AIDSWEEKLY Plus; Monday, January 14, 2008
Staff Medical Writers

NewsRx -- New research, 'Impact of nucleoside reverse transcriptase inhibitors on mitochondria in human immunodeficiency virus type 1-infected children receiving highly active antiretroviral therapy,' is the subject of a report (see also HIV/AIDS). According to recent research from the United States, "Mitochondrial toxicity induced by nucleoside reverse transcriptase inhibitors (NRTIs) has been reported to be responsible for various adverse effects. The relative impact of NRTIs on the mitochondria of human immunodeficiency virus (HIV) type 1 (HIV-1)-infected children receiving highly active antiretroviral therapy (HAART) is unknown."

"Mitochondrial DNA (mtDNA) levels were quantified longitudinally from peripheral blood mononuclear cells (PBMCs) in 31 HIV-1-infected children from Pediatric AIDS Clinical Trial Group Study 382 who were receiving HAART, including nelfinavir, efavirenz, and different NRTIs, and who had had undetectable plasma HIV-1 RNA levels for >2 years. The median mtDNA levels in PBMCs increased from 137 copies/cell at the baseline to 179 copies/cell at week 48 (p=0.01) and 198 copies/cell at week 104 (p <0.001). Before the initiation of HAART, children who received regimens containing didanosine had mtDNA levels persistently lower than those in children not receiving didanosine (106 versus 140 copies/cell; p=0.008). During HAART, the median increase in the mtDNA level from the baseline to week 104 was the lowest in children who received regimens containing didanosine (+26 copies/cell) compared to those in children who received other regimens (+79 copies/cell) (p=0.02). A multivariate analysis also demonstrated that didanosine, as part of HAART, was the only NRTI associated with the change in mtDNA levels (p=0.007). Children receiving didanosine-containing antiretroviral regimens have the lowest mtDNA levels in PBMCs and may be at greater risk for long-term adverse effects due to mitochondrial toxicity," wrote A. Saitoh and colleagues, University of California, Department of Pediatrics.

The researchers concluded: "This may be of particular importance in resource-limited countries where didanosine is widely used for the treatment of HIV-infected children."

Saitoh and colleagues published their study in Antimicrobial Agents and Chemotherapy (Impact of nucleoside reverse transcriptase inhibitors on mitochondria in human immunodeficiency virus type 1-infected children receiving highly active antiretroviral therapy. Antimicrob Agents Chemother. 2007 Dec;51(12):4236-42.

For additional information, contact A. Saitoh, University of California, University of California, Dept. of Pediatrics, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0672 USA..

Publisher contact information for the journal Antimicrobial Agents and Chemotherapy is: American Society Microbiology, 1752 N St. NW, Washington, DC 20036-2904, USA.

Keywords: United States, La Jolla, HIV/AIDS, AIDS, Acquired Immune Deficiency Syndrome, Acquired Immunodeficiency Syndrome, Anti-Infectives, Antimicrobials, Antivirals, Chemotherapy, Clinical Trial Research, DNA, Drug Therapy, Drugs, Efavirenz, Enzyme Research, Enzymes, Enzymology, HAART, HIV, Human Immunodeficiency Virus, Immunology, Nelfinavir, Nucleoside Reverse Transcriptase Inhibitor, Pediatric, Pharmaceuticals, Proteins, Proteomics, Sexually Transmitted Disease, Therapy, Treatment, Viral, Virology.

This article was prepared by AIDS Weekly editors from staff and other reports.

2008-01-14
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