Anyways, I think there is something else, that BP

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Anyways, I think there is something else, that BP is saying you want those inflammatory non-classical, S1 presenting monocytes adhering to endothelial walls to stay put so as to keep the inflammation from spreading to vessels in the brain and heart.

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Those monocytes elsewhere will send out cytokines to call macrophages and monocytes to that site. No chemotaxi because CCL5 and CCL4 are blocked.

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I wonder if BP is correct about wanting to use both a statin to lower fractalkine and CCR5i to block monocyte motility (no matter that he says low motility is a cause of PASC). or maybe will CCR5i alone lower fractalkine and inhibity damaging non-classical monocyte motility?

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I've never tried to hunt down the level of effect CCR5 has on fractalkine but with the effect on TNF-a and IFNy it should be significant and our longhaulers trial seems to support that.