 Microbiology and Immunology Graduate Program
B.S., Pharmacology and Toxicology from the University of the Sciences in Philadelphia
Email: liudmila.mazaleuskaya@drexel.edu
Advisor: Sonia Navas-Martin, Ph.D.
Thesis Research Summary:
I received a Bachelor of Science in pharmacology and toxicology from the University of the Sciences in Philadelphia (USP). While attending USP, I spent two years in the lab of Dr. Diane Morel researching on the role of oxidative stress in the development of chronic diseases, such as ischemic heart disease and age-related macular degeneration. Using cell culture models, I assessed the degree of oxidative stress upon exposure to various oxidizing agents and the potential antioxidant capacity of carotenoids. Throughout this time, I gained valuable experience in laboratory techniques and developed a passion for biomedical research.
I came to Drexel to get a graduate degree in pharmacology and physiology with an interest in drug discovery and development. I began thesis research in the Department of Microbiology and Immunology in the laboratory of Dr. Sonia Navas-Martin. Currently, my thesis work is focused on understanding the role of Toll-Like Receptors in the mouse model of viral-induced CNS disease. In particular, I work with murine CoVs, collectively called Mouse Hepatitis Virus (MHV), that provide models of acute and chronic viral infection of the central nervous system. Highly neurovirulent MHV-JHM and mildly virulent MHV-A59 are used to study virus-induced lethal encephalitis and chronic demyelination, respectively. MHV-induced demyelination is associated with infiltrating macrophages and resident microglia in the CNS white matter. However, specific contribution of these cell types to demyelination and encephalitis is still poorly understood.
My research efforts aim at understanding if MHVs induce inflammation through the activation of macrophage/microglia Toll-Like Receptors (TLRs), germline-encoded receptors sensing viral nucleic acids and structural proteins among other microbial components. TLR2 and TLR4 may detect viral glycoproteins, while TLR3 and TLR7 sense viral dsRNA and ssRNA, respectively. Using in vitro and in vivo models, molecular biology techniques and pharmacological tools, I intend to determine if TLRs activate the antiviral defense mechanism or contribute to CoV pathogenesis. I have also developed a strong interest in TLR ligand pharmacology and structure-activity relationship of TLR agonists, and hope to continue research on TLRs in my future career. |