*The co-authors JM Llibre and A Bonjoch contributed equally to this article.
Targeting only reverse transcriptase with zidovudine/lamivudine/abacavir plus tenofovir in HIV-1-infected patients with multidrug-resistant virus: a multicentre pilot study
Article first published online: 15 MAY 2008
© 2008 British HIV Association
Volume 9, Issue 7, pages 508–513, August 2008
How to Cite
Llibre, J., Bonjoch, A., Iribarren, J., Galindo, M., Negredo, E., Domingo, P., Pérez-Alvarez, N., Martinez-Picado, J., Schapiro, J., Clotet, B. and the HIV Conference Call study group (2008), Targeting only reverse transcriptase with zidovudine/lamivudine/abacavir plus tenofovir in HIV-1-infected patients with multidrug-resistant virus: a multicentre pilot study. HIV Medicine, 9: 508–513. doi: 10.1111/j.1468-1293.2008.00581.x
These data were presented in part at the XVI International HIV Drug Resistance Workshop, Barbados, West Indies, June 2007 [Abstract 71] and at the 8th International Congress on Drug Therapy in HIV Infection, Glasgow, UK, November 2006 [Abstract P225].
- Issue published online: 12 AUG 2008
- Article first published online: 15 MAY 2008
- Received: 27 January 2008, accepted 27 March 2008
Vol. 10, Issue 6, 396, Article first published online: 5 MAY 2009
- HIV-1 resistance;
- holding regimen;
- multidrug failure;
To evaluate the safety, immunological outcome and HIV-1 evolution in the reverse transcriptase (RT) in patients with multidrug resistance receiving zidovudine/lamivudine/abacavir (TZV) plus tenofovir (TDF).
Pilot analysis of highly experienced patients (n=28), with ≥1 thymidine-associated mutation (TAM) and the M184V mutation.
Median of 8.5 treatment regimens, 58% Centers for Disease Control stage C. Baseline (nadir) CD4 count 363 (112) cells/μL. There was a sustained 24-week drop in viral load (VL) of 0.71 HIV-1 RNA copies/mL (P<0.001), with 35.7% (10/28) achieving a VL of <50 copies/mL. The median 24-week decrease in CD4 was −53 cells/μL and only −17 cells/μL when baseline CD4 was <350 cells/μL. There was no evolution in RT mutations, TAMs, accessory mutations or K65R. No clinical progression and one out of 28 suspected abacavir Hypersensitivity Reaction (HSR). Lower probability of achieving VL<400 copies/mL was associated with D67N (P=0.007), D67N/M41L (P=0.01), ≥3 TAMs (P=0.07) and VL>10 000 copies/mL (P=0.01). Mutations conferring zidovudine hypersusceptibility (Y181C, K65R and L74V) did not improve virological or immunological outcomes. Better CD4 outcomes were seen in patients without M41L (P=0.04) or with baseline VL<10 000 copies/mL (P=0.01).
A bridging regimen with TZV+TDF prevents significant immunological decline and may forestall viral evolution in HIV-1 RT despite persistent viral replication.