Amy Adamson, Associate Professor
In my lab we study how viruses interact with human cells and how such interactions might cause disease. We currently work with two different human viruses: Epstein-Barr virus (EBV), which infects about 95% of the world's population and causes infectious mononucleosis and some cancers; and Influenza, which causes "the flu" and has in the past caused major epidemics and pandemics. We are interested in how the virus manipulates the host's cellular proteins and pathways to aid in infection/replication, and how such interactions can be altered to inhibit viral infection or replication. Recent Findings: For Influenza:a genetic screen in Drosophila identified several genetic modifiers of Influenza M2 function. Such modifiers, which are genes involved in the cellular activity of M2 (the viral proton channel), included specific subunits of the cellular V1V0-ATPase, a proton pump which regulates intracellular pH. In mammalian cells, we have used these findings to show that manipulating individual V1V0-ATPase subunits directly affects Influenza viral infection and replication within cells (see the publication "A Drosophila Model for Genetic Analysis of Influenza Viral/Host Interactions", listed below). In addition, we have found that glucose metabolism indirectly affects influenza viral infection via activity of the V1V0-ATPase pump (see the publication "Glycolytic Control of Vacuolar-Type ATPase Activity: A Mechanism to Regulate Influenza Viral Infection," listed below). For EBV:: a genetic screen in Drosophila also identified several genetic modifiers of EBV BRLF1 and BZLF1 function. Of great interest is our finding that Drosophila Tor (Target of rapamycin) is a potent modifier of both BRLF1 and BZLF1 functions. Translation to human cells has shown that the mTOR pathway is a key regulator of EBV lytic replication. This pathway, which promotes mRNA translation, cell growth, autophagy, mitochondrial metabolism, angiogenesis, and adipogenesis, is a potential target for anti-cancer therapy, and perhaps anti-EBV therapy (see the publications "A Study of Epstein-Barr Virus BRLF1 Activity in a Drosophila Model System" and "Inhibition of mTOR inhibits lytic replication of Epstein-Barr virus in a cell-type specific manner", listed below). |
Recent Grant Awards: 2012-2015 "Inhibition of mTOR Alters Epstein-Barr Virus Lytic Replication", PI, NIH. |
Recent Publications: Adamson, A. Inhibition of mTOR inhibits lytic replication of Epstein-Barr virus in a cell-type specific manner. In preparation. |
Classes:
Principles of Biology I (BIO 111) |
Contact: 201 Eberhart Building
|
Research:
