Other possible mechanisms by which SARS-CoV-2 could induce a hyperinflammatory syndrome are: i) the autoantibodies formation through “molecular mimicry”, as in Acute Rheumatic Fever (although this mechanism would not justify the occurrence of shock); ii) a vascular damage secondary to the deposition of immune-complexes as in acute serum sickness; iii) an antibody-dependent enhancement (ADE) with IgG immune complexes that enhance virus infection in Fc-receptor-bearing cells. Intriguingly, this phenomenon is the cause of Dengue vascular permeability syndrome, which, again, shares some similarities with PeCOHS [78]. ADE were demonstrated in SARS-CoV infection years ago, mediated by antibodies directed to the envelope spike proteins [79].