A comparison of herpes simplex virus plaque development after viral treatment with anti-DNA or antilipid agents.
The plaque development of Herpes simplex virus type 1 (HSV) is slower for viruses treated with two anti-DNA agents: ultraviolet radiation (UV) or n-acetoxy-2-acetyl-aminofluorene. For HSV treated with three antimembrane agents--butylated hydroxytoluene, acridine plus near UV radiation, or ether--the plaque development time is the same as for untreated viruses. These differences hold even for viruses that survived treatment that lowered viability below the 1% level. Gamma ray inactivation of HSV produces no change in plaque development even though this agent is believed to preferentially affect viral DNA.
D015073:2-Acetylaminofluorene / Q000031:analogs & derivatives*; D000099:Acetoxyacetylaminofluorene / Q000494:pharmacology*; D000166:Acridines / Q000494:pharmacology*; D002084:Butylated Hydroxytoluene / Q000494:pharmacology*; D004261:DNA Replication / Q000187:drug effects / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D004986:Ether / Q000494:pharmacology; D018139:Simplexvirus / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects; D014466:Ultraviolet Rays; D010948:Viral Plaque Assay; D014779:Virus Replication / Q000187:drug effects / Q000528:radiation effects
D000166:Acridines; D004986:Ether; D002084:Butylated Hydroxytoluene; D000099:Acetoxyacetylaminofluorene; D015073:2-Acetylaminofluorene