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PeterMedveczky

Peter Medveczky, MD

Professor, COLLEGE OF MEDICINE MOLECULAR MEDICINE
  • We are virologists and molecular biologists interested in oncogenic and neurotropic herpesviruses. These large DNA viruses cause cancer and neurodegenerative diseases.
  • Project 1 involves experiments on the Kaposi's sarcoma Associated Herpesvirus (KSHV) related to latency and oncogenic transformation. In this context we also study the role of marijuanas major compound THC and its receptors in modulation of oncogenic herpesviruses. Project is funded by a 5 year NIH grant.

  • Project 2 is molecular biology of the viral interleukin-6 (vIL-6) of KSHV that is possibly involved in the oncogenic transformation process. Funding is pending.

  • Project 3 Identification novel oncogenic viruses in AIDS lymphomas (50% has no known etiology). Funding is pending.

  • Project 4 Human herpesvirus 6 (HHV-6) is implicated in the pathogenesis of multiple sclerosis (M.S.). Recent data show that variant HHV-6A infected marmosets develop an MS-like disease but variant B infected animals remain healthy suggesting that variant A virus encodes specific genes responsible for this phenotype. About 65 genes of the two variant genomes are highly homologous; however, about 15 genes show significant sequence divergence. Currently we are developing a system to identify genes of interest e.g. involved in neurotropism and M.S. Funded by a small grant and other grants are pending.

  • Project 5 HHV-6 is a unique human virus as we discovered that its genome integrates into telomeres of human chromosomes. We have identified families with integrated HHV-6 in chromosomes 17 and 18. These patients are diagnosed with various CNS conditions and show weakened immune responses.

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MichaelCheung

Michael Cheung, BS, MS

Graduate Research Assistant, COLLEGE OF MEDICINE MOLECULAR MEDICINE
  • My research interests focus on mesenchymal stem cells (MSCs), also known as multipotent stromal cells, and their role in modulating immune responses. In particular, our work has revealed that respiratory syncytial virus (RSV) may infect MSCs and increase the expression of immune regulatory factors including IFN-beta and indoleamine-2,3-dioxygenase (IDO), which down-regulate T cell proliferation and may be responsible for the lack of development of protective immunity to the virus despite recurrent infections. The use of the IDO-specific inhibitor 1-methyltryptophan on infected MSCs successfully reversed this effect. Future directions may include the use of an IDO inhibitor as a way to increase the immune response to the virus and lead to better outcomes in patients.
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