PB , thank for the response. A few more are coming!
RTIs prevent HIV conversion, IIs (not in clinical ye, as I figure) prevents HIV 'residence', & PIs prevent HIV maturation. They are in both ends of HIV's life cycle. What about the virus already incorporated, & worse keep making v-RNA----active virus? will Anti-sense approaches work? How far have these compounds progressed in trials? Since PIs used alone don't prevent viral replication, the clinical measurement of 'v- RNA' is not a real test of their efficacy, & v-particles might be more relavent. But you have to get rid off the v-RNA somehow, sometime. Certainly the sooner the better. In that case I think the next ingredients in the 'cocktail' treatment of HIV-positive patients lay somewhere between RTI-PI, don't you agree? Who are further ahead?
If you are a director of drug discovery, which particular step(s) of HIV's life cycle is considered as a 'bottle-neck' between the three mentioned above? If this target(s) is chosen, how you would like to setup a relavent assay(s) to screen for future drugs? Too bad I am just a little guy, but might be someone else on this thread is in the position to push this field forward.
Any comments, thoughts or links are highly appreciated.
regards |
