ArticlePLoS pathogens2010
Murine gamma-herpesvirus 68 hijacks MAVS and IKKbeta to initiate lytic replication.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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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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
41 citing papers in PubMed, 59 citations in OpenAlex.
- Herpesviruses hijack ISGylation to promote viral capsid assembly.Science advances · 2026Article
- Apolipoprotein E selectively supports gammaherpesvirus replication in macrophages.Journal of virology · 2025Article
- Hijacking of nucleotide biosynthesis and deamidation-mediated glycolysis by an oncogenic herpesvirus.Nature communications · 2024Article
- The Role of the Nuclear Factor-Kappa B (NF-κB) Pathway in SARS-CoV-2 Infection.Pathogens (Basel, Switzerland) · 2024Review
- Lytic Replication and Reactivation from B Cells Is Not Required for Establishing or Maintaining Gammaherpesvirus LatencyJournal of virology · 2022Article
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- Article
- Conserved Herpesvirus Kinase ORF36 Activates B2 Retrotransposons during Murine Gammaherpesvirus Infection.Journal of virology · 2020Article
- Deamidation Shunts RelA from Mediating Inflammation to Aerobic Glycolysis.Cell metabolism · 2020Article
- A role of hypoxia-inducible factor 1 alpha in Murine Gammaherpesvirus 68 (MHV68) lytic replication and reactivation from latency.PLoS pathogens · 2019Article
- Epstein-Barr Virus and Innate Immunity: Friends or Foes?Microorganisms · 2019Review
- Review
- Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression.PLoS pathogens · 2018Article
- Viral FGARAT ORF75A promotes early events in lytic infection and gammaherpesvirus pathogenesis in mice.PLoS pathogens · 2018Article
- Recognizing the SINEs of Infection: Regulation of Retrotransposon Expression and Modulation of Host Cell Processes.Viruses · 2017Review
- Host Noncoding Retrotransposons Induced by DNA Viruses: a SINE of Infection?Journal of virology · 2017Review
- Genome-wide mapping of infection-induced SINE RNAs reveals a role in selective mRNA export.Nucleic acids research · 2017Article
- RTA Occupancy of the Origin of Lytic Replication during Murine Gammaherpesvirus 68 Reactivation from B Cell Latency.Pathogens (Basel, Switzerland) · 2017Article
- A Viral Deamidase Targets the Helicase Domain of RIG-I to Block RNA-Induced Activation.Cell host & microbe · 2016Article
- IκB Kinase ε Is an NFATc1 Kinase that Inhibits T Cell Immune Response.Cell reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Upon viral infection, the mitochondrial antiviral signaling (MAVS)-IKKbeta pathway is activated to restrict viral replication. Manipulation of immune signaling events by pathogens has been an outstanding theme of host-pathogen interaction. Here we report that the loss of MAVS or IKKbeta impaired the lytic replication of gamma-herpesvirus 68 (gammaHV68), a model herpesvirus for human Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus. gammaHV68 infection activated IKKbeta in a MAVS-dependent manner; however, IKKbeta phosphorylated and promoted the transcriptional activation of the gammaHV68 replication and transcription activator (RTA). Mutational analyses identified IKKbeta phosphorylation sites, through which RTA-mediated transcription was increased by IKKbeta, within the transactivation domain of RTA. Moreover, the lytic replication of recombinant gammaHV68 carrying mutations within the IKKbeta phosphorylation sites was greatly impaired. These findings support the conclusion that gammaHV68 hijacks the antiviral MAVS-IKKbeta pathway to promote viral transcription and lytic infection, representing an example whereby viral replication is coupled to host immune activation.
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Identifiers
What OpenQuestion holds
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.