ArticleJournal of virology2004
Cells lacking NF-kappaB or in which NF-kappaB is not activated vary with respect to ability to sustain herpes simplex virus 1 replication and are not susceptible to apoptosis induced by a replication-incompetent mutant virus.
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 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Host-directed clearance of nuclear tegument U14 terminates NF-κB signaling and supports HHV-6A replication.PLoS pathogens · 2026Article
- The producer cell type of HSV-1 alters the proteomic contents and infectious capacity of virions.Journal of virology · 2025Article
- Pseudorabies Virus Infection Triggers NF-κB Activation via the DNA Damage Response but Actively Inhibits NF-κB-Dependent Gene Expression.Journal of virology · 2021Article
- Autophagy receptors as viral targets.Cellular & molecular biology letters · 2021Review
- Pseudorabies Virus Infection of Epithelial Cells Leads to Persistent but Aberrant Activation of the NF-κB Pathway, Inhibiting Hallmark NF-κB-Induced Proinflammatory Gene Expression.Journal of virology · 2020Article
- The ICP0 Protein of Herpes Simplex Virus 1 (HSV-1) Downregulates Major Autophagy Adaptor Proteins Sequestosome 1 and Optineurin during the Early Stages of HSV-1 Infection.Journal of virology · 2019Article
- HSV-1-induced activation of NF-κB protects U937 monocytic cells against both virus replication and apoptosis.Cell death & disease · 2016Article
- miR-H28 and miR-H29 expressed late in productive infection are exported and restrict HSV-1 replication and spread in recipient cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- HSV-1 degrades, stabilizes, requires, or is stung by STING depending on ICP0, the US3 protein kinase, and cell derivation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Type I interferon and NF-κB activation elicited by herpes simplex virus gH/gL via αvβ3 integrin in epithelial and neuronal cell lines.Journal of virology · 2013Article
- The virion host shutoff RNase plays a key role in blocking the activation of protein kinase R in cells infected with herpes simplex virus 1.Journal of virology · 2013Article
- Classical swine fever virus failed to activate nuclear factor-kappa b signaling pathway both in vitro and in vivo.Virology journal · 2012Article
- αvβ3-integrin is a major sensor and activator of innate immunity to herpes simplex virus-1.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- The TIM and TAM families of phosphatidylserine receptors mediate dengue virus entry.Cell host & microbe · 2012Article
- Herpes simplex virus glycoproteins gH/gL and gB bind Toll-like receptor 2, and soluble gH/gL is sufficient to activate NF-κB.Journal of virology · 2012Article
- Article
- A limited innate immune response is induced by a replication-defective herpes simplex virus vector following delivery to the murine central nervous system.Journal of neurovirology · 2009Article
- Cross-regulation between herpesviruses and the TNF superfamily members.Nature reviews. Immunology · 2008Review
- Detection and diagnosis of herpes simplex virus infection in adults with acute liver failure.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2008Article
- Herpes simplex virus type 1 ICP4 deletion mutant virus d120 infection failed to induce apoptosis in nerve growth factor-differentiated PC12 cells.Journal of neurovirology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Earlier we reported that NF-kappaB is activated by protein kinase R (PKR) in herpes simplex virus 1-infected cells. Here we report that in PKR(-/-) cells the yields of wild-type virus are 10-fold higher than in PKR(+/+) cells. In cells lacking NF-kappaB p50 (nfkb1), p65 (relA), or both p50 and p65, the yields of virus were reduced 10-fold. Neither wild-type nor mutant cells undergo apoptosis following infection with wild-type virus. Whereas PKR(+/+) and NF-kappaB(+/+) control cell lines undergo apoptosis induced by the d120 (Deltaalpha4) mutant of HSV-1, the mutant PKR(-/-) and NF-kappaB(-/-) cell lines were resistant. The evidence suggests that the stress-induced apoptosis resulting from d120 infection requires activation of NF-kappaB and that this proapoptotic pathway is blocked in cells in which NF-kappaB is not activated or absent. Activation of NF-kappaB in the course of viral infection may have dual roles of attempting to curtain viral replication by rendering the cell susceptible to apoptosis induced by the virus and by inducing the synthesis of proteins that enhance 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.