title: Viral transcripts in cells infected with defective interfering particles of equine herpesvirus type 1.
abstract: Equine herpesvirus type 1 (EHV-1) preparations enriched in defective interfering particles (DIPs) have previously been demonstrated to mediate the coestablishment of persistent infection and oncogenic transformation in primary hamster embryo fibroblasts. In this study, it was demonstrated that infection of a rabbit kidney (RK) cell line with EHV-1 DIP-enriched preparations also results in the establishment of persistent infection. Viral transcription was characterized in RK cells infected with DIP-enriched stocks and compared to viral transcription in RK cells infected with standard (STD) EHV-1. During the first 8 hr of infection with the DIP-enriched EHV-1 preparation, viral DNA sequences which are conserved in the DIP genome were predominantly expressed. Thus, these transcripts originate from DNA sequences that contain the components of the defective genome which originates from DNA sequences mapping at 0.00-0.04 of the Long region terminus and within two portions of the Short region inverted repeats (IR), 0.78-0.79 and 0.83-0.865 of the internal IRs and 0.99-1.00 and 0.915-0.95 of the terminal IRs. The overwhelming majority of viral transcripts that were synthesized in the DIP-enriched infections appeared to correspond to transcripts expressed in STD infection as assessed by Northern hybridization analysis but the synthesis of transcripts originating from sequences not conserved in the defective genome was significantly delayed. However, some high molecular weight RNA species that were synthesized in STD infections were not detected in DIP-enriched infections. Studies utilizing metabolic inhibitors indicated that viral transcription in DIP-enriched infections, like that of STD cytocidal infection, is regulated in an immediate early, early and late manner.
authors.affiliation: Department of Microbiology and Immunology, Louisiana State University Medical Center, Shereveport 71130.
authors.forename: W L
authors.initials: WL
authors.lastname: Gray
authors.forename: R
authors.initials: R
authors.lastname: Yalamanchili
authors.forename: B
authors.initials: B
authors.lastname: Raengsakulrach
authors.forename: R P
authors.initials: RP
authors.lastname: Baumann
authors.forename: J
authors.initials: J
authors.lastname: Staczek
authors.forename: D J
authors.initials: DJ
authors.lastname: O'Callaghan
mesh_terms: D015152:Blotting, Northern; D003513:Cycloheximide / Q000494:pharmacology; D004261:DNA Replication / Q000187:drug effects; D004279:DNA, Viral / Q000235:genetics*; D003673:Defective Viruses / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects; D006564:Herpesviridae / Q000235:genetics*; D004861:Herpesvirus 1, Equid / Q000235:genetics* / Q000254:growth & development; D010746:Phosphonoacetic Acid / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics*; D012367:RNA, Viral / Q000235:genetics*; D015183:Restriction Mapping; D014158:Transcription, Genetic; D014762:Viral Interference
chemical_list: D004279:DNA, Viral; D012333:RNA, Messenger; D012367:RNA, Viral; D003513:Cycloheximide; D010746:Phosphonoacetic Acid