Virus-induced changes in peroxisomal markers among HIV-infected patients

Relevance. It is been currently known that viruses rewire the metabolic machinery host’s cell to promote successful viral replication via reprogramming host energy flows, resource, metabolic tools and further, the reorganization of cellular structures. Recent studies indicate that the human immunodeficiency virus significantly reduces the number of peroxisomes in infected cells. However, there is still no clear understanding of the reasons for this apparent HIV intervention. The aim of the study was to confirm the hypothesis about the causes of the decrease in the number of peroxisomes in HIV infection. In this study, changes in several hematological markers of peroxisomal metabolism were assessed in connection with data on the unique role of these organelles in the catabolism of the amino acid L-lysine, the level of which correlates with the level of viral RNA in the blood plasma of HIV-infected individuals. Materials and Methods. A study was conducted on the levels of total cholesterol, catalase, L-lysine, and its derivative L-carnitine among HIV-infected individuals (controllers and patients with rapidly progressive disease) in comparison with similar indicators in cohorts of HIV-infected patients and healthy individuals. Results and Discussion. The study confirms the presence of significant differences in plasma levels of markers associated with peroxisomal metabolism, such as catalase, cholesterol, and the amino acid L-lysine, in the compared groups of HIV controllers and patients with rapidly progressing disease. The most negative changes in peroxisomal markers were detected among patients with accelerated HIV disease progression and, to a lesser extent, in individuals from the overall cohort. Conclusion. The results of this study indicate that HIV interference with host peroxisome biogenesis is accompanied by a concomitant dysregulation of peroxisomal enzyme systems and L-lysine-related substrates. Virus-induced reprogramming of the catabolism of this essential amino acid indirectly confirms the hypothesis of a key role of L-lysine in the HIV life cycle and is a factor in the successful implementation of the reproductive strategy of the human immunodeficiency virus.