Dr. Sajal Ghosh

Assistant Professor


M.Sc. in Biochemistry, Calcutta University, India

Ph.D. in Biochemistry, Calcutta University, India

Post-Doc, Molecular Virology, Univ. Alabama at Birmingham, USA

General field of research:

Viral Oncology

Affiliations other than medicine:

Evans Center for Interdisciplinary Biomedical Research
Cancer Research Center

Contact information:

72 East Concord Street, R-908 BUSM
Phone: (617)-638 5615

Housman Building, R-906
Phone: (617)-638 5615
Fax: (617)-638 5609



FeLV; EBV; Non-coding RNA; Gene Transactivaion; TLR-signaling

Summary of research interest:

My research interest is to understand molecular basis of oncogenesis caused by leukemia virus and Epstein barr virus (EBV). Leukemia viruses are oncogene deficient simple retroviruses but how their infection in animals causes tumor development in a predicable manner is poorly understood.

We have demonstrated using feline leukemia virus as a model that the long-terminal region (LTR) of these viruses independently activates AP-1 and NFκB signaling pathways in the host cells. We hypothesized that such activities may aid in tumorigenesis. We found that the U3-LTR region makes small non-coding RNA, whose production is directly related to the transactivation potential of the LTR. Our recent studies demonstrated that toll-like receptor 3 (TLR3) expression is necessary for such activity.

Our current research effort is dedicated to understand the regulation of expression of the LTR-transcript and how it activates TLR3 signaling. EBV, on the other hand, is a large DNA tumor virus, associated with several human malignancies. However, EBV maintains a latent state of infection in these cancers and it is believed that the latent gene products play a discrete role in the genesis or maintenance of EBV-associated tumors. Our interest is to determine the contribution of EBV latent gene products in tumorigenesis.

Recent publications:

Forman, L. W., Pal-Ghosh, R., Spanjaard, R. A., Faller, D. V., and Ghosh, S. K. 2009. Identification of LTR-specific small non-coding RNA in FeLV infected cells. FEBS Letters 583: 1386-1390.

Zhao, X., Patton, J. R., Ghosh, S. K., Fischel-Ghodsian, N., Shen, L., and Spanjaard, R. A. 2007. Pus3p and Pus1p-Dependent Pseudouridylation of Steroid Receptor RNA Activator Controls a Functional Switch that Regulates Nuclear Receptor Signaling. Molecular Endocrinology 21: 686-699.

Ghosh, S. K., Forman, L. W., Akinsheye, I., Perrine, S. P., and Faller, D. V. 2007. Short, Discontinuous Exposure to Butyrate Effectively Sensitizes Latently EBV-Infected Lymphoma Cells to Nucleoside Analogue Antiviral Agents. Blood Cells Molecules and Diseases 38: 57-65.

Abujamra, A. L., Spanjaard, R. A., Akinsheye, I., Zhao, X., Faller, D. V., and Ghosh, S. K. 2006. Leukemia Virus Long Terminal Repeat Activates NFκB Pathway by a TLR3-dependent Pathway. Virology. 345: 390-403.

Abujamra, A. L., Faller, D. V., and Ghosh, S. K. 2003. Mutations That Abrogate Transactivational Activity of the Feline Leukemia Virus Long Terminal Repeat Do Not Affect Virus Replication. Virology 309: 294-305.

Ghosh, S. K., Roy-Burman, P. and Faller, D. V. 2000. Long Terminal Repeat Regions from Exogenous but not Endogenous Feline Leukemia Viruses Transactivate Cellular Gene Expression Journal of Virology 74: 9742-9748.

Ghosh, S. K. and Faller, D. V. 1999. Feline leukemia virus long terminal repeat activates collagenase IV expression through AP-1. Journal of Virology 73: 4931-4940.

Wei, X., Ghosh, S.K., Taylor, M.E., Johnson, V.A., Emini, E.A., Deutsch, P., Lifson, J.D., Bonhoeffer, S., Nowak, M.A., Hahn, B.H., Saag, M.S., and Shaw, G.M. 1995. Viral dynamics in human immunodeficiency virus type 1 infection. Nature 373: 117-122, 1995.

Technologies available for sharing upon request:

Real-time PCR analysis; Reverse Transcriptase assay for retrovirus replication