role of mitochondria in hiv infection and associated metabolic disorders: focus on nonalcoholic fatty liver disease and lipodystrophy syndrome

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ID: 190107
2013
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Abstract
Highly active antiretroviral therapy (HAART) has considerably improved the prognosis of HIV-infected patients. However, prolonged use of HAART has been related to long-term adverse events that can compromise patient health such as HIV-associated lipodystrophy syndrome (HALS) and nonalcoholic fatty liver disease (NAFLD). There is consistent evidence for a central role of mitochondrial dysfunction in these pathologies. Nucleotide reverse transcriptase inhibitors (NRTIs) have been described to be mainly responsible for mitochondrial dysfunction in adipose tissue and liver although nonnucleoside transcriptase inhibitors (NNRTIs) or protease inhibitors (PIs) have also showed mitochondrial toxicity, which is a major concern for the selection and the long-term adherence to a particular therapy. Several mechanisms explain these deleterious effects of HAART on mitochondria, and evidence points to other mechanisms beyond the “Pol-γ hypothesis.” HIV infection has also direct effects on mitochondria. In addition to the negative effects described for HIV itself and/or HAART on mitochondria, HIV-infected patients are more prone to develop a premature aging and, therefore, to present an increased oxidative state that could lead to the development of these metabolic disturbances observed in HIV-infected patients.
Reference Key
prez-matute2013oxidativerole Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;P. Pérez-Matute;L. Pérez-Martínez;J. R. Blanco;J. A. Oteo
Journal journal of aoac international
Year 2013
DOI
10.1155/2013/493413
URL
http://dx.doi.org/10.1155/2013/493413
Keywords
cytology

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