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Thus, as the study suggests, the virus does not replicate efficiently when certain signaling pathways are disturbed. A disturbance such as preventing a protein kinase from activating a transcription factor may reduce HSV1's ability to subvert the pathway.

"Our studies here also suggests that HSV1 alters a repertoire of cellular transcription factors. Some are inhibited while others are activated in the interest of viral replication," Bachenheimer said. Among these is NF-kappaB, a transcription factor that prevents programmed cell death.

"So one could envision drugs that specifically target viral proteins that affect the kinds of cell signal transduction pathways and transcription factors we are studying here. But these would have to be targeted to the viral part of the equation not the normal cellular part, as these signaling activities occur in every cell," Bachenheimer said.

"Part of our effort now is to identify the viral proteins which trigger these effects."

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Contact: Karen Stinneford or Lynn Wooten
Lwooten@unch.unc.edu
919-966-3366
University of North Carolina School of Medicine
13-Oct-1999