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Thursday, 07/16/2020 11:41:19 AM

Thursday, July 16, 2020 11:41:19 AM

Post# of 1047
EIGR Antiviral Anti ARDS Mechanism of Action -Derek Lowe : “Compared to influenza A virus infection in the same ferret model, the coronavirus transcriptional response was much less dramatic, but very distinctive. The team was even able to check transcription in human lung tissue (2 post-mortem samples compared to 2 different healthy patients). That’s a very small sample, necessarily, but it showed a very similar profile: no interferon upregulation and plenty of cytokine transcription. They were able to check circulating levels of these in a larger number of patients (24 infected cases versus 24 uninfected controls), and these results were also consistent: they tested negative for interferon, but showed elevation of CXCL9 (which attracts T cells) and CXCL16 (which attracts NK cells), CCL8 and CCL2 (recruiting monocytes and/or macrophages), and CXCL8 (which attracts neutrophils). A sudden oversupply of these cell types might be behind the pathology of the disease, which could be characterized, if these hypotheses are correct, as a uniquely imbalanced response: far too little interferon and far too many cytokines, too early.

I expect we’ll see quite a few other papers in this area; we’ll see if this picture holds up. But it certainly seems consistent with what people have been seeing in the clinic, and it bodes well for the therapies that are aiming to dampen the cytokine response pathways. Does this mean that administration of IFN-I or IFN-III would also be beneficial?”
https://blogs.sciencemag.org/pipeline/archives/2020/05/21/there-may-be-a-unique-coronavirus-immune-response