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HIV type 1 DNA development during long-term supervised therapy interruption

Lars E Eriksson1, Kerstin I Falk, Göran A Bratt

  • 1Department of Virology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden. Lars.Eriksson@omv.ki.se

AIDS Research and Human Retroviruses
|June 14, 2003
PubMed

Insights

Human immunodeficiency virus type 1 (HIV-1) DNA increases after stopping long-term supervised therapy interruption (LT-STI). Rapid CD4(+) cell decline before treatment predicts therapy interruption failure.

Area of Science:

  • Virology
  • Immunology
  • Antiretroviral Therapy

Background:

  • Long-term supervised therapy interruption (LT-STI) is a strategy explored in managing HIV-1 infection.
  • Effective protease inhibitor-based antiretroviral therapy (PI-ART) suppresses HIV-1 RNA to <50 copies/ml.
  • Understanding HIV-1 DNA dynamics during LT-STI is crucial for treatment strategies.

Purpose of the Study:

  • To investigate the pattern of HIV-1 DNA changes during LT-STI.
  • To identify associations between HIV-1 DNA development and other HIV-related factors.
  • To determine predictors of LT-STI success or failure.

Main Methods:

  • Quantification of HIV-1 DNA in CD4(+) cells using real-time polymerase chain reaction.
  • Simultaneous amplification of HIV-1 pol gene and human albumin gene.
  • Analysis of HIV-1 RNA levels, CD4(+) cell counts, and HIV-1 DNA values.

Main Results:

  • HIV-1 DNA in CD4(+) cells increased in all patients during LT-STI, with an average doubling time of 2 months.
  • Observed patterns included rapid initial increase, rapid continuous increase, and slow increase.
  • HIV-1 DNA slope correlated positively with HIV-1 RNA levels and baseline HIV-1 DNA, and inversely with CD4(+) cell decline.

Conclusions:

  • HIV-1 DNA persists in CD4(+) cells despite long-term PI-ART and increases after therapy interruption.
  • Rapid CD4(+) cell decline before PI-ART is a significant predictor of LT-STI failure.
  • Continuing treatment may be advisable for patients with a steep pre-PI-ART CD4(+) cell decline.

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