Research Interests
Dr. Levy’s laboratory studies the virus-mediated induction of lymphoma as a model to understand the early stages of malignancy, the defining events of the disease process and the role of oncogenes. We study three animal models of virus-induced lymphoma to address these issues:
Feline leukemia virus (FeLV)-induced lymphoma in the domestic cat is an important model for human viral disease because FeLV is a natural pathogen that infects a naturally outbreeding mammalian species. Our studies have shown that the variable clinical outcome of FeLV infection is linked to genetic variability among natural isolates. Further, because the molecular mechanism of tumor induction involves the activation of host oncogenes, FeLV has proved to be a useful model system for the discovery of new cellular oncogenes associated with lymphoma. Murine leukemia virus (MuLV) infection in the laboratory mouse is a useful model for studies of pathogenesis because the virus reliably induces T-cell lymphoma with short latency. For this reason, we are using the MuLV model to study early, preclinical changes that lead to malignancy. Analyses have implicated involvement of bone marrow progenitors, particularly hematopoietic progenitors and an early prothymocyte. Simian AIDS-associated lymphoma in the rhesus macaque is an important model for human AIDS-related lymphoma. Our studies with this model are focused on identifying predictive epidemiologic factors that may be useful in evaluating risk of lymphoma in AIDS patients, and on dissecting the positive and negative growth regulatory pathways operative in the tumor microenvironment.
Recent Publications:
Habis, A., G.B. Baskin, L. Simpson, I. Fortgang, M. Murphey-Corb, and L.S. Levy. 2000. Rhesus lymphocryptovirus infection during the progression of SAIDS and SAIDS-associated lymphoma in the rhesus macaque. AIDS Res. Human Retrovir. 16: 163-171.
Fortgang, I., P. Didier, and L.S. Levy. 2000. B-cell leukemia in a rhesus macaque (Macaca mulatta) infected with simian immunodeficiency virus. Leukemia and Lymphoma 37: 657-662.
Rulli, K., P.A. Lobelle-Rich, A. Trubetskoy, J. Lenz, and L.S. Levy. 2001. Tissue distribution and timing of appearance of polytropic envelope recombinants during infection with SL3-3 MuLV or its weakly pathogenic mutant SL3DMyb5. J. Virol. 75: 522-526.
Fortgang, I., T. Rege, G.B. Baskin, M. Murphey-Corb, and L.S. Levy. 2001. Variation in SIV env V1 region in SAIDS-associated lymphoma. AIDS Res. Human Retrovir. 17:459-465.
Baskin, G.B, K.J. Cremer, and L.S. Levy. 2001. Comparative pathobiology of HIV- and SIV-associated lymphoma. AIDS Res. Human Retrovir., 17: 745-751.
Rulli, K., J. Lenz , and L.S. Levy. 2002. Disruption of hematopoiesis and thymopoiesis in the early premalignant stages of infection with SL3-3 MuLV. J. Virol., 76:2363-2374.
Ruff, K., G.B. Baskin, L. Simpson, M. Murphey-Corb, and L.S. Levy. 2003. Rhesus rhadinovirus infection in healthy and SIV-infected macaques. J. Med. Primatol., 32: 1-6.
Fortgang, I., T. Rege, G.B. Baskin, M. Murphey-Corb, and L.S. Levy. 2001. Variation in SIV env V1 region in SAIDS-associated lymphoma. AIDS Res. Human Retrovir. 17:459-465
Chandhasin, C., P.A. Lobelle-Rich and L.S. Levy. 2004. Feline leukemia virus LTR variation and disease association in a geographic and temporal cluster. J. Gen. Virol. 85: 2937-2942.
Finstad, S., S. Prabhu, K.R. Rulli and L.S. Levy. 2004. Regulation of FeLV-945 by c-Myb binding and CBP recruitment to the LTR. Virology Journal (Biomed Central) 1: 3.
Johnson, C., P. A. Lobelle-Rich, A. Puetter and L.S. Levy. 2005. Substitution of FeLV LTR sequences into MuLV alters the pattern of insertional activation and identifies new common insertion sites. J. Virol. 79: 57-66.
Chandhasin, C., P.N. Coan and L.S. Levy. 2005. Subtle mutational changes in the SU protein of a natural FeLV-A isolate alter disease spectrum. J. Virol. 79: 1351-1360.
Chandhasin, C., P.N. Coan, I. Pandrea, C.K. Grant, P.A. Lobelle-Rich, A. Puetter and L.S. Levy. 2005. Unique LTR and SU gene sequences of feline leukemia virus as determinants of disease outcome. J. Virol. 79: 5278-5287.
Johnson, C., and L.S. Levy. 2005. Matrix attachment regions as targets for retroviral integration. Virology Journal (Biomed Central) 2: 68.
Contact: llevy@tulane.edu