Conclusions
The pathogenesis of the HIV-T. cruzi coinfection in astrocytes leads to an oxidative misbalance as a key mechanism, which exacerbates ROS generation and promotes positive feedback to parasite growth in the CNS.
Methods
We evaluated the interplay between both pathogens in human astrocytes and its consequences on the host cell pro-oxidant condition self-propitiated by the parasite - using its EVs - or by HIV infection. For this goal, we challenged cultured human primary astrocytes with both pathogens and the efficiency of infection and multiplication were measured by microscopy and flow cytometry and parasite DNA quantification. Mitochondrial and cellular ROS levels were measured by flow cytometry in the presence or not of scavengers with a concomitant evaluation of the cellular apoptosis level.
Results
We observed that increased mitochondrial and cellular ROS production boosted significantly T. cruzi infection and multiplication in astrocytes. Such oxidative condition was promoted by free trypomastigotes-derived EVs as well as by HIV infection. Conclusions: The pathogenesis of the HIV-T. cruzi coinfection in astrocytes leads to an oxidative misbalance as a key mechanism, which exacerbates ROS generation and promotes positive feedback to parasite growth in the CNS.