THE EFFECTS OF ULTRAVIOLET LIGHT ON HOST CELL REACTIVATION AND PLAQUE SIZE OF Herpes simplex VIRUS TYPE I IN C3H/lOT1/2 MOUSE CELLS

Abstract

—Herpes simplex virus — type 1 (HSV‐I) plaque‐forming ability and plaque size were measured on C3H/1OT1/2 cell monolayers as functions of pretreatment dose with UV light at different times before inoculation with virus, in order to determine if UV‐enhanced reactivation (ER) of UV‐irradiated virus. as well as associated phenomena, could be obtained in this cell system. The number of virus plaques observed (i.e. the capacity of the cells to support virus growth) and the size of the plaques were found to increase substantially with pretreatment of the cells with UV light. However, no significant ER was observed. Therefore, the mechanisms responsible for the increases in plaque size and cell capacity seem to be independent of those responsible for ER. In work by others. C3H/l0T1/2 cells have hcen transformed by UV light at doses similar to those used in this study; the absence of ER of UV‐irradiated virus in this study indicates that the mechanism underlying ER is not required for transformation.

THE EFFECTS OF ULTRAVIOLET RADIATION EXPOSURE OF ADJACENT CELLS ON PLAQUE FORMATION WITH Herpes simplex VIRUS TYPE I

“…Why irradiated cells may produce complete virus earlier than unirradiated cells is still unclear, since HSV codes for its own DNA polymerase. At low fluences of UV and with inoculation delays similar to those used in the present study, UV may actually cause an increase in cellular viral capacity (Montes and Taylor, 1986), and can act as a stimulant to cellular DNA replicative synthesis in confluent human fibroblast cell monolayers (Cohn et al, 1984). In addition, the results of Cornelis et al, 1980, show that SV40, a mammalian virus that does not code for its own DNA polymerase, also exhibits a LPE when assayed on a different strain of monkey kidney cells (BSC-1).…”

“…They also showed that UV irradiated cells make virus earlier, make more virus, exhibit ultraviolet enhanced reactivation (UVER), and required appropriate delays for the expression of all of these phenomena suggesting the presence of an inducible process. It is interesting to note that the delay between cell irradiation and viral infection that is necessary for the LPE with CV-1P cells, is not required for C3W10T1/2 cells (Montes and Taylor, 1986). Whether this challenges the conclusion of Babich et al (1982) that delayed expression of the LPE and its inhibition by cycloheximide suggest that the LPE is an inducible phenomenon is unclear.…”

“…Some inducible phenomena, such as Weigle Reactivation (WR) in bacteria, also exhibit timing differences, similar to those shown here for mammalian cells, if different strains of bacteria are treated (Fields, 1980). In addition, while Babich et al (1981) reported that UVER and the LPE behaved in a similar fashion in CV-1P cells, Montes and Taylor (1986) reported that C3H/lOT1/2 cells exhibit a LPE but no UVER.…”

“…The resulting plaques formed after such an infection are considerably larger than those formed when infecting unirradiated cells. Under appropriate conditions, the LPE can give rise to a five-fold increase in plaque area (Montes and Taylor, 1986). With African green monkey kidney cells (strain CV-lP), no LPE is measurable unless a delay of at least 12 h is allowed between cell irradiation and viral infection, and a maximum LPE is obtained if a delay of at least 48 h is employed (Coohill et a f .…”

“…For C3H/lOT1/2 mouse embryo fibroblast cells, which are deficient in excision repair, the reverse is true, i.e. cells infected with HSV immediately after being exposed to UV give the largest LPE which decreases as the time between cell irradiation and viral inoculation increases (Montes and Taylor, 1986). 'To whom correspondence should be sent: Mail Stop 125-112, JPUCaltech, 4800 Oak Grove Drive, Pasadena, CA 91109, USA.…”