Dr. Maryam Ahmed

Education:

  • Ph.D. Wake Forest University School of Medicine, Winston-Salem, NC
  • B.A. University of Virginia, Charlottesville, VA

Professional Experience:

  • Research Assistant Professor: Department of Biochemistry; Wake Forest University School of Medicine, Winston-Salem, NC
  • Post-doctoral: Department of Microbiology and Immunology; University of Pennsylvania School of Medicine, Philadelphia, PA

Areas of Interest:

  • Virus-host interactions
  • Viral pathogenesis
  • Immune responses to virus infections
  • Development of oncolytic viruses
  • Cancer therapies

Research:

Studying the response of different cells to virus infections is critical in understanding viral pathogenesis and developing virus-based therapeutics. My research focuses on the mechanisms by which specific cells, such as cancer cells and immune cells, respond to a prototype negative strand RNA virus, vesicular stomatitis virus (VSV).

VSV is currently being developed as an oncolytic agent due to its ability to potently kill a variety of cancer cells. However, the success of VSV-based cancer therapies is determined by several factors including the permissiveness of cancer cells to virus infection, the ability of the virus to spread through tumor tissues, and the ability of the host immune response to promote anti-tumor responses. We are interested in determining the potential of VSV as an anti-tumor agent for the treatment of highly aggressive tumors by investigating these factors in cell culture models and in small animal models of breast and prostate cancers. Furthermore, we are currently developing combination therapeutic strategies that may serve to promote tumor cell killing by VSV and enhance anti-tumor immune responses.

Selected Publications:

1. Ahmed, M., S. Puckett, S. Arimilli, S. Mizel, G. Parks, and D.S. Lyles. 2010. Stimulation of human dendritic cells by VSV vectors engineered to express flagellin. J. Virology. 84(22): 12093-8.
2. Ahmed, M., S. Puckett, and D.S. Lyles. 2010. Breast cancer therapies with an oncolytic matrix protein mutant of vesicular stomatitis virus. Cancer Gene Therapy.17(12):883-92.
3. Ahmed, M., K. L. Brzoza-Lewis, S. Puckett, L. M. Mitchell, and E. M. Hiltbold. 2009. M protein mutant vesicular stomatitis virus stimulates maturation of TLR7-positive dendritic cells through TLR-dependent and -independent mechanisms. J.Virology. 83(7)2962-75.
4. Carey, B. L., M. Ahmed, S. Puckett, and D. S. Lyles. 2008. Early steps of the virus replication cycle are inhibited in prostate cancer cells resistant to oncolytic vesicular stomatitis virus. J. Virology. 82(24):12104-15
5. Ahmed, M., T. R. Marino, S. Puckett, N. D. Kock, and D. S. Lyles. 2008. Immune response in the absence of neurovirulence in mice infected with M protein mutant vesicular stomatitis virus. J. Virology. 82(18):9273-7.
6. Ahmed, M., K. L. Brzoza, and E. M. Hiltbold. 2006. Matrix protein mutant of vesicular stomatitis virus stimulates maturation of myeloid dendritic cells. J. Virology 80(5):2194-205.
7. 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: 34-49.

Title: Associate Professor , Viral Pathogenesis and Immunity
Department: Department of Biology

Email address: Email me

Phone: (828) 262-2677

Office address
Rankin Science North 215