On June 5, 2020, George Mason University in Virginia, announced that two of its scientists--Fatah Kashanchi, PhD, Director, Laboratory of Molecular Virology, School of Systems Biology, and Lance Liotta, MD, PhD, Co-Director and Co-Founder, Center for Applied Proteomics and Molecular Medicine--are working to mitigate virally driven HIV pathogenesis in the central nervous system (CNS). Preliminary data the researchers have gathered suggests that cannabinoids—specifically, cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC)--may be effective in reducing HIV-1 transcription of both short, non-coding RNA such as trans-activating response (TAR) RNA, and full-length genomic RNA, thereby resulting in decreased production of virus. The researchers have also found that the reduction in transcription results in a decreased incorporation of HIV-1 RNA into extracellular vesicles (EVs)/exosomes released from infected cells. This has been previously shown to contribute to dysfunction in recipient cells, including activation of the NF-kB pathway, a protein complex that controls transcription of DNA, cytokine production, and cell survival through toll-like receptor 3 (TLR3), and to increased susceptibility to infection. TLR3 is a member of the toll-like receptor family of pattern-recognition receptors of the innate immune system. The researchers hypothesize that cannabinoid treatment may affect host cell pathways, including autophagy and the endosomal sorting complexes required for transport (ESCRT) pathways, to alter EV/exosome release which can potentially mitigate EV/exosome-related dysfunction during viral infection of the CNS. The researchers have two aims for their work. First, they intend to define the mechanisms of cannabinoid-mediated decreased EV/exosome production and release in HIV-1 infected cells.Login Or Register To Read Full Story