The cellular pharmacology of nucleoside- and nucleotide-analogue reverse-transcriptase inhibitors and its relationship to clinical toxicities

Clin Infect Dis. 2004 Mar 1;38(5):743-53. doi: 10.1086/381678. Epub 2004 Feb 18.

Abstract

Nucleoside- and nucleotide-analogue reverse-transcriptase inhibitors (NRTIs) require intracellular phosphorylation for anti-human immunodeficiency virus (HIV) activity and toxicity. Long-term toxicities associated with NRTIs may be related to overactivation of this process. In vitro experiments have shown increased rates of NRTI and endogenous nucleoside phosphorylation to be associated with cellular activation. Patients with advanced HIV disease often have overexpression of cytokines, which corresponds to an elevated cellular activation state. These patients also have higher rates of NRTI phosphorylation and NRTI toxicity, suggesting an interaction between a proinflammatory biological state, NRTI phosphorylation, and toxicity. Studies suggest that women may have higher rates of NRTI phosphorylation than do men, as well as increased risk for NRTI-induced toxicity. Future research is needed to understand the NRTI activation process and improve the long-term toxicity profile of NRTIs. Such research should include comparisons of NRTI phosphorylation according to sex and cellular activation state (i.e., elevated vs. low).

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Antiviral Agents / pharmacology
  • Female
  • HIV Infections / metabolism*
  • HIV Reverse Transcriptase / antagonists & inhibitors*
  • Humans
  • Male
  • Nucleosides / adverse effects
  • Nucleosides / blood
  • Nucleosides / metabolism
  • Nucleosides / pharmacology
  • Phosphorylation
  • Reverse Transcriptase Inhibitors / adverse effects
  • Reverse Transcriptase Inhibitors / blood
  • Reverse Transcriptase Inhibitors / metabolism
  • Reverse Transcriptase Inhibitors / pharmacology*

Substances

  • Antiviral Agents
  • Nucleosides
  • Reverse Transcriptase Inhibitors
  • HIV Reverse Transcriptase