Alcohol use is known to exacerbate the progression of human immunodeficiency virus associated acquired immunodeficiency syndrome or HIV/AIDS in the brain, known as the NeuroAIDS. The mechanisms of this accelerated progression are still poorly understood. The purpose of my thesis is to review the parameters contributing to the co-morbid effects of alcohol in the progression of NeuroAIDS. The first aim will evaluate the exacerbating effects of alcohol on HIV-1 transmission, infection, and the role of metabolic energy imbalance during NeuroAIDS progression, which will enable me to formulate the possible mechanism for NeuroAIDS progression. The second aim will help me establish the technique of rat embryonic neuronal isolation, which will be used for testing the neurotoxicity of HIV proteins (Tat, gp120) in the setting of interactive neuroimmune cell culture (brain endothelial cells, astrocytes, microglia, and neurons) with or without the presence of alcohol. The synergistic effect of alcohol on HIV associated neurotoxicity will pave the future research path to examine the unique mechanism for HIV/AIDS progression and a possible cure for HIV/AIDS with active antiretroviral drug(s)
