ArticleVirology2008
Biological and genotypic properties of defective interfering particles of equine herpesvirus 1 that mediate persistent infection.
Article in Virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- The EHV-1 UL4 protein that tempers viral gene expression interacts with cellular transcription factors.Virology · 2014Article
- RNA-mediated interference and reverse transcription control the persistence of RNA viruses in the insect model Drosophila.Nature immunology · 2013Article
- Deletion of the UL4 gene sequence of equine herpesvirus 1 precludes the generation of defective interfering particles.Virus genes · 2012Article
- The early UL3 gene of equine herpesvirus-1 encodes a tegument protein not essential for replication or virulence in the mouse.Virology · 2011Article
- Article
- Article
- Properties of an equine herpesvirus 1 mutant devoid of the internal inverted repeat sequence of the genomic short region.Virology · 2011Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Infection with equine herpesvirus 1 (EHV-1) preparations enriched for defective interfering particles (DIP) leads to a state of persistent infection in which infected cells become lysis resistant and release both infectious (standard) virus and DIP. EHV-1 DIP are unique in that the recombination events that generate DIP genomes produce new open reading frames (ORFs; Hyb1.0 and Hyb2.0) consisting of 5' sequences of varying lengths of the early regulatory gene IR4 fused to 3' sequences of varying lengths of the UL5 regulatory gene. Only two additional ORFs (UL3 and UL4) are conserved. Because persistently infected cells release a heterogeneous mixture of DIP, characterization of the elements responsible for this altered state of infection has proved difficult. Here we describe a method for studying persistent infection using recombinant DIP (rDIP). Infection with rDIP resulted in the production of recombinant DIP that replicated faithfully to, at least, five passages and mediated a rapid progression to persistent infection as measured by: 1) production of cells resistant to lysis by the standard virus; and 2) infected cells that released both standard virus and DIP. High concentrations of rDIP also resulted in interference with the standard virus replication, another hallmark of persistent infection. rDIP deleted of UL3, UL4, and either Hyb gene, the only functional genes conserved in the DIP genome, replicated but exhibited markedly reduced ability to interfere with standard virus replication. Restoring only the Hyb genes (either Hyb1.0 or Hyb2.0), the IR4 gene, or specific portions of the IR4 gene restored interference. These data suggest that residues 144 to 196 of the IR4 protein within the HYB proteins are important for DIP interference and that persistent infection results from recombination events that produce DIP genomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.