/virology , Immunity, Humoral , Immunization, Passive/methods , Immunoglobulin G/biosynthesis , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , Pneumonia, Viral/virology , Receptors, Complement/immunology , Receptors, Complement/metabolism , SARS-CoV-2 , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/immunology , Severe Acute Respiratory Syndrome/virology , Severity of Illness Index , COVID-19 SerotherapySubject(s)
Antigen-Antibody Complex/biosynthesis , Betacoronavirus/pathogenicity , Coronavirus Infections/immunology , Cytokine Release Syndrome/immunology , Immune Complex Diseases/immunology , Pneumonia, Viral/immunology , Severe Acute Respiratory Syndrome/immunology , Vasculitis/immunology , Antibodies, Viral/biosynthesis , Antigen-Antibody Complex/drug effects , Betacoronavirus/immunology , Blood Vessels/drug effects , Blood Vessels/immunology , Blood Vessels/pathology , Blood Vessels/virology , COVID-19 , Complement C3/antagonists & inhibitors , Complement C3/biosynthesis , Complement Inactivating Agents/therapeutic use , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Coronavirus Infections/virology , Cytokine Release Syndrome/complications , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/virology , Humans , Immune Complex Diseases/complications , Immune Complex Diseases/drug therapy , Immune Complex Diseases/virology , Immunity, Humoral/drug effects , Interleukin 1 Receptor Antagonist Protein/therapeutic use , Interleukin-6/antagonists & inhibitors , Interleukin-6/biosynthesis , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , Pneumonia, Viral/virology , Receptors, Interleukin-1/antagonists & inhibitors , Receptors, Interleukin-1/biosynthesis , SARS-CoV-2 , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/drug therapy , Severe Acute Respiratory Syndrome/virology , Severity of Illness Index , Vasculitis/complications , Vasculitis/drug therapy , Vasculitis/virologyABSTRACT
Coronavirus Disease 2019 (COVID-19) is an ongoing public health emergency and new knowledge about its immunopathogenic mechanisms is deemed necessary in the attempt to reduce the death burden, globally. For the first time in worldwide literature, we provide scientific evidence that in COVID-19 vasculitis a life-threatening escalation from type 2 T-helper immune response (humoral immunity) to type 3 hypersensitivity (immune complex disease) takes place. The subsequent deposition of immune complexes inside the vascular walls is supposed to induce a severe inflammatory state and a cytokine release syndrome, whose interleukin-6 is the key myokine, from the smooth muscle cells of blood vessels.