Wail Hassan, Ph.D., M(ASCP)CM
Enderis Hall, Room 469
Phone: (414) 229-3124
Fax: (414) 229-2619
- Ph.D., Department of Biological Sciences, The University of Southern Mississippi, 2004
- Diploma, Parasitology and Medical Entomology, High Institute of Public Health, Alexandria University, Egypt, 1993
- B.S., Microbiology, Faculty of Science, Alexandria University, Egypt, 1990
- Alzheimer’s Disease
Interests & Expertise
HIV-1 pathogenesis: Human immunodeficiency virus type one (HIV-1) infection is generally a fatal disease. Most infected individuals develop acquired immunodeficiency syndrome (AIDS) after an average of 10 years if left untreated. Some, however, control the virus to low, or even undetectable, levels and may survive for more than 20 years without developing AIDS. Multiple criteria are known to influence disease progression in HIV-1 disease and many of these criteria are established early during acute infection. Dr. Hassan’s goal is to understand the underlying mechanisms of the early events that take place during acute HIV-1 infection, which seem to impact both the severity of the disease during the chronic phase and the timing of disease progression. Better understanding of these events is needed to define the initial insults exerted by the virus against the immune system, define the mechanisms leading to the initial failures of the immune system, and define correlates of protection that can be used as prognostic and vaccine development tools.
Alzheimer’s disease: Multiple neurodegenerative diseases, including Alzheimer’s disease (AD), are linked to alterations in proteostasis of aggregation-prone proteins. Beta amyloid (AB) is a hallmark of AD pathogenesis. Cellular mechanisms involving AB homeostasis may be key defense mechanisms against AB toxicity. His group has identified a proteasomal regulatory protein, AIP-1, that alleviates proteotoxicity resulting from expressing human AB in a transgenic Caenorhabditis elegans model of AD. Dr. Hassan is currently testing the involvement of AIP-1 homologues in mammalian systems (AIRAP and AIRAPL) in AB homeostasis.
Hassan, W. M., Merin, D. A., Fonte, V., & Link, C. D. (2009). AIP-1 ameliorates β-amyloid peptide toxicity in a Caenorhabditis elegans Alzheimer’s disease model. Human Molecular Genetics, 18(15), 2739-2747.
Eberly, M., Kader, M., Hassan, W., Rogers, K. A., Zhou, J., Mueller, Y., Mattapallil, M., Piatak Jr., M., Lifson, J. D., Katsikis, P. D., Roederer, M., Villinger, F., & Mattapallil, J. J. (2009). IL-15 induced upregulation of CD4 is the primary cause for increased permissibility to SIV during acute infection. Journal of Immunology, 182(3), 1439-1448.
Kader, M., Hassan, W. M., Eberly, M., Piatak, M., Lifson, J. D., Roederer, M., & Mattapallil, J. J. (2008). Anti-retroviral therapy prior to acute viral replication preserves CD4 T cells in the periphery but not in rectal mucosa during acute simian immunodeficiency virus infection. Journal of Virology, 82(22), 11467-11471.
Hassan, W. M., Ellender, R. D., & Wang, S. Y. (2007). Fidelity of bacterial source tracking: Escherichia coli vs Enterococcus spp and minimizing assignment of isolates from non-library sources. Journal of Applied Microbiology, 102, 591-598.