Nazira El-Hage, Ph.D.
Ph.D. University of Kentucky
M.S. University of Kentucky
B.S. University of Kentucky
I became a scientist because I always asked the question “why” and because of my desire to make an intellectual and practical contribution to the world. After I received my Master’s degree in Biological Sciences, I got a job as a laboratory technician in the Department of Microbiology and Immunology, at the University of Kentucky. I worked with the bacterium Legionella pneumophila which is responsible for most cases of Legionnaires' disease. I became very interested in learning more about infectious diseases, and decided to continue my education and earned my Ph.D. degree in Microbiology and Immunology at the University of Kentucky. My research project was on the spirochete Borrelia burgdorferi, a tick-borne obligate parasite that causes Lyme disease in humans. After completion of my degree I took a job in academia, as a post-doctoral scholar in the Department of Virology. I was interested in a career as a virologist, because I wanted to work with viruses that have no cure or vaccine against them. Human Immunodeficiency Virus and to some extend Hepatitis C Virus, are two viruses that fit into that category.
For the past 11 years, my research interest has focused on identifying the underlying mechanisms by which Human Immunodeficiency Virus (HIV) and drug abuse or drug pharmacotherapy causes toxicity and injury in the central nervous system (CNS), leading to neurological dysfunction and NeuroAIDS. In addition, my laboratory focuses on the interactive effects of HIV-1 and Hepatitis C Virus (HCV) co-infection on the host immune response and cell function, as nearly 40 % of HIV-1 infected subjects suffers comorbidity with HCV infection. The central nervous system (CNS) is preferentially vulnerable to HIV infection as chronic exposure to HIV in the brain can lead to neurocognitive impairment (NCI). HIV/AIDS and opiate drug abuse are interlinked epidemics among injection drug users, and morphine, the main bioactive product of heroin in the brain, can increase HIV replication, as well as neuronal toxicity in the presence of HIV infection. Autophagy is a key process involved in proper cellular maintenance and its disruption has been implicated as a contributing factor in neurodegenerative diseases. However, whether alterations of autophagy may be a contributing factor in these interactive effects is largely unknown in HIV disease. My lab is involved in studying for the first time (i) the role of the autophagy pathway in the pathogenesis of HIV-1 in microglial cells and determines whether opiates converge at this point, and (ii) the role of autophagy in the pathogenesis of HIV-neurodegenerative disorder in the context of opioid abuse. My lab also studies the role of autophagy among the different HIV clades (B/C) in context of drug of abuse. The existence of multiple subtypes of HIV worldwide has created new challenges to control HIV infection and associated neuropathogenesis. Both HIV clade C (HIV-C) and HIV clade B (HIV-B) can cause cognitive impairment, with studies indicating clade B being more neuropathogenic than clade C. However, the exact mechanism underlying the differences in the neuropathogenesis by both the subtypes remains elusive. My lab is investigating (i) the effect of opiates on the neuropathogenesis among the different clades, and (ii) the role of the autophagy pathway as a mechanism regulating the divergence in the neuropathogenesis of HIV clade B/C. We are also developing an on-demand controlled released nano-formulation using state- of -the art magneto-electro nanoparticles (MENPs) and biodegradable liposome encapsulation for efficient drug delivery across the blood brain barrier that would target HIV-1 latency in drug abusing individuals.