Abstract
Background: There may be a possible link between the use of HAART and oxidative
stress-related mitochondrial dysfunction in HIV patients. We evaluated the mitochondrial and
oxidative impacts of short and long-term administration of HAART on HIV patients attending the
Enugu State University Teaching (ESUT) Hospital, Enugu, Nigeria following short and long-term
therapy.
Methods: 96 patients categorized into four groups of 24 individuals were recruited for the study.
Group 1 comprised of 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 of 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 the 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, TRNALEU
uur) in the long-term treatment group.
Conclusion: Long-term treatment with HAART increases oxidative stress and causes mitochondrial
alterations in HIV patients.
Keywords:
HIV/AIDS, HAART, mitochondrial dysfunction, oxidative stress, biochemical alterations, necrosis.
Graphical Abstract
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