Possible mechanisms of HIV neuro-infection in alcohol use: Interplay of oxidative stress, inflammation, and energy interruption.
Review
Overview
abstract
Alcohol use and HIV-1 infection have a pervasive impact on brain function, which extends to the requirement, distribution, and utilization of energy within the central nervous system. This effect on neuroenergetics may explain, in part, the exacerbation of HIV-1 disease under the influence of alcohol, particularly the persistence of HIV-associated neurological complications. The objective of this review article is to highlight the possible mechanisms of HIV/AIDS progression in alcohol users from the perspective of oxidative stress, neuroinflammation, and interruption of energy metabolism. These include the hallmark of sustained immune cell activation and high metabolic energy demand by HIV-1-infected cells in the central nervous system, with at-risk alcohol use. Here, we discussed the point that the increase in energy supply requirement by HIV-1-infected neuroimmune cells as well as the deterrence of nutrient uptake across the blood-brain barrier significantly depletes the energy source and neuro-environment homeostasis in the CNS. We also described the mechanistic idea that comorbidity of HIV-1 infection and alcohol use can cause a metabolic shift and redistribution of energy usage toward HIV-1-infected neuroimmune cells, as shown in neuropathological evidence. Under such an imbalanced neuro-environment, meaningless energy waste is expected in infected cells, along with unnecessary malnutrition in non-infected neuronal cells, which is likely to accelerate HIV neuro-infection progression in alcohol use. Thus, it will be important to consider the factor of nutrients/energy imbalance in formulating treatment strategies to help impede the progression of HIV-1 disease and associated neurological disorders in alcohol use.
