ArticleJournal of virology2013
Inhibition of the host translation shutoff response by herpes simplex virus 1 triggers nuclear envelope-derived autophagy.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 31 citations in OpenAlex.
- Caspase-8 is required for HSV-1-induced apoptosis and promotes effective viral particle release via autophagy inhibition.Cell death and differentiation · 2023Article
- Interplay between Autophagy and Herpes Simplex Virus Type 1: ICP34.5, One of the Main Actors.International journal of molecular sciences · 2022Review
- Review
- Article
- Nonstructural protein 6 of porcine epidemic diarrhea virus induces autophagy to promote viral replication via the PI3K/Akt/mTOR axis.Veterinary microbiology · 2020Article
- Herpes Simplex Virus: The Hostile Guest That Takes Over Your Home.Frontiers in microbiology · 2020Review
- Seeking Closure: How Do Herpesviruses Recruit the Cellular ESCRT Apparatus?Journal of virology · 2019Review
- Autophagic degradation of lamins facilitates the nuclear egress of herpes simplex virus type 1.The Journal of cell biology · 2019Article
- Dendritic cells mature to resist lamin degradation and herpes virus release.The Journal of cell biology · 2019Article
- Programmed cell death: the battlefield between the host and alpha-herpesviruses and a potential avenue for cancer treatment.Oncotarget · 2018Review
- Therapeutic Opportunities in Eukaryotic Translation.Cold Spring Harbor perspectives in biology · 2018Review
- Autophagy-Virus Interplay: From Cell Biology to Human Disease.Frontiers in cell and developmental biology · 2018Article
- Review
- Exocytosis of Varicella-Zoster Virus Virions Involves a Convergence of Endosomal and Autophagy Pathways.Journal of virology · 2016Article
- The regulation of autophagy during exercise in skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Review
- Review
- Degradation-mediated protein quality control at the inner nuclear membrane.Nucleus (Austin, Tex.) · 2016Review
- HSV targeting of the host phosphatase PP1α is required for disseminated disease in the neonate and contributes to pathogenesis in the brain.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Hippuristanol - A potent steroid inhibitor of eukaryotic initiation factor 4A.Translation (Austin, Tex.)Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Macroautophagy is a cellular pathway that degrades intracellular pathogens and contributes to antigen presentation. Herpes simplex virus 1 (HSV-1) infection triggers both macroautophagy and an additional form of autophagy that uses the nuclear envelope as a source of membrane. The present study constitutes the first in-depth analysis of nuclear envelope-derived autophagy (NEDA). We established LC3a as a marker that allowed us to distinguish between NEDA and macroautophagy in both immunofluorescence and flow cytometry. NEDA was observed in many different cell types, indicating that it is a general response to HSV-1 infection. This autophagic pathway is known to depend on the viral protein γ34.5, which can inhibit macroautophagy via binding to beclin-1. Using mutant viruses, we were able to show that binding of beclin-1 by γ34.5 had no effect on NEDA, demonstrating that NEDA is regulated differently than macroautophagy. Instead, NEDA was triggered in response to γ34.5 binding to protein phosphatase 1α, an interaction used by the virus to prevent host cells from shutting off protein translation. NEDA was not triggered when late viral protein production was inhibited with acyclovir or hippuristanol, indicating that the accumulation of these proteins might stress infected cells. Interestingly, expression of the late viral protein gH was sufficient to rescue NEDA in the context of infection with a virus that otherwise does not support strong late viral protein expression. We argue that NEDA is a cellular stress response triggered late during HSV-1 infection and might compensate for the viral alteration of the macroautophagic response.
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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.