Amy Adamson, Professor | UNCG Biology
We are interested in how viral proteins interact with and modify the function of host cellular proteins, and how these interactions affect both viral replication and host cell function.
We are working with the Epstein-Barr virus (EBV) immediate-early proteins BZLF1 (Z) and BRLF1 (R).
We also express viral proteins in the developing Drosophila eye to search for genetic interactors of viral proteins.
Here, R over-expression causes over-proliferation of eye cells. We performed a genetic screen in Drosophila with tumor suppressor mutants to see which pathways were affected by R activity. One interesting interactor was Tor (Target of rapamycin), whose mammalian homolog (mTOR) is a key regulator of cell growth.
Translation of this finding to human cells showed that suppression of mTOR inhibits EBV lytic replication in B cells.
Studies to determine the exact mechanism of this inhibition are ongoing.
We are working with the influenza proteins M2, NP, and NS1.
Within Drosophila tissues, M2 localizes and functions the same as in mammalian tissues.
Here, over-expression of M2, at 29°C, causes a severe mutant phenotype, with loss of eye tissue. M2 functions as an intracellular proton channel, and alters the pH of intracellular compartments.
A genetic screen identified important modifiers of M2 activity, such as specific subunits of the host vacuolar V1V0-ATPase. Modulation of these specific subunits greatly affects influenza infection and replication within mammalian cells.
Here, over-expression of individual subunits of the V1V0-ATPase increases the ability of influenza virus to replicate within MDCK cells (as noted by increased HA (red) staining).
post: Amy Adamson, UNCG Biology, 201 Eberhart Bldg., Greensboro, NC 27402-6170
phone: (336) 256-0312
fax: (336) 334-5839