Thanks for sharing mtruong34! Going through t

Thanks for sharing mtruong34!

Going through the referenced works I noticed this article which I hadn't seen before from 2009

https://link.springer.com/article/10.1186/1471-2172-10-35

It sounds like the RANTES/CCL-5 connection was also made in the SARS outbreak in 2003.

Quote:

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Interestingly, the SARS-CoV infected DCs showed low expression of antiviral cytokines (IFN-α, IFN-β, IFN-γ and IL-12p40), moderate upregulation of proinflammatory cytokines (TNF-α and IL-6) but significant upregulation of inflammatory chemokines (macrophage inflammatory protein (MIP)-1α/CCL3, regulated upon activation, normal T cell expressed and secreted (RANTES)/CCL-5 , interferon-inducible protein of 10 kD (IP-10)/CXCL10 and monocyte chemotactic protein (MCP)-1/CCL2. We postulated that this lack of antiviral cytokine response against a background of intense chemokine upregulation could represent a mechanism of immune evasion by SARS-CoV.

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But that CCR3 may have been the "QB"? (would love for someone with the molecular biology chops to chime in...)

Quote:

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Among the CCRs studied, the upregulation of CCR-3 is the strongest (Fig. 3). It has been reported that the expression of CCR-3, unlike CCR-5 and CCR-7, are independent of the maturation status of DCs [13, 14].

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Given this paper I am a little surprised that the FDA was as difficult to convince early on in the pandemic. It seems that a CCR5 antagonist would be a great drug to try given this paper.