The CCR5 receptor also responds to chemokine (a cytokine that recruits immune cells to the site of infection/damage). So, leronlimab may work by reducing inflammation rather than preventing SARS-CoV-2 entry, according to some sources I encounter (see links below).

Also, the D614G mutation doesn’t change the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein. So, the RBD should still bind to the ACE2 receptor.

I have not seen any research papers showing/suggesting that CCR5 can be a receptor for SARS-CoV-2, so I think it remains a possibility.

Leronlimab shows promise as a treatment for COVID-19 - GlobalData

Disruption of the CCL5/RANTES-CCR5 Pathway Restores Immune Homeostasis and Reduces Plasma Viral…