Replies to post #50673 on Biotech Values

[DewDiligence]

>In almost every infected individual there is already a population of virus that is dependent on CXCR4 for entry. No mutations necessary.<

I think you’re mixing two issues: i) viral mutation; and ii) preferential selection among multiple (non-mutated) viral strains.

[microcapfun]

>> Not at all. In almost every infected individual there is already a population of virus that is dependent on CXCR4 for entry.

I don't think that's true. In a significant majority of treatment-naive HIV+ patients, most have no CXCR4 tropic virus at all. After CCR5 inhibitor therapy, a small fraction of those who were thought to be CXCR4 tropic negative display CXCR4 tropism fairly rapidly, and it is thought this is due to an insensitive tropism assay. After the first few R4's show up, the rate of R5-->R4 conversion seems to be very slow.

Certainly the mutation from CCR5 to CXCR4 will happen eventually with a CCR5 inhibitor, but apparently the mean time for this to happen is several years if the patient starts out with no CXCR4 tropism.

(I think I've got this right, but if I screwed up somebody will be kind enough to let me know!)

For this reason, and for the reason that mutations render all HIV drugs ineffective eventually, CCR5 inhibitors should become a significant component of HIV therapy.

micro