Joy E. Ikekpeazu, Oliver C. Orji, Ikenna K. Uchendu* and Lawrence U.S. Ezeanyika Pages 1-14 (14)
Methods: 96 patients categorized into four groups of 24 individuals were recruited for the study. Group 1 comprised age-matched, apparently healthy, sero-negative individuals (the No HIV group); group 2 consisted of HIV sero-positive individuals who had not started any form of treatment (the Treatment naïve group). Individuals in group 3 were known HIV patients on HAART for less than one year (Short-term treatment group), while group 4 comprised HIV patients on HAART for more than one year (Long-term treatment group). All patients were aged between 18 to 60 years and attended the HIV clinic at the time of the study. Determination of total antioxidant status (TAS in nmol/l), malondialdehyde (MDA in mmol/l), CD4+ count in cells/μl, and genomic studies were all done using standard operative procedures.
Results: We found that the long-term treatment group had significantly raised levels of MDA, as well as significantly diminished TAS compared to the Short-term treatment and No HIV groups (P<0.05). In addition, there was significantly elevated variation in the copy number of mitochondrial genes (mtDNA: D-loop, ATPase 8, TRNALEUuur) in long-term treatment group.
Interpretation and Conclusion: Long-term treatment with HAART increases oxidative stress and causes mitochondrial alterations in HIV patients.
HIV/AIDS, HAART, Mitochondrial dysfunction, Oxidative Stress, Biochemical alterations
Department of Medical Biochemistry, University of Nigeria Enugu Campus, Department of Medical Laboratory Science, Faculty of Health Science and Technology, College of Medicine, University of Nigeria Enugu Campus, Enugu State, Department of Medical Laboratory Science, Faculty of Health Science and Technology, College of Medicine, University of Nigeria Enugu Campus, Enugu State, Department of Biochemistry, University of Nigeria