HIV associated
neurocognitive disorders (HAND) is a unique form of neurological impairment that stems from HIV. This disease and its characteristics can be accredited to incorporation of
DNA and
mRNA of HIV-1 into the CNS. A proper understanding of the intricacies of HAND and the underlying mechanisms associated with corresponding immune reactions are vital for the potential development of a reliable treatment for HAND. A common phenomenon observed in CNS cells, specifically microglia, that are infected with HAND is
inflammation, which is a consequence of the activation of innate immune response due to a variety of stimuli, in this case, being the
HIV infection. The CNS based
inflammation is mediated by the production of
cytokines,
chemokines,
reactive oxygen species, and secondary messengers, which occurs at CNS glia, endothelial cells and peripherally derived immune cells.
Inflammasomes play a significant role with regard to
neuroinflammation due to their ability to dictate the activation of various inflammatory responses. Certain stimuli can result in the activation of
caspase-1; hence, leading to the processing of interleukin-1β and
interleukin-18 pro-inflammatory
cytokines. The processed IL-1β and
IL-18 activate signaling pathways that begin the process of
neuroinflammation. Due to the fact that the NLRP3
inflammasome is the most abundant in the CNS, it is the most extensively investigated
inflammasome with regard to the nervous system. Due to the importance of
neuroinflammation in the evolution of HAND and proliferation of
neuroinflammation due to HAND, it can be concluded that there exists a relationship between HAND and
inflammasomes. The aim of our review is to consolidate current knowledge of important mechanisms in HAND, specifically related to its relationship with
neuroinflammation and
inflammasomes to shed light on a possible improved treatment for HAND.