ArticleJournal of virology2003
Strain-dependent structural variants of herpes simplex virus type 1 ICP34.5 determine viral plaque size, efficiency of glycoprotein processing, and viral release and neuroinvasive disease potential.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Enhanced Pathogenic Consequences Induced by a Seven-Amino-Acid Extension in the G Protein of the HRSV BA9 Genotype.International journal of molecular sciences · 2025Article
- Impact of the interaction between herpes simplex virus 1 ICP22 and FACT on viral gene expression and pathogenesis.Journal of virology · 2024Article
- Article
- Advanced progress in the genetic modification of the oncolytic HSV-1 virus.Frontiers in oncology · 2024Review
- Towards a comprehensive view of the herpes B virus.Frontiers in immunology · 2023Review
- Interplay between Autophagy and Herpes Simplex Virus Type 1: ICP34.5, One of the Main Actors.International journal of molecular sciences · 2022Review
- Human Adenovirus Type 4 Comprises Two Major Phylogroups with Distinct Replicative Fitness and Virulence Phenotypes.Journal of virology · 2022Article
- The herpesvirus accessory protein γ134.5 facilitates viral replication by disabling mitochondrial translocation of RIG-I.PLoS pathogens · 2021Article
- Viral infection of human neurons triggers strain-specific differences in host neuronal and viral transcriptomes.PLoS pathogens · 2021Article
- Herpes simplex virus-1 KOS-63 strain is virulent and causes titer-dependent corneal nerve damage and keratitis.Scientific reports · 2021Article
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- Review
- Genotypic and Phenotypic Diversity of Herpes Simplex Virus 2 within the Infected Neonatal Population.mSphere · 2019Article
- Selective Editing of Herpes Simplex Virus 1 Enables Interferon Induction and Viral Replication That Destroy Malignant Cells.Journal of virology · 2019Article
- Herpes Simplex Virus 1 γJournal of virology · 2018Article
- A new era in cytomegalovirus vaccinology: considerations for rational design of next-generation vaccines to prevent congenital cytomegalovirus infection.NPJ vaccines · 2018Review
- Shared ancestry of herpes simplex virus 1 strain Patton with recent clinical isolates from Asia and with strain KOS63.Virology · 2017Article
- Analysis of the Protective Immunity Induced by Herpes Simplex Virus 1 Strain M3 with an Attenuated Phenotype Due to Mutations in the ViralFrontiers in microbiology · 2017Article
- Relating plaque morphology to respiratory syncytial virus subgroup, viral load, and disease severity in children.Pediatric research · 2015Article
- Up to four distinct polypeptides are produced from the γ34.5 open reading frame of herpes simplex virus 2.Journal of virology · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ability of certain strains of herpes simplex virus type 1 (HSV-1) to cause encephalitis or neuroinvasive disease in the mouse upon peripheral infection is dependent on a combination of activities of specific forms of viral proteins. The importance of specific variants of ICP34.5 to neuroinvasive disease potential and its correlation with small-plaque production, inefficient glycoprotein processing, and virus release were suggested by comparison of ICP34.5 from the SP7 virus, originally obtained from the brain of a neonate with disseminated disease, and the tissue culture-passaged progeny of SP7 (SLP5 and SLP10) and the KOS321 virus. SLP5, SLP10, and KOS321 are attenuated and exhibit a large-plaque phenotype, including efficient glycoprotein processing and viral release. We show that expression of the KOS321 ICP34.5 protein in cells infected with SP7 or ICP34.5 deletion mutants promotes large plaque formation and efficient viral glycoprotein processing, while expression of the SP7 ICP34.5 protein decreases efficiency of viral glycoprotein processing. In addition, a recombinant virus, 4hS1, with the SP7 ICP34.5 gene replacing the KOS321-like ICP34.5 gene in the SLP10a background, rescues the small-plaque phenotype and neuroinvasive disease. The major difference in the ICP34.5 gene product is the number of Pro-Ala-Thr repeats in the middle region of the protein, with 18 for SP7 and 3 for KOS321. Strain-dependent differences in the ICP34.5 protein can therefore alter the tissue culture behavior and the virulence of HSV-1.
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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.