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.
Publication Date: 1989-09-01 PubMed ID: 2549705DOI: 10.1016/0042-6822(89)90101-3Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- Non-P.H.S.
- Research Support
- U.S. Gov't
- P.H.S.
Summary
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This study explains how the infection of a rabbit kidney cell line with Defective Interfering Particles (DIPs) of Equine Herpesvirus Type 1 (EHV-1) results in persistent infection similar to previous findings in Primary Hamster Embryo Fibroblasts. The research also examined and compared the viral transcription process in both standard EHV-1 and DIP-enriched infections.
Research Background
- The study focuses on the cell infection process using Defective Interfering Particles (DIPs) of Equine Herpesvirus Type 1 (EHV-1), a variant of herpesvirus observed in horses.
- Prior studies revealed that DIPs are capable of mediating the coestablishment of persistent infection and oncogenic (cancer initiating) transformation in Primary Hamster Embryo Fibroblasts.
Research Methodology
- To assess whether this pattern is consistent across different species and cell types, the researchers observed the infection’s impact on the Rabbit Kidney (RK) cell line using enriched DIPs.
- A comparison was made between viral transcription in Rabbit Kidney (RK) cells infected with DIP-enriched EHV-1 and those infected with a standard (STD) version of EHV-1.
- The researchers examined which viral DNA sequences were predominantly expressed during the first eight hours of DIP-enriched EHV-1 infection.
Research Findings
- The study confirmed that the infection of a Rabbit Kidney (RK) cell line with DIP-enriched preparations also resulted in the establishment of a persistent infection, similar to the effects in Primary Hamster Embryo Fibroblasts.
- In DIP-enriched EHV-1 infections, viral transcripts were found to originate from DNA sequences containing components of the defective genome.
- However, synthesis of transcripts originating from sequences not preserved in the defective genome was found to be significantly delayed.
- It was also noticed that some high molecular weight RNA species which were synthesized in standard infections did not appear in DIP-enriched infections.
- Through the use of metabolic inhibitors, the researchers established that viral transcription in DIP-enriched infections is regulated in an immediate early, early, and late manner, similar to the process in normal cytocidal (cell-killing) infections.
Significance of the Research
- The results of this study offer valuable insights into the nature of viral transcription in both standard EHV-1 and DIP-enriched infections.
- The research provides an enhanced understanding of the persistent infection process, supporting further explorations into viral transmission and potential therapeutic responses.
Cite This Article
APA
Gray WL, Yalamanchili R, Raengsakulrach B, Baumann RP, Staczek J, O'Callaghan DJ.
(1989).
Viral transcripts in cells infected with defective interfering particles of equine herpesvirus type 1.
Virology, 172(1), 1-10.
https://doi.org/10.1016/0042-6822(89)90101-3 Publication
Researcher Affiliations
- Department of Microbiology and Immunology, Louisiana State University Medical Center, Shereveport 71130.
MeSH Terms
- Blotting, Northern
- Cycloheximide / pharmacology
- DNA Replication / drug effects
- DNA, Viral / genetics
- Defective Viruses / genetics
- Gene Expression Regulation / drug effects
- Herpesviridae / genetics
- Herpesvirus 1, Equid / genetics
- Herpesvirus 1, Equid / growth & development
- Phosphonoacetic Acid / pharmacology
- RNA, Messenger / genetics
- RNA, Viral / genetics
- Restriction Mapping
- Transcription, Genetic
- Viral Interference
Grant Funding
- AI 21996 / NIAID NIH HHS
- AI 22001 / NIAID NIH HHS
Citations
This article has been cited 10 times.- Charvat RA, Zhang Y, O'Callaghan DJ. Deletion of the UL4 gene sequence of equine herpesvirus 1 precludes the generation of defective interfering particles.. Virus Genes 2012 Oct;45(2):295-303.
- Charvat RA, Breitenbach JE, Ahn B, Zhang Y, O'Callaghan DJ. The UL4 protein of equine herpesvirus 1 is not essential for replication or pathogenesis and inhibits gene expression controlled by viral and heterologous promoters.. Virology 2011 Apr 10;412(2):366-77.
- Chen M, Harty RN, Zhao Y, Holden VR, O'Callaghan DJ. Expression of an equine herpesvirus 1 ICP22/ICP27 hybrid protein encoded by defective interfering particles associated with persistent infection.. J Virol 1996 Jan;70(1):313-20.
- Harty RN, Colle CF, Grundy FJ, O'Callaghan DJ. Mapping the termini and intron of the spliced immediate-early transcript of equine herpesvirus 1.. J Virol 1989 Dec;63(12):5101-10.
- Roux L, Simon AE, Holland JJ. Effects of defective interfering viruses on virus replication and pathogenesis in vitro and in vivo.. Adv Virus Res 1991;40:181-211.
- Labbé M, Charpilienne A, Crawford SE, Estes MK, Cohen J. Expression of rotavirus VP2 produces empty corelike particles.. J Virol 1991 Jun;65(6):2946-52.
- Valenzuela S, Pizarro J, Sandino AM, Vásquez M, Fernández J, Hernández O, Patton J, Spencer E. Photoaffinity labeling of rotavirus VP1 with 8-azido-ATP: identification of the viral RNA polymerase.. J Virol 1991 Jul;65(7):3964-7.
- Harty RN, O'Callaghan DJ. An early gene maps within and is 3' coterminal with the immediate-early gene of equine herpesvirus 1.. J Virol 1991 Jul;65(7):3829-38.
- Holden VR, Yalamanchili RR, Harty RN, O'Callaghan DJ. ICP22 homolog of equine herpesvirus 1: expression from early and late promoters.. J Virol 1992 Feb;66(2):664-73.
- Zhao Y, Holden VR, Harty RN, O'Callaghan DJ. Identification and transcriptional analyses of the UL3 and UL4 genes of equine herpesvirus 1, homologs of the ICP27 and glycoprotein K genes of herpes simplex virus.. J Virol 1992 Sep;66(9):5363-72.
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