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Dr. Mathes, Director of the CRR and Director of the Viral Oncogenesis Program of the OSU Comprehensive Cancer Center/James Cancer Hospital Research Institute, is a Professor of Veterinary Bioscience in the College of Veterinary Medicine. Dr. Mathes' research has provided critical knowledge of immunosuppressive factors in retrovirus infections and neoplastic disease. He has a long-standing interest in treatment and prevention of retrovirus disease and has established a research program to evaluate anti-retrovirus drug therapy. He currently supports 1 graduate student. He is Director of the Imaging Core in the Department of Veterinary Biosciences, which offers flow cytometry, confocal microscopy, and in vivo imaging (IVIS).
NIH, RO1 CA51485 (Subcontract), Pathogenic Mechanisms in Feline Leukemia, L. Mathes, Ph.D. (Principal Investigator)
Research conducted in collaboration with Dr. Pradip Roy-Burman, University of Southern California has demonstrated that infectious feline leukemia virus may be altered biologically because of homologous recombination with non-infectious endogenous FeLV (enFeLV). We hypothesize that recombinants arising de novo in the infected animals, while only poorly replicated compared to FeLV wild type strains in the host, might have enhanced pathogenicity in certain target cells (potentially erythroid progenitor cells) which are eliminated by the associated cytopathic effects. We have shown that exogenous/endogenous recombination takes place in the first 8 wks of infection in vivo (J. Virol. 74:5796-5801, 2000).
NIH, NIDA, RO1-DAB13815 Psycostimulants & Lentiviral Infection of Neural Cells. L. Mathes, Ph.D. (Principal Investigator).
The major focus of this grant is to investigate the synergism between psycostimulants and neurotropic FIV infection in cats. We have shown that methamphetamine (METH) and other psycostimulatory greatly enhance FIV infection of feline astrocyte culters (J. NeuroVirology 8:240-249, 2002). The objective of the current studies is to determine the mechanism of this enhancement. We hypothesize that METH upregulates expression of the virus receptor CXCR4 which in turn increases the rate and extent of infection. Our current quest is to understand how METH modulates CXCR4 expression.