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Department of Biochemistry at Wake Forest University Graduate School of Arts and Sciences

Maryam Ahmed

Maryam AhmedResearch Assistant Professor, Biochemistry
B.A., University of Virginia, 1992
Ph.D. (Microbiology and Immunology), Wake Forest University School of Medicine, 1997

Telephone: (336) 716-2270
Fax: (336) 716-7671
E-mail: mahmed@wfubmc.edu

Determining the mechanisms by which viruses target and kill tumor cells is the central theme of my research. Several viruses are currently being developed as oncolytic agents to treat cancers. The challenge is to enhance the selectivity of these viruses for tumors, while minimizing disease. My work focuses on the prototype negative stranded RNA virus, vesicular stomatitis virus (VSV). The basis for the selectivity of anti-tumor therapies using VSV and other viruses appears to be due to the development of defects in anti-viral responses, such as the type I interferon (IFN) response, during tumorigenesis. However, our studies have shown that not all tumor cells are susceptible to infection and killing by VSV. Therefore, in order to assess the outcome of therapies using VSV, our goal is to determine the molecular pathways that lead to VSV sensitivity or resistance in specific cancers.

Immune responses initiated by dendritic cells (DC) are important for tumor immunosurveillance and destruction. However, the contribution of DC during anti-tumor therapies using VSV has not been elucidated. Using both cell culture and animal models, one of our main goals is to determine the role of DC during VSV pathogenesis and therapies, in order to develop viruses with enhanced selectivity for tumor cells.

Recent publications:

Ahmed, M., S. Cramer, and D. S. Lyles. 2004. Sensitivity of prostate tumors to wild-type and M protein mutant vesicular stomatitis viruses. Virology. 330(1): 34-49.

Ahmed, M., M. O. McKenzie, S. Puckett, M. Hojnacki, L. Poliquin, and D. S. Lyles. 2003. Ability of the matrix protein of vesicular stomatitis virus to suppress beta interferon gene expression is genetically correlated with the inhibition of host RNA and protein synthesis. J. Virology. 77(8): 4646-4657.

Ahmed, M, M. Lock, C. G. Miller, and N. W. Fraser. 2002. Regions of the Herpes Simplex Virus Type 1 Latency-Associated-Transcript (LAT) that Protect Cells from Apoptosis in vitro and Protect Neuronal Cells in vivo. J. Virology. 76(2): 717-729.

Ahmed, M., and N. W. Fraser. 2001. The Herpes Simplex Virus Type 1 2-kb LAT Intron Associates with Ribosomal Proteins and Splicing Factors. J. Virology. 75(24): 12070-12080.

Ahmed, M., and D.S. Lyles. 1998. Effect of Vesicular Stomatitis Virus Matrix Protein on Transcription Directed by Host RNA Polymerases I, II and III. J. Virology. 72: 8413-8419.

Ahmed, M., and D.S. Lyles. 1997. Identification of a Consensus Mutation in M Protein of Vesicular Stomatitis Virus from Persistently Infected Cells that Affects Inhibition of Host-Directed Gene Expression. Virology. 237: 378-3.

Lyles, D.S., M.O. McKenzie, M. Ahmed, and S.C. Woolwine. 1996. Potency of Wild-Type and Temperature Sensitive Vesicular Stomatitis Virus Matrix Protein in Inhibition of Host-Directed Gene Expression. Virology. 225: 172-180.