Thanks for your postings, good thinking and interesting links.
I agree that Viracept appears to have a unique resistance profile, not shared by other PI's. Can we assume that starting with another PI and then switching to Viracept would not decrease Viracept's potency? It seems that the motivation for beginning treatment with Viracept is due to its comparably milder side effects.
From my brief reading of the St. Petersburg summary, I was impressed that currently there are no imminent clinically promising methods under development. Also, that nelfinavir and saquinavir have fewer mutation sites than the other listed PI's. (Table 2).
I am curious if there is any data for the amount of time it takes to develop resistance to Viracept. If the drug knocks down the virus level to non-detection, then mutations should be slowed down too. Is there data indicating the expected duration of treatment with Viracept before a new drug is needed to combat resistant strains?
Table 2. Resistance mutations associated with protease inhibitor use.
Drug Mutations
Overall: L10I, K20M, L24I, V32I, M46I, I54V, L63P, A71V, V82A/F,
I84V, L90M
saquinavir: G48V, L90M
ritonavir: M36I, M46I, I54V/L, A71V, V82F, I84V, L90M
indinavir: L10I, V32I, M46I, I54V, L63P, A71V, V82A/T, I84V, L90M
nelfinavir: D30N, A71V, N88D |
