ArticleJournal of virology2006
Functional genomic analysis of herpes simplex virus type 1 counteraction of the host innate response.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 61 citations in OpenAlex.
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- Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.Nature communications · 2025Article
- Transcriptomics ofMicroorganisms · 2024Article
- Apoptosis and Phagocytosis as Antiviral Mechanisms.Sub-cellular biochemistry · 2023Article
- Interplay between Autophagy and Herpes Simplex Virus Type 1: ICP34.5, One of the Main Actors.International journal of molecular sciences · 2022Review
- Oncolytic Virus Encoding a Master Pro-Inflammatory Cytokine Interleukin 12 in Cancer Immunotherapy.Cells · 2020Review
- Article
- A bimodal switch in global protein translation coupled to eIF4H relocalisation during advancing cell-cell transmission of herpes simplex virus.PLoS pathogens · 2018Article
- Multifunctional viral protein γ34.5 manipulates nucleolar protein NOP53 for optimal viral replication of HSV-1.Cell death & disease · 2018Article
- Functional prediction of differentially expressed lncRNAs in HSV-1 infected human foreskin fibroblasts.Virology journal · 2016Article
- Cellular responses to HSV-1 infection are linked to specific types of alterations in the host transcriptome.Scientific reports · 2016Article
- Role of the DNA Sensor STING in Protection from Lethal Infection following Corneal and Intracerebral Challenge with Herpes Simplex Virus 1.Journal of virology · 2015Article
- Selective recruitment of host factors by HSV-1 replication centers.Dong wu xue yan jiu = Zoological research · 2015Article
- Doxorubicin synergizes with 34.5ENVE to enhance antitumor efficacy against metastatic ovarian cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Up to four distinct polypeptides are produced from the γ34.5 open reading frame of herpes simplex virus 2.Journal of virology · 2014Article
- Recognition of herpes simplex viruses: toll-like receptors and beyond.Journal of molecular biology · 2014Review
- Bugs in the system.Immunological reviews · 2013Review
- Herpes simplex virus 1 infection induces activation and subsequent inhibition of the IFI16 and NLRP3 inflammasomes.Journal of virology · 2013Article
- Permissive and restricted virus infection of murine embryonic stem cells.The Journal of general virology · 2012Article
- HSV-2 inhibits type-I interferon signaling via multiple complementary and compensatory STAT2-associated mechanisms.Virus research · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) mutants lacking the ICP34.5 gene are severely attenuated in mouse models and have a significant growth defect in confluent mouse embryo fibroblasts. Previously, ICP34.5 was demonstrated to have a crucial role in evading the innate immune response to infection by mediating the dephosphorylation of eIF2alpha, a translation initiation factor phosphorylated by PKR during the antiviral response. To further understand the role of ICP34.5 in evasion of the antiviral response, we used transcriptional profiling to examine host cell gene expression in both wild-type and ICP34.5-null virus-infected mouse embryo fibroblasts over a time course of infection. Our study revealed that cells responded to infection within 3 h through PKR-dependent eIF2alpha phosphorylation and that the majority of up-regulated genes at 3 h postinfection were involved in the antiviral response. HSV-1 counters this response through early expression of ICP34.5 and dephosphorylation of eIF2alpha. By 12 h postinfection, the differences between the number and functional classification of genes differentially up- and down-regulated between wild-type and ICP34.5-null virus-infected cells were maximal. Specifically, in wild-type virus-infected cells, the majority of changed genes were involved in metabolic and biosynthetic processes, while in ICP34.5-null virus-infected cells, mostly antiviral genes were up-regulated. Further, ICP34.5-null virus-infected cells produced greater amounts of beta interferon than wild-type virus-infected cells. These results indicate that ICP34.5 expression and function at early times postinfection have a pivotal role in the ability of HSV-1 to gain control of the host cell and maintain an environment for successful viral replication.
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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.