Mitochondria are sensors for HIV drugs.
Highly active anti-retroviral therapy (HAART) has drastically altered the course of HIV-1 infection, resulting in a major decrease in morbidity and mortality. However, adverse drug reactions and long-term toxicities associated with HAART are now a concern. A major toxicity that has been highlighted by the increased use of HAART is related to mitochondrial side-effects. At the same time, analysis of the biochemical pathways involved in programmed cell death has revealed that mitochondria are main sensors in this process. In this article, the regulation of mitochondrial damage following the use of nucleoside analogue reverse transcriptase inhibitors (NRTIs) and protease inhibitors is discussed, with a particular focus on the putative molecular mechanisms involved.
Petit
Frédéric
F
Unité de Physiopathologie des Infections Lentivirales, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris cedex 15, France.
Fromenty
Bernard
B
Owen
Andrew
A
Estaquier
Jérôme
J
D019380:Anti-HIV Agents / Q000009:adverse effects* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D015658:HIV Infections / Q000188:drug therapy*; D015497:HIV-1 / Q000187:drug effects*; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000502:physiology
D019380:Anti-HIV Agents