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One difference is that HIV regularly switches to use another co-receptor, CXCR4, in place of CCR5. So, if you take away CCR5 it just uses the other receptor and still causes infection. I haven't read the paper, but it sounds like this work might impact HIV receptor binding more broadly.
The other problem with the CCR5 inhibition approach is that there are side-effects. For example, the mutation in CCR5 you're referring to does have some negative effects - I believe individuals with that mutation are more susceptible to developing West Nile virus encephalitis, for example.