Interleukin-12 upregulates furin gene expression. Thus one can see a situation where an effective Th1 response to virus could potentiate viral entry, as well as up-regulating other pro-inflammatory proteins dependent on furin pro-protein cleavage. This could be the positive feedback loop leading to ARDS. The other important information from chinese pre-prints, is the activation of complement by viral coded proteins. (Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2- mediated complement over-activation Authors: Ting Gao1#, Mingdong Hu3, 5#, Xiaopeng Zhang1, 4#, Hongzhen Li6,) Stable anaphylatoxin products such as C3a des arg should be measured in patients with severe COVID pneumonia. There are two marketed complement cascade inhibitors out there!
We are looking at repurposing of TLR-9 agonist immunostimulatory oligonucleotides (CpG ODNs) to induce type 1 interferons and provide prophylaxis against COVID infection.
Does anyone know if furin expression is up regulated or down-regulated by induction of the interferon response genes?
