In the latter, TNF-α and IL-1β upregulation was observed at 24 hpi [23], whereas in the former, TNF-α upregulation was seen as a consequence of viral replication at 48 and 72 hpi, and VEGF, G-CSF and GM-CSF were found to be upregulated at 72 hpi; all upregulation levels became significant when virus inoculation was in combination with an antibody against FCoV S protein that is known to induce ADE [18,19]. This evidence concerns the gene IL1B and acute disseminated encephalomyelitis.