The individualized genetic barrier predicts treatment response in a large cohort of HIV-1 infected patients

PLoS Comput Biol. 2013;9(8):e1003203. doi: 10.1371/journal.pcbi.1003203. Epub 2013 Aug 29.

Abstract

The success of combination antiretroviral therapy is limited by the evolutionary escape dynamics of HIV-1. We used Isotonic Conjunctive Bayesian Networks (I-CBNs), a class of probabilistic graphical models, to describe this process. We employed partial order constraints among viral resistance mutations, which give rise to a limited set of mutational pathways, and we modeled phenotypic drug resistance as monotonically increasing along any escape pathway. Using this model, the individualized genetic barrier (IGB) to each drug is derived as the probability of the virus not acquiring additional mutations that confer resistance. Drug-specific IGBs were combined to obtain the IGB to an entire regimen, which quantifies the virus' genetic potential for developing drug resistance under combination therapy. The IGB was tested as a predictor of therapeutic outcome using between 2,185 and 2,631 treatment change episodes of subtype B infected patients from the Swiss HIV Cohort Study Database, a large observational cohort. Using logistic regression, significant univariate predictors included most of the 18 drugs and single-drug IGBs, the IGB to the entire regimen, the expert rules-based genotypic susceptibility score (GSS), several individual mutations, and the peak viral load before treatment change. In the multivariate analysis, the only genotype-derived variables that remained significantly associated with virological success were GSS and, with 10-fold stronger association, IGB to regimen. When predicting suppression of viral load below 400 cps/ml, IGB outperformed GSS and also improved GSS-containing predictors significantly, but the difference was not significant for suppression below 50 cps/ml. Thus, the IGB to regimen is a novel data-derived predictor of treatment outcome that has potential to improve the interpretation of genotypic drug resistance tests.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Anti-HIV Agents / therapeutic use*
  • Bayes Theorem
  • Cohort Studies
  • Drug Resistance, Viral
  • Female
  • HIV Infections / drug therapy*
  • HIV Infections / genetics*
  • HIV Infections / virology
  • HIV-1*
  • Humans
  • Logistic Models
  • Male
  • Middle Aged
  • Models, Biological*
  • Models, Genetic
  • Models, Statistical
  • Odds Ratio
  • ROC Curve
  • Treatment Outcome

Substances

  • Anti-HIV Agents

Grants and funding

This work was supported by the Swiss HIV Cohort Study [grant numbers 470, 528, 569, 629]; the Swiss HIV Cohort Study Research Foundation; the Swiss National Science Foundation [grant numbers 33CS30-134277, 3247B0-112594 to HFG and SY, 324730-130865 to HFG, CR32I2_127017 to NB and HFG]; the Collaborative HIV and Anti-HIV Drug Resistance Network [grant number 223131] of the European Community's Seventh Framework Programme [grant number FP7/2007–2013]; a research grant of the Union Bank of Switzerland, in the name of a donor to HFG; an unrestricted research grant from Gilead, Switzerland to the SHCS Research Foundation and by the University of Zurich's Clinical Research Priority Program (CRPP) “Viral infectious diseases: Zurich Primary HIV Infection Study” (to HFG). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.