ArticleJournal of virology2009
Herpes simplex virus type 1 regulatory protein ICP0 aids infection in cells with a preinduced interferon response but does not impede interferon-induced gene induction.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- The producer cell type of HSV-1 alters the proteomic contents and infectious capacity of virions.Journal of virology · 2025Article
- Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity.Frontiers in microbiology · 2025Review
- Article
- pUL36 Deubiquitinase Activity Augments Both the Initiation and the Progression of Lytic Herpes Simplex Virus Infection in IFN-Primed Cells.Journal of virology · 2022Article
- A 77 Amino Acid Region in the N-Terminal Half of the HSV-1 E3 Ubiquitin Ligase ICP0 Contributes to Counteracting an Established Type 1 Interferon Response.Microbiology spectrum · 2022Article
- Host Intrinsic and Innate Intracellular Immunity During Herpes Simplex Virus Type 1 (HSV-1) Infection.Frontiers in microbiology · 2019Review
- Targeting Swine Leukocyte Antigen Class I Molecules for Proteasomal Degradation by the nsp1α Replicase Protein of the Chinese Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Strain JXwn06.Journal of virology · 2016Article
- Novel roles of cytoplasmic ICP0: proteasome-independent functions of the RING finger are required to block interferon-stimulated gene production but not to promote viral replication.Journal of virology · 2014Article
- Murine cytomegalovirus protein pM92 is a conserved regulator of viral late gene expression.Journal of virology · 2014Article
- Herpes simplex virus 1-encoded tegument protein VP16 abrogates the production of beta interferon (IFN) by inhibiting NF-κB activation and blocking IFN regulatory factor 3 to recruit its coactivator CBP.Journal of virology · 2013Article
- Inhibition of Indoleamine-2,3-dioxygenase (IDO) in Glioblastoma Cells by Oncolytic Herpes Simplex Virus.Advances in virology · 2012Article
- Varicella-zoster virus immediate-early protein ORF61 abrogates the IRF3-mediated innate immune response through degradation of activated IRF3.Journal of virology · 2011Article
- The herpes simplex virus immediate-early ubiquitin ligase ICP0 induces degradation of the ICP0 repressor protein E2FBP1.Journal of virology · 2011Article
- HSV-1 ICP0: paving the way for viral replication.Future virology · 2011Article
- Human cytomegalovirus IE1 protein elicits a type II interferon-like host cell response that depends on activated STAT1 but not interferon-γ.PLoS pathogens · 2011Article
- Viral takeover of the host ubiquitin system.Frontiers in microbiology · 2011Article
- Cellular localization of the herpes simplex virus ICP0 protein dictates its ability to block IRF3-mediated innate immune responses.PloS one · 2010Article
- Depletion of CoREST does not improve the replication of ICP0 null mutant herpes simplex virus type 1.Journal of virology · 2010Article
- Comparison of the biological and biochemical activities of several members of the alphaherpesvirus ICP0 family of proteins.Journal of virology · 2010Article
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Several independent lines of evidence indicate that interferon-mediated innate responses are involved in controlling herpes simplex virus type 1 (HSV-1) infection and that the viral immediate-early regulatory protein ICP0 augments HSV-1 replication in interferon-treated cells. However, this is a complex situation in which the experimental outcome is determined by the choice of multiplicity of infection and cell type and by whether cultured cells or animal models are used. It is now known that neither STAT1 nor interferon regulatory factor 3 (IRF-3) play essential roles in the replication defect of ICP0-null mutant HSV-1 in cultured cells. This study set out to investigate the specific role of ICP0 in HSV-1 resistance to the interferon defense. We have used a cell line in which ICP0 expression can be induced at levels similar to those during the early stages of a normal infection to determine whether ICP0 by itself can interfere with interferon or IRF-3-dependent signaling and whether ICP0 enables the virus to circumvent the effects of interferon-stimulated genes (ISGs). We found that the presence of ICP0 was unable to compromise ISG induction by either interferon or double-stranded RNA. On the other hand, ICP0 preexpression reduced but did not eliminate the inhibitory effects of ISGs on HSV-1 infection, with the extent of the relief being highly dependent on multiplicity of infection. The results are discussed in terms of the relationships between ICP0 and intrinsic and innate antiviral resistance mechanisms.
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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.