As in FiP, a normally harmless coronavirus virus to become, in vivo, a lethal killer. This occurs with SARS-CoV-2. SARS-CoV-2 toxifies two key receptors, the ACE 2 receptor and the nAChR receptor. The autoantibodies against ACE 2 decrease/deplete ACE 2. This causes the vascular damage. and cytokine storms being observed. Induction of cytokine expression in epithelial cells lacking Ace2 contribute to the primed inflammatory response in the Ace2?/? mice. ACE2 deficiency impaired endothelial function in cerebral arteries from adult mice and augmented endothelial dysfunction during aging. Oxidative stress plays a critical role in cerebrovascular dysfunction induced by ACE2 deficiency and aging. The neuological manifestations are caused by the nAChR autoantibodies. There is a disease which involves these autoantibodies and it is a carbon copy of COVID-19s neurological manifestations. Autoimmune autonomic ganglionopathy is the disease. Please read the referenced paper.