Evolution of HIV resistance during treatment interruption in experienced patients and after restarting a new therapy

J Clin Virol. 2005 Dec;34(4):277-87. doi: 10.1016/j.jcv.2005.08.007. Epub 2005 Sep 26.

Abstract

Background: To analyse the evolution of resistance patterns in patients undergoing treatment interruption (TI) and re-initiating highly active anti-retroviral therapy (HAART).

Methods: HIV-RT and -PR gene-sequences were analysed in 14 patients (>5 failing prior drugs) before and during TI and under a new HAART. Genotypes were interpreted using two bioinformatics systems. Additionally, virus load (VL) and CD4(+)-T-cell counts were measured.

Results: Six patients (42%) achieved sustained undetectable VL up to one year after TI (responders), while 8 (57%) maintained VL of more than 2,000 copies/mL (non-responders). Different patterns of resistance-mutations evolution were detected. During TI loss of all mutations was observed in three patients, a reduction of mutations was detected in seven patients, and no alteration was seen in four patients. In the responders, 87.5% of protease inhibitor (PI)-resistance mutations waned during TI and remained undetectable under the new treatment. In contrast, in the non-responder group most PI-resistance mutations continued noticeable under the new therapy. Loss of primary PI-resistance mutations and the presence of one fully active PI in the new regimen significantly correlated with success of subsequent treatment (p=0.028). In two patients new reverse transcriptase associated mutations were detected during TI, G190A (NNRTI mutation) and K70R (NRTI mutation). Appearance of K70R could be explained by a reverse direction of a previously described pathway of thymidin analogues mutation resistance development, while G190A could be due to prolonged subinhibitory drug levels after cessation of NNRTIs.

Conclusion: In the evolution of HAART-resistance, different patterns were observed in responders and non-responders during but not before TI. Absence of PI-resistance associated mutations during and after TI and administration of a predicted fully active PI for the new therapy correlated with success. Newly detected mutations during TI may indicate reversibility of previously described mutational pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Retroviral Agents / pharmacology*
  • Anti-Retroviral Agents / therapeutic use
  • Antiretroviral Therapy, Highly Active
  • Drug Resistance, Viral / genetics*
  • Evolution, Molecular*
  • HIV / drug effects*
  • HIV / genetics
  • HIV Infections / drug therapy
  • HIV Infections / virology*
  • HIV Protease Inhibitors / pharmacology
  • Humans
  • Mutation
  • Protease Inhibitors / pharmacology
  • RNA-Directed DNA Polymerase / genetics
  • Species Specificity
  • Treatment Outcome
  • Withholding Treatment

Substances

  • Anti-Retroviral Agents
  • HIV Protease Inhibitors
  • Protease Inhibitors
  • RNA-Directed DNA Polymerase