ArticleJournal of virology2006
ICP0 prevents RNase L-independent rRNA cleavage in herpes simplex virus type 1-infected cells.
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 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Article
- Article
- Orchestrated efforts on host network hijacking: Processes governing virus replication.Virulence · 2020Review
- The Race between Host Antiviral Innate Immunity and the Immune Evasion Strategies of Herpes Simplex Virus 1.Microbiology and molecular biology reviews : MMBR · 2020Review
- Impact of Type I Interferon on the Safety and Immunogenicity of an Experimental Live-Attenuated Herpes Simplex Virus 1 Vaccine in Mice.Journal of virology · 2017Article
- Interferons, signal transduction pathways, and the central nervous system.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Foreign RNA induces the degradation of mitochondrial antiviral signaling protein (MAVS): the role of intracellular antiviral factors.PloS one · 2012Article
- Illuminating viral infections in the nervous system.Nature reviews. Immunology · 2011Review
- Interferon regulatory factor 3-dependent pathways are critical for control of herpes simplex virus type 1 central nervous system infection.Journal of virology · 2010Article
- Cellular localization of the herpes simplex virus ICP0 protein dictates its ability to block IRF3-mediated innate immune responses.PloS one · 2010Article
- Article
- Control of herpes simplex virus replication is mediated through an interferon regulatory factor 3-dependent pathway.Journal of virology · 2009Article
- Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling.Virology · 2008Article
- Herpes simplex virus-infected cell protein 0 blocks the silencing of viral DNA by dissociating histone deacetylases from the CoREST-REST complex.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The classical interferon (IFN)-dependent antiviral response to viral infection involves the regulation of IFN-stimulated genes (ISGs), one being the gene encoding cellular endoribonuclease RNase L, which arrests protein synthesis and induces apoptosis by nonspecifically cleaving rRNA. Recently, the herpes simplex virus type 1 (HSV-1) protein ICP0 has been shown to block the induction of ISGs by subverting the IFN pathway upstream of the 2'-5'-oligoadenylate synthetase (OAS)/RNase L pathway. We report that ICP0 also prevents rRNA degradation at late stages of HSV-1 infection, independent of its E3 ubiquitin ligase activity, and that the resultant rRNA degradation is independent of the classical RNase L antiviral pathway. Moreover, the degradation is independent of the viral RNase vhs and is independent of IFN response factor 3. These studies indicate the existence of another, previously unidentified, RNase that is part of the host antiviral response to viral infection.
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Registered trials
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