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Department of Microbiology Dr. Lagunoff's Microbiology Department web site Michael Lagunoff received his bachelors degree in Chemistry from Oberlin College and his Ph.D. in Virology from the University of Chicago. He went on to do his post-doctoral training at the University of California, San Francisco where he began work on the molecular biology of Kaposi's Sarcoma-associated Herpesvirus. Michael is an associate professor in the Department of Microbiology and has an adjunct appointment in Immunology. The laboratory studies the molecular virology of Kaposi's Sarcoma-associated herpesvirus (KSHV). KSHV is the infectious cause of Kaposi's Sarcoma (KS). KS is a highly vascularized hyperplasia that is the most common tumor in AIDS patients and is currently the most commonly reported tumor in regions of Africa. KSHV is also associated with two B-cell lymphoproliferative diseases, primary effusion lymphoma and AIDS-associated multicentric Castleman's disease. The laboratory is interested in how the virus alters the host cell to induce tumors. KSHV encodes over 80 genes and many are involved in altering host cell signal transduction. The laboratory focuses on how initiation of signal transduction pathways by viral genes leads to viral pathogenesis in endothelial and B-cells. We are currently working on how KSHV induced signaling through the gp130 receptor induces persistent STAT3 activation and subsequent AKT activation, pathways commonly activated in tumors. This pathway is also involved in KSHV driven differentiation of blood endothelial cells to lymphatic endothelium and we are interested the role of differentiation in the biology of KSHV. We also have a major focus on viral induced angiogenesis. KS tumors are highly vascularized and KSHV induces many genes involved in angiogenesis. Ongoing studies in the lab examine the role of KSHV induced angiogenesis in KSHV biology. Current Students: Valerie Morris, Tracie Delgado Representative Publications: Carroll, P.A., Brazeau, E., and Lagunoff, M. 2004. Kaposi’s sarcoma-associated herpesvirus infection of blood endothelial cells induces lymphatic differentiation. Virology 328:7-18. Chen, L and Lagunoff, M. 2005. Establishment and Maintenance of Kaposi’s Sarcoma-associated herpesvirus latency in cultured B-cells. Journal of Virology, 79:14383-91 Carroll, P.A., Kenerson, H.L., Yeung, R.S. and M. Lagunoff. 2006. Latent Kaposi’s Sarcoma-associated herpesvirus infection of endothelial cells induces Hypoxia induced transcription factors. Journal of Virology, 80:10802-12. Rose, P.P, J.M. Carroll, V.R. DeFilippis, P.A. Carroll, M. Lagunoff, A.V. Moses, C.T. Roberts jr. and K. Fruh. 2007. The Insulin Receptor is essential for virus-induced tumorigenesis of Kaposi’s Sarcoma. Oncogene, 26:1995-2005. Chen, L. and Lagunoff M. 2007. The KSHV viral Interleukin-6 is not essential for latency or lytic replication in BJAB cells. 359:425-435. Virology. Punjabi, A.S., Carroll, P.A., Chen, L. and M. Lagunoff. 2007. Persistent activation of STAT3 by latent KSHV infection of endothelial cells. 81:2449-2458. Journal of Virology. Orr, M.T., Mathis, M.A., Lagunoff, M., Sacks, J.A. and Wilson C.B. 2007. CD8 T cell control of HSV reactivation from latency is abrogated by viral inhibition of MHC class I. Cell Host and Microbe. COS Expertise
Profile Updated August 2007
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