My non-medical interpretation: leronlimab kicks Ma

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My non-medical interpretation: leronlimab kicks Maraviroc’s ass due to the extraordinary way it inhibits CCR5 that supports innate immune response verses Maraviroc that deep buries into the CCR5 receptor and hinders immune response. Accurate or not?

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Maraviroc binds shallow near the entry of the CCR5 receptor and doesn't even bind the n terminus. It works by changing the shape of the receptor so HIV and ligands like CCL5 can't bind. Although I have an inkling that in some rare cases ligands may be able to bind or even knock maraviroc loose. Leronlimab on the other hand binds deep including binding the deepest binding site the n terminus that all ligands bind too. I've read the very long paper on how maraviroc binds in the CCR5 and a very long paper on the structure of CCR5 and how ligands bind. It's how I figured out that Cytodyn's claim that CCLs can bind CCR5 when leronlimab was used was false.

What both maraviroc and leronlimab do is switch from an M2 (anti-inflammatory, anti-iimmune) macrophage response to an M-1 (inflammatory, killer immune) macrophage response. The trick is by blocking CCLs both lower inflammatory cytokines and rely on the other CCR receptors to bring about a normal immune response.