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Can anyone help me out here? I thought low migration of intermediate monocytes was the proposed cause of PASC, so why would reducing the migration further with LL help the condition?

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A very low state of CCL4 exists in Covid increasing the non-classical monocytes which differentiate from classical when reintroduced into the bone marrow. The blocking of CCL4 by leronlimab would lower that further very insignificantly. The viral particles are shed and introduced into non-classical monocytes during the Covid active phase.

In longhaulers the low state of CCL4 exists with again a very insignificant amount of difference caused by leronlimab. Those viral particle containing non-classical monocytes will not use CCL4 as a chemotaxi and leronlimab will block the CCL5. In addition CCR5 blockade downregulates TNF-a and IFNy which are necessary for fracktaline production. TNF-a is also necessary for non-classical monocytes for endothelial cell adhesion.