ArticleProceedings of the National Academy of Sciences of the United States of America2003
Relationship of herpes simplex virus genome configuration to productive and persistent infections.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 144 citations in OpenAlex.
- DNA damage responses in HCMV infection: emerging mechanisms and outstanding questions.Journal of virology · 2026Review
- HSV-1 origin binding protein UL9 forms intermolecular DNA tethers and intramolecular DNA loops.Nature communications · 2026Article
- Viral and cellular insulators promote sustained HSV vector-mediated transgene expression in brain.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Kaposi's sarcoma herpesvirus exploits the DNA damage response to circularize its genome.Nucleic acids research · 2024Article
- Review
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- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- The HSV-1 ubiquitin ligase ICP0: Modifying the cellular proteome to promote infection.Virus research · 2020Review
- Protocol Optimization for the Production of the Non-Cytotoxic JΔNI5 HSV Vector Deficient in Expression of Immediately Early Genes.Molecular therapy. Methods & clinical development · 2020Article
- HSV-1 Hijacks the Host DNA Damage Response in Corneal Epithelial Cells through ICP4-Mediated Activation of ATM.Investigative ophthalmology & visual science · 2020Article
- Early Nuclear Events after Herpesviral Infection.Journal of clinical medicine · 2019Review
- Macaca arctoides gammaherpesvirus 1 (strain herpesvirus Macaca arctoides): virus sequence, phylogeny and characterisation of virus-transformed macaque and rabbit cell lines.Medical microbiology and immunology · 2019Article
- Herpes simplex virus 1 ICP8 mutant lacking annealing activity is deficient for viral DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019Review
- Ubiquitination at the interface of tumor viruses and DNA damage responses.Current opinion in virology · 2018Review
- Promyelocytic leukemia (PML) nuclear bodies (NBs) induce latent/quiescent HSV-1 genomes chromatinization through a PML NB/Histone H3.3/H3.3 Chaperone Axis.PLoS pathogens · 2018Article
- Herpes Simplex Virus Vectors for Gene Transfer to the Central Nervous System.Diseases (Basel, Switzerland) · 2018Review
- The Exonuclease Activity of Herpes Simplex Virus 1 UL12 Is Required for Production of Viral DNA That Can Be Packaged To Produce Infectious Virus.Journal of virology · 2017Article
- Article
- Duck enteritis virus (DEV) UL54 protein, a novel partner, interacts with DEV UL24 protein.Virology journal · 2017Article
12 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
Infection of susceptible cells by herpes simplex virus (HSV) can lead to productive infection or to latency, where the genomes persist in the nuclei of peripheral neurons in a quiescent state. Using the HSV strain d109, which does not express any viral genes and thus establishes a quiescent state in most cells, we observed that a fraction of genomes circularized upon infection. The expression of infected cell protein (ICP) 0, which is known to be involved in reactivation from latency and the promotion of productive infection, inhibited the formation of circular genomes. Circular genomes were not observed upon infection of fully permissive cells by wild-type virus, in either the presence or absence of viral DNA replication. However, productive infection in the absence of ICP0 resulted in the accumulation of a subpopulation of circular genomes. The proportion of circular genomes formed during infection with an ICP0 mutant was greater at low multiplicity of infection, a condition in which ICP0 mutants replicate poorly. In the complete absence of viral gene expression, it was found that only circular genomes persisted in cells. These results suggest that circularization of the HSV genome may not occur early in the productive phase of wild-type HSV infection, but rather during establishment of a quiescent state or latency, providing a possible strategy for long-term persistence. Additionally, the circularization and possible fate of HSV genomes are regulated by an activity of ICP0.
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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.