WELCOME TO THE EUGENINLAB

HIV infection of the central nervous system (CNS) can result in neurologic dysfunction with devastating consequences in a significant number of individuals with AIDS. The major CNS complications in individuals with HIV are encephalitis, dementia, and/or cognitive impairment that are characterized by leukocyte infiltration into the CNS, microglia activation, aberrant chemokine expression, blood-brain barrier (BBB) disruption, and eventual damage and/or loss of neurons. As the HIV-infected population lives longer, an understanding of the impact of the virus on chronic disease processes such as NeuroAIDS becomes increasingly relevant. NeuroAIDS has been associated with the presence of elevated CNS inflammatory factors, such as cytokines, PAF, excitatory aminoacids (especially glutamate) and their receptors, soluble viral proteins, and chemokines, as determined in post-mortem examination of tissue. These observations in vivo have been correlated with in vitro findings that support the participation of these factors as mediators of neurodegeneration. The mechanism that triggers these abnormalities are not always associated with high viral replication but rather with inflammation. To study the development of NeuroAIDS we examine two different, but interrelated, potential mechanisms of pathogenesis.
Our focus is to examine the role of HIV infection of astrocytes in the pathogenesis of NeuroAIDS as well as in immune cells, macrophages and T cells, with special emphasis in the role of gap junction channels, hemichannels of pannexins and connexin, ATP receptors and a new system of communication named TNT. We examined how these systems amplify inflammation and toxicity and how these communication systems are altered by HIV infection in vitro and in vivo. 
These studies are essential to understand the mechanism by which HIV remains in the brain, as a reservoir of the virus, and to explore the question of how HIV changes the phenotype of HIV-infected cells to its advantage. Experimental approach: We use cellular and molecular biological techniques to study the expression, post-transcriptional modifications, and intercellular trafficking of neurotransmitters and their receptors, chemokines/cytokines as well as electrophysiology. Our approach involves the use of primary immune and CNS cells and tissues and samples obtained from individuals with NeuroAIDS.