, San Jose, CA, USA.
Inflammopharmacology. 2020 Oct;28(5):1219-1222. doi: 10.1007/s10787-020-00739-x. Epub 2020 Jul 7.
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.
2019 年在中国武汉出现的新型冠状病毒(SARS-CoV-2)与已知源自蝙蝠病毒的严重急性呼吸综合征(SARS)病毒大约有 80%的基因组匹配。在当前或以前感染过 SARS-CoV-2 的一组儿科患者中,已观察到川崎病的一般症状和不典型川崎病。病毒感染,如 SARS-CoV-2 病毒感染,可能导致大量抗原抗体免疫复合物在一部分患者中无法迅速清除,从而导致 III 型超敏反应免疫反应,并导致川崎病或川崎病症状(也称为多系统炎症综合征)在一部分患者中。抗体广泛结合病毒抗原会产生抗原抗体免疫复合物,如果某些补体系统功能障碍的个体不能消除这些复合物,就会引发炎症性 III 型超敏反应症状,包括蛋白酶释放,从而破坏上皮、间皮和内皮基底膜,并在全身引发广泛炎症。如果第一轮针对基底膜的蛋白酶攻击产生了新的自身抗体和新的未清除的抗原抗体免疫复合物,那么在 SARS-CoV-2 感染结束后,这种情况可能会持续存在。