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Posted On: 06/10/2019 12:28:04 PM
Post# of 154952
I research this some, the difference in death rate (though there has been a lot debate on twitter, having the author recant some conclusions (also n=11))
It seems the big difference is the higher death rate from flu with ccr5 delta 32. The biggest issue with flu is not clearly the virus from the lungs. Going back again, with studies in mice, it looks like it is not that ccr5 is deleted. It is that since it is deleted the chemokines that normally bind to ccr5, bind to other receptors causing the issue (since ccr5 is gone). With leronimab not greatly inhibiting these chemokines at lower does or at least allowing the important one MCP-1 bind (we know because less side effects), this should not be an issue with leronlimab.
https://ajp.amjpathol.org/article/S0002-9440(...7/fulltext
It seems the big difference is the higher death rate from flu with ccr5 delta 32. The biggest issue with flu is not clearly the virus from the lungs. Going back again, with studies in mice, it looks like it is not that ccr5 is deleted. It is that since it is deleted the chemokines that normally bind to ccr5, bind to other receptors causing the issue (since ccr5 is gone). With leronimab not greatly inhibiting these chemokines at lower does or at least allowing the important one MCP-1 bind (we know because less side effects), this should not be an issue with leronlimab.
https://ajp.amjpathol.org/article/S0002-9440(...7/fulltext
Quote:
However, macrophages were the predominant cell type infiltrating at day 2 postinfection in CCR5−/− lungs,
Quote:
this accelerated macrophage accumulation is likely to be linked to enhanced expression of MCP-1 and RANTES (Figure 6A), and possibly of IP-10, and their binding to other intact chemokine receptors on the CCR5-deficient macrophages.
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