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Posted On: 01/12/2021 10:05:49 PM
Post# of 148917
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.
But that CCR3 may have been the "QB"? (would love for someone with the molecular biology chops to chime in...)
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.
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:
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.
But that CCR3 may have been the "QB"? (would love for someone with the molecular biology chops to chime in...)
Quote:
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].
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.
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