Jun 22, 2012
Good Day Dr. Young, I wrote before this section a month ago (http://www.thebody.com/Forums/AIDS/Meds/Q222497.html) asking for some information. Recently, my doctor have received the answer of the mexican federal comission in order to switch my meds to EFV, TDF and DRV/r. I used the Stanford University HIV Drug Resistant Database and I realized that EFV have a high level resistance because the K103N mutation. However I have read too that T215Y mutation may lead to hypersusceptibility to NNRTIs. My doctor explained me that , because I never have used a NNRTI before, it could work and in the case it doesnt work I have the enough time to change to ETR, I showed the Stanford University HIV analysis and he get really surprised but he just doesnt want to go against the federal comission conclusion about my treatment. This is no a surprise for me, I have been asking answers to doctors of here and nobody can explain me anything with a scientific rigor. I am trying to contact hight level doctors. Another data I think you should know is like I said I never have used NNRTIs before, and K103N mutation and other ones are new on this year, I compared with my genotype test of 2011 and my virus hadnt that mutations. So the question is, should I trust this new treatment? or is it better to use ETR instead of EFV?
THANKS A LOT DOCTOR YOUNG! I REALLY APPRECIATE YOUR HELP!
Here is my actual genotype profile(Feb, 2012): Complete Mutations Profile: Reverse Trancriptase Gene: M41L, D67N, T69D, K103N, M184V, T215Y, K43R, A98S, S105A, E122K, D123E, S163T, Q174A, D177E, Q207E, R211K, L214F, P272A, R277K, R284K, T286A, E297K, K311R, G335D Protease Gene: L10F, D30N, L33F, K43T, M46I, I54V, V82A, N88D, V3I, I13V, K20R, E35D, M36I, S37N, R57Q, D60E, Q61E, I62V, L63P, I64V, I93L
And Genotype Test results on May, 2011 : Reverse Trancriptase Gene: M41L, D67N, T69D, M184V, T215D/Y Protease Gene: L10F, D30N, L33F, K43T, M46I, I54V, V82A/V, K20K/R, M36I, L63P, I64I/V
Response from Dr. Young
Hello and good to hear from you.
I'm happy to hear that you used the online Stanford drug resistance resource. I have to agree with you and respectfully disagree with my Mexican colleagues.
Your virus (2012) is actually quite a bit more resistant that I had first thought- it likely has high level resistance to several drug classes (NRTIs, NNRTIs and PIs). I would not agree with the idea that your virus has susceptibility to EFV, though it should be sensitive to the second generation NNRTIs, like etravirine.
I don't know how to explain the differences in the two genotypic results, especially with regards to the K103N mutation, but when ever I'm in doubt about these, I'll pragmatically err on the side of the worse case (or most drug resistant) scenario.
In my opinion, it would be better to use ETV over EFV; since your virus is already resistant to all PIs except for darunavir, and since the Standford DB predicts low-leve resistance to tenofovir (TDF), I'd be very careful about assembling as potent a regimen as possible and therefore reluctant to use EFV. If my (or Stanford's) interpretation is right, a regimen of TDF+ETV +DRV/r would have two fully active agents (ETV and DRV) while the TDF+EFV+DRV/r would only have 1 active agent.
An alternative to using ETV would be (as we discussed earlier) maraviroc or raltegravir- either of which should be fully active against your virus.
Buenos suerte, BY
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