Thanks ohm, yes I recall the mucosal lining noted by Dr. Sacha after your statement. I also thought the X4 was due to current drugs and/or resistance as it seemed more prevelant in patients that had been on treatment for many years, but couldn't recall any specific science data to support.

Due to leronlimab allowing normal immune functions and other drugs to still bind/function, would this potentially support keeping the disease from mutating to X4 or cancer from finding other pathways?

Quote:

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Due to its selectivity and target specific mechanism of action, Leronlimab allows chemokine binding (CCL3, CCL4) at therapeutic doses and does not have agonist activity of the CCR5 receptor (it does not activate the immune function of the receptor). This target specificity separates Leronlimab from other CCR5 antagonists.

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