Major Research Interest:
Herpes simplex virus 2 (HSV-2)
The current focus of the lab is Herpes simplex virus 2 (HSV-2) causes recurrent genital infections and life-threatening neonatal disease. Epstein-Barr virus (EBV) causes infectious mononucleosis and plays an important role in the development of several B cell and epithelial cell cancers. Like other herpesviruses, both have a lipid envelope containing many membrane proteins, and their entry into cells, and for HSV-2 its subsequent spread to adjacent cells, requires membrane fusion. Transient coexpression of HSV-2 membrane proteins gB, gD, gH and gL, or EBV proteins gB, gH and gL, causes cell fusion in the absence of infection, in a process that in many respects mimics fusion between the virus and cell membranes. Three-dimensional structures are known for gB and the gH/gL complex of both viruses, and there is some limited information from mutagenesis studies about which residues lie within functionally important parts of the proteins. The activity of gB in fusion is generally believed to be triggered by an interaction with gH/gL, but the location of the binding sites on either protein is not clear. Determination of the binding site on gB may facilitate the design of drugs able to interfere with the interaction and thus block membrane fusion and virus entry into cells.
