Even in the HAART era where the viral load is below detection levels, the prevalence of HIV-1 associated neurocognitive disorders (HAND) remains high due to many reasons, such as latent virus reactivation and drugs' inability to efficiently cross the blood brain barrier (BBB). Therefore, it is important to understand the mechanisms leading to neuronal deregulation in HIV-1-infected patients in the HAART era. The lack of productive infection of neurons by HIV-1 suggests that viral and cellular proteins with neurotoxic activities that are released from HIV-1 infected target cells, or reservoirs cells for latent active virus, cause this neuronal deregulation. The viral proteins Tat, Vpr and gp120 have been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells. The mechanisms and the cellular factors used by these proteins to cause neuronal damage remain unclear. Therefore, research in the Molecular Studies of Neurodegenerative Diseases (MSND) Lab mainly focuses on the identification of these mechanisms, utilizing molecular, virological and cellular approaches to determine the cellular factors used by the viral proteins, as well as their interplay with microRNAs to cause neuronal dysfunction.

The outcome of these studies will advance the understanding of HIV-1 pathogenesis and will decipher the mechanisms used by HIV-1 Tat, Vpr and gp120 proteins that lead to neuronal degeneration.