NEW YORK (Reuters Health) – It has been hypothesized that antiretroviral-induced mitochondrial toxicity may be the first step leading to lipodystrophy in HIV-infected patients. However, a new report suggests that the mitochondria of HIV-infected children with lipodystrophy function normally and are not prone to apoptosis.
Dr. Andrea Cossarizza, from the University of Modena and Reggio Emilia School of Medicine in Modena, Italy, and colleagues compared the peripheral blood lymphocyte mitochondria of HIV-infected children with or without lipodystrophy to those of healthy children. All of the HIV-infected children were receiving highly active antiretroviral therapy (HAART).
The investigators used flow cytometry to determine mitochondrial membrane potential, mitochondrial mass, intra-mitochondrial cardiolipin distribution, and apoptosis in fresh and cultured lymphocytes. The mitochondrial DNA content in fresh lymphocytes was also determined.
The mitochondria of all three groups were found to be similar in functionality and in their apoptosis potential, the researchers state in the February 1st issue of The Journal of Infectious Diseases. Furthermore, the lymphocytes of HIV-infected children with lipodystrophy had similar amounts of mitochondrial DNA as those of healthy children.
While "drug- or virus-induced mitochondrial damages in the pathogenesis of lipodystrophy have been hypothesized, there is a substantial lack of direct analysis of the functionality of these organelles," the authors note. "Our data seem to exclude the presence of HAART-induced mitochondrial damage in lymphocytes from children with lipodystrophy."