ArticleJournal of virology2004
Efficient replication by herpes simplex virus type 1 involves activation of the IkappaB kinase-IkappaB-p65 pathway.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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.
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Who cites it
67 citing papers in PubMed, 121 citations in OpenAlex.
- Article
- Neural-Cell-Intrinsic NF-κB Signaling Enhances Reovirus Virulence.Journal of virology · 2023Article
- Herpes simplex virus type I glycoprotein L evades host antiviral innate immunity by abrogating the nuclear translocation of phosphorylated NF-κB sub-unit p65.Frontiers in microbiology · 2023Article
- Inhibitory activity and mechanism of silver nanoparticles against herpes simplex virus type 1.Archives of virology · 2022Article
- Article
- Porcine circovirus type 3 capsid protein induces NF-κB activation and upregulates pro-inflammatory cytokine expression in HEK-293T cells.Archives of virology · 2021Article
- Wogonin inhibits in vitro herpes simplex virus type 1 and 2 infection by modulating cellular NF-κB and MAPK pathways.BMC microbiology · 2020Article
- MG132 exerts anti-viral activity against HSV-1 by overcoming virus-mediated suppression of the ERK signaling pathway.Scientific reports · 2020Article
- Herpes Simplex Virus 1 UL2 Inhibits the TNF-α-Mediated NF-κB Activity by Interacting With p65/p50.Frontiers in immunology · 2020Article
- Effect of Loss-of-function of the Herpes Simplex Virus-1 microRNA H6-5p on Virus Replication.Virologica Sinica · 2019Article
- NF-κB-Dependent Production of ROS and Restriction of HSV-1 Infection in U937 Monocytic Cells.Viruses · 2019Article
- HSV-1\EGFP stimulates miR-146a expression in a NF-κB-dependent manner in monocytic THP-1 cells.Scientific reports · 2019Article
- Bowman‒Birk Inhibitor Suppresses Herpes Simplex Virus Type 2 Infection of Human Cervical Epithelial Cells.Viruses · 2018Article
- Herpes Simplex Virus 1 Dramatically Alters Loading and Positioning of RNA Polymerase II on Host Genes Early in Infection.Journal of virology · 2018Article
- Suppression of Oncolytic Adenovirus-Mediated Hepatotoxicity by Liver-Specific Inhibition of NF-κB.Molecular therapy oncolytics · 2017Article
- BX-795 inhibits HSV-1 and HSV-2 replication by blocking the JNK/p38 pathways without interfering with PDK1 activity in host cells.Acta pharmacologica Sinica · 2017Article
- HSV-1-induced activation of NF-κB protects U937 monocytic cells against both virus replication and apoptosis.Cell death & disease · 2016Article
- Oncolytic virotherapy for urological cancers.Nature reviews. Urology · 2016Review
- NF-κB promotes leaky expression of adenovirus genes in a replication-incompetent adenovirus vector.Scientific reports · 2016Article
- Non-Canonical Role of IKKα in the Regulation of STAT1 Phosphorylation in Antiviral Signaling.PloS one · 2016Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Infection by herpes simplex virus type 1 (HSV-1) induces a persistent nuclear translocation of NFkappaB. To identify upstream effectors of NFkappaB and their effect on virus replication, we employed mouse embryo fibroblast (MEF)-derived cell lines with deletions of either IKK1 or IKK2, the catalytic subunits of the IkappaB kinase (IKK) complex. Infected MEFs were assayed for virus yield, loss of IkappaBalpha, nuclear translocation of p65, and NFkappaB DNA-binding activity. Absence of either IKK1 or IKK2 resulted in an 86 to 94% loss of virus yield compared to that of normal MEFs, little or no loss of IkappaBalpha, and greatly reduced NFkappaB nuclear translocation. Consistent with reduced virus yield, accumulation of the late proteins VP16 and gC was severely depressed. Infection of normal MEFs, Hep2, or A549 cells with an adenovirus vector expressing a dominant-negative (DN) IkappaBalpha, followed by superinfection with HSV, resulted in a 98% drop in virus yield. These results indicate that the IKK-IkappaB-p65 pathway activates NFkappaB after virus infection. Analysis of NFkappaB activation and virus replication in control and double-stranded RNA-activated protein kinase-null MEFs indicated that this kinase plays no role in the NFkappaB activation pathway. Finally, in cells where NFkappaB was blocked because of DNIkappaB expression, HSV failed to suppress two markers of apoptosis, cell surface Annexin V staining and PARP cleavage. These results support a model in which activation of NFkappaB promotes efficient replication by HSV, at least in part by suppressing a host innate response to virus infection.
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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.