Hah, I have a feeling NP was confused on this one so only he can make sense of what he was thinking. I thought it surprising and telling on one of the latest calls that NP admitted he wasn't up on all the science, and deferred to someone else to answer some of the questions pertaining to topics beyond his understanding. Truly wise to do so.

If he wasn't confused, then he did a poor job of explaining what he meant. How can CCR5 RO explain who will be an HIV responder? As MDV hypothesized, if NP confused HIV tropism testing with RO then his comments might make sense .. as only CCR5 tropic HIV will respond to CCR5 blockade, not R4=CXCR4 tropic infection. But if he wasn't confused, how can RO predict response to LL in HIV? If at baseline lots of CCR5 is occupied by HIV, then maybe that would be similar to tropism testing? Possibly CXCR4 tropic does not have as much CCR5 receptor in bound form? Who knows???

I just know they are doing something with RO to satisfy FDA in BLA for HIV, as part justification.

I think if we are saying 350 or 525 mg is enough but FDA wants 700, we may need to show that upping dose does not increase RO and thus not worth it, or alternatively, to show that RO does not correlate with viral load reduction or CD4 counts or some other marker for HIV status. Either our dose is high enough, or show that RO is irrelevant (maybe a ceiling effect or something like that one of the maraviroc papers showed that not important to rely on routine RO testing).