NP said Leronlimab could mimic the CCR5-delta 32 m

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NP said Leronlimab could mimic the CCR5-delta 32 mutation for bone marrow transplants and thus cure HIV.
However, how does it work with diseases that are related to CCR5 delta 32 such as MS, lupus, OCD? Can it also bind to the CCR5 mutation?

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There are two different types of CCR5 delta 32. The first type is single allele where a lowered amount of CCR5 is produced. The second is double allele deletion where no CCR5 receptors exist.

Where leronlimab would mimic the Berlin bone marrow transplant patient would be total blockage of CCR5 would be the same as no CCR5 receptors.

In single allele it would be easier for leronlimab to cover the CCR5 receptors that do exist. In double allele there are no CCR5 receptors to bind to. In double allele you would see other receptors taking over for CCR5 with an increased binding affinity for chemokines.

One of the reasons leronlimab would not react exactly like CCR5 delta 32 double allele and would work to address diseases is that with CCR5 delta 32 secondary chemokines for predominately CCR1, CCR3, CCR4 would be highly competitive with primary chemokines. Doing so would imbalance chemokines that would be helpful in reducing certain diseases. With leronlimab you'd see low binding affinity to other receptors with minimal disruption.

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Also, can it down regulate immuno-moodilin?

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There's a correlation between increased CCR5 expression and increased levels of Annexin-A1 which produces immuno-moodulin. Annexin-A1 is preferentially expressed on autoimmune prone T-cells which would lead me to believe leronlimab would downregulate it. It also brings up interesting possibilities for leronlimab in treating psychiatric disorders.