Rebecca Conner

Publication Date


Advisor(s) - Committee Chair

Thomas Coohill, Larry Elliott, Frank Toman

Degree Program

Department of Biology

Degree Type

Master of Science


In mammalian cell-virus systems, it has been observed that damage caused by exposure of the cell to ultraviolet radiation (UV) will result in an increase in viral plaque development rate. This phenomenon is termed the Large Plaque Effect (LPE). Apparently, viral plaque development increases at a faster rate for Herpes Simplex Virus (HSV) when it is assayed on certain UV-irradiated mammalian cells. The consequence of this increase in plaque development rate is that viral plaques appear larger on irradiated monolayers of cells when compared to plaques that developed on unirradiated cellular monolayers.

The cause of the LPE is not yet understood. It is though that the enhancement of plaque development, due to UV damage, is a manifestation of the excision repair mechanisms operating on the cellular genome. It is known that agents that act like UV and inhibit DNA synthesis, such as hydroxyurea, caffeine, and the carcinogen N-acetoxy-2-acetylaminofluorene, can produce the LPE. Conversely, cyclohexamide, which inhibits de novo protein synthesis, can completely prevent the LPE caused by UV. There is also some evidence of a cellular membrane effect involved in generating a non-UV LPE as observed in work with dimethyl sulfoxide. In addition, certain syncytial mutants of HSV are known to enhance membrane fusion.


Biology | Cell and Developmental Biology | Cell Biology | Life Sciences