Hi Dr. Holodniy:

I'd be lost without this website. Thanks to you and your colleagues for your time. I'm HIV+ at least 10yrs. Started AZT monotherapy in '90, added DDC in '93, switched DDC for 3TC in '96, and added Viracept in '97. (I know this is all taboo now, but my HIV doc was following current procedures way back then.) Since 1994, VL has bounced from undetectable to a max of 1500...it was undetectable by ultrasensative test for a few months after starting Viracept. CD4% was in 40's until mid-'96, in 30's until end of '98, and is now 25. I stopped combo of AZT/3TC/Viracept about 6 weeks ago when VL was 1000 and CD4% 31. This week VL is 5000, CD4% 25. VL and CD4 have consistently been in this range since I stopped antivirals. Not currently on any antivirals. My plan is to closely monitor my VL and CD4 and go back on medications if the VL approaches 10,000.

I was very proud of my ability to understand my lab reports until along comes my first genotype, which was taken one week after I stopped drugs. Reported mutations: RT gene: 62V, 184V, 215Y, 214F. PI gene: 30N, 63P, 77I, 88D. I have a Dr appt after July 4th and I want to be as informed as I can be. At my last appt (before the genotypoe was back) my Dr suggested that I start a combo of DDI, D4T, Sustiva and maybe HU. A copule of questions, please:

(1) What is your interpretation of my genotype mutations. Do I have any viable drug combinations left? (2) Would the combo that my HIV doc suggested be prudent? and (3) What would be your recommendation for a new combo given my drug history and genotype?

Thanks so much for your time. I hope that you realize what a service this site provides to the HIV+ community. Dave.

Dear Dave, your genotype indicates the following: primary resistance to AZT (215Y, and precursor AZT mutation 214F), primary resistance to 3TC (184V) and possible secondary resistance to ddC and ddI (184V), although this has not been shown to be clinically relevant; in the protease gene, you have primary resistance to nelfinavir (30N) and secondary resistance to nelfinavir (77I, 88D). The 63P is a naturally occurring mutation which in and of itself does not confer any resistance, but can contribute to resistance to PIs if other primary mutations are present. The regimen your doctor recommends is great. There should be no demonstrable cross resistance. Given your viral load now, that regimen should have no problem getting your viral load to <50 and keeping it there.

MH