KRT18 and infection: The pattern of CNS involvement varies with model design: in K18-hACE2 mice, high neuronal ACE2 expression drives neuron-centric infection and death that can be fatal [54,57], whereas in MA10 and endogenous-promoter hACE2 contexts, pathology is predominantly vascular and immune-mediated, with selective neuronal dysfunction [47,55,60,61].