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JAC Advance Access originally published online on March 28, 2003
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Journal of Antimicrobial Chemotherapy (2003) 51, 1091-1093
© 2003 The British Society for Antimicrobial Chemotherapy

Leading Article

Nucleoside analogues and HIV: the combined cost to mitochondria

Catherine L. Cherry1,3,* and Steven L. Wesselingh1,3

1 Department of Medicine, Monash University, Melbourne; 2 Infectious Diseases Unit, The Alfred Hospital, Melbourne; 3 Burnet Institute for Medical Research and Public Health, Melbourne, Australia

Keywords: nucleoside analogue, mitochondria, HIV

The first 150 words of the full text of this article appear below.

Highly active antiretroviral therapy (HAART) has revolutionized human immunodeficiency virus (HIV) care in the developed world. Since the introduction of HAART the morbidity and mortality associated with HIV infection have decreased dramatically,1 but this benefit has been associated with the emergence of a diverse range of antiretroviral toxicities.

Nucleoside reverse transcriptase inhibitors (NRTIs) are central to effective HAART, with current antiretroviral guidelines recommending the inclusion of at least two of these agents in each regimen. However, NRTIs also contribute significantly to the toxicities of HAART. Here we review the known mechanism of action of NRTIs, the proposed mechanism by which they may cause toxicities through mitochondrial damage, the evidence that HIV infection may predispose individuals to overt mitochondrial dysfunction, and potential future methods of monitoring and preventing these problems.

Nucleoside analogues act as alternative substrates for DNA polymerases. Because NRTIs lack a hydroxyl group in the 3'-position (required for the . . . [Full Text of this Article]


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