Open AccessChanges in Mitochondrial DNA in Peripheral Blood Mononuclear Cells from HIV‐Infected Patients with Lipoatrophy Randomized to Receive Abacavir
Author(s) -
Jennifer Hoy,
Michelle E. Gahan,
Andrew Carr,
Don Smith,
Sharon R. Lewin,
Steve Wesselingh,
David A. Cooper
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/422602
Subject(s) - abacavir , lipoatrophy , peripheral blood mononuclear cell , mitochondrial dna , stavudine , mitochondrial toxicity , medicine , virology , mitochondrial disease , biology , immunology , pharmacology , viral disease , human immunodeficiency virus (hiv) , viral load , zidovudine , genetics , in vitro , antiretroviral therapy , gene
It has been suggested that lipoatrophy associated with exposure to nucleoside analogues is caused by depletion of mitochondrial DNA (mtDNA). The aim of the present study was to determine whether switching treatment from a thymidine analogue to abacavir was associated with an increase in the mtDNA copy number in peripheral blood mononuclear cells (PBMCs). Of 111 patients with lipoatrophy who were randomized to have treatment switched to abacavir or to continue treatment with thymidine analogues, 94 patients had PBMCs obtained at baseline and at weeks 4, 12, and 24, for quantification of the mtDNA copy number. During the 24-week study, there was no significant change in mtDNA copy numbers in PBMCs in either treatment group, despite improvement in peripheral lipoatrophy among patients whose treatment was switched to abacavir.
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