There does seem to be some selective blocking going on. We just don't know what kind which is why I bemoan the fact there is so little basic research on leronlimab. Dr. Patterson's tests are sorting that out a bit.

But with GPCRs and chemokines there's a secondary pathway through either CCR1 or CCR3 receptors. There's less binding affinity and much fewer of those receptors. You will get an immune response absent CCR5 just a milder one. Of course with CCR5 delta 32 double allele gene deletion you still have a fairly strong response because CCR1, CCR3 and binding ramp up to take the place of CCR5.