The antiviral activity exerted by vaccinia virus on the growth of herpes simplex virus in BS-C-1 cells.
The growth of herpes simplex virus type 2 (HSV-2) in BS-C-1 cells, was inhibited following super-infection with vaccinia virus. This inhibition was efficiently induced by both the intracellular mature virus (IMV) form of vaccinia virus and the extracellular enveloped virus (EEV), containing an additional external viral membrane. Treatment of vaccinia IMV with the detergents NP-40, Brij-58 or n-octyl-alpha-D-glucopyranoside, abolished its ability to inhibit the growth of HSV-2. Ultraviolet irradiation of vaccinia virus, that completely inactivated the infectivity of the virus, resulted in partial loss of the capability to inhibit the growth of HSV-2: 16-fold more irradiated virus was needed for the inhibition. Electron microscopy showed that the irradiated vaccinia virus adsorbed and penetrated into the HSV-infected cells but remained morphologically intact within the cells for at least 22 h. When the steps in the growth of HSV affected by the irradiated vaccinia virus were followed, it was found that while the synthesis of HSV DNA was partially decreased, the synthesis of HSV proteins was very strongly inhibited and virus particles were not formed.
Keywan
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Department of Virology, Hebrew University-Hadassah Medical School, P. O. Box 12272, 91120, Jerusalem, Israel.
Katz
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D000818:Animals; D002460:Cell Line; D004279:DNA, Viral / Q000096:biosynthesis; D018258:Herpesvirus 2, Human / Q000254:growth & development* / Q000502:physiology / Q000648:ultrastructure; D008854:Microscopy, Electron; D015163:Superinfection / Q000821:virology; D014466:Ultraviolet Rays; D014616:Vaccinia virus / Q000502:physiology* / Q000528:radiation effects / Q000648:ultrastructure; D014762:Viral Interference / Q000502:physiology* / Q000528:radiation effects
D004279:DNA, Viral