In that specific case they're talking about COVID-19 variants which is nonsensical in that context because COVID-19 doesn't bind to CCR5. Leronlimab may have the ability to reduce COVID-19 viral replication but that runs through it's downregulation of the mTORc1 pathway.
With HIV the 7 contact points for CCR5 and the one for the N terminus are so exacting that I would expect any genomic change would render that HIV variant non-viable.
Now we come to CCR5 binding chemokines. It's a key that fits a specific lock and after millions of years of evolution any mutations are at a competitive disadvantage.
One claim made by Cytodyn that I now think may possibly be untrue is that leronlimab selectively blocks chemokines. Being large molecule it never really made sense to me and I've never seen any testing for it.