ArticleJournal of virology2010
The interferon-induced gene ISG15 blocks retrovirus release from cells late in the budding process.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
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
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- BST2/Tetherin is constitutively expressed on human thymocytes with the phenotype and function of Treg cells.European journal of immunology · 2015Trial
- Therapeutic modulation of HIV-1 using miRNAs and lncRNAs: from bench to bedside.Virology journal · 2026Review
- Single cell RNA transcriptome response to fentanyl use in persons with HIV infection.Scientific reports · 2026Article
- Persistent type I interferon signaling within the brain of people with HIV on ART with cognitive impairment.PLoS pathogens · 2025Article
- Review
- Interferons in HIV-1 infection: mechanisms, antiviral potentials, and therapeutic challenges.Frontiers in immunology · 2025Review
- The emerging roles of ubiquitin-like modifications in regulating HIV replication and host defense.Frontiers in cellular and infection microbiology · 2025Review
- Review
- Macrophages treated with interferons induce different responses in lymphocytes via extracellular vesicles.iScience · 2024Article
- Review
- ISG15-LFA1 interactions in latent HIV clearance: mechanistic implications in designing antiviral therapies.Frontiers in cell and developmental biology · 2024Article
- Interaction of TSG101 with the PTAP Motif in Distinct Locations of Gag Determines the Incorporation of HTLV-1 Env into the Retroviral Virion.International journal of molecular sciences · 2023Article
- Several cell-intrinsic effectors drive type I interferon-mediated restriction of HIV-1 in primary CD4Cell reports · 2023Article
- Several cell-intrinsic effectors drive type I interferon-mediated restriction of HIV-1 in primary CD4bioRxiv : the preprint server for biology · 2023Article
- The HIV Restriction Factor Profile in the Brain Is Associated with the Clinical Status and Viral Quantities.Viruses · 2023Article
- ISG15 deficiency restricts HIV-1 infection.PLoS pathogens · 2022Article
- YAP ISGylation increases its stability and promotes its positive regulation on PPP by stimulating 6PGL transcription.Cell death discovery · 2022Article
- ISG15 and ISGylation in Human Diseases.Cells · 2022Review
- The diverse roles of miRNAs in HIV pathogenesis: Current understanding and future perspectives.Frontiers in immunology · 2022Review
41 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
4 authors at 1 institution in 1 country.
Funding
Abstract
The release of retroviruses from cells requires ubiquitination of Gag and recruitment of cellular proteins involved in endosome sorting, including the ESCRT-III proteins and the Vps4 ATPase. In response to infection, cells have evolved an interferon-induced mechanism to block virus replication through expression of the interferon-stimulated gene 15 (ISG15), a dimer homologue of ubiquitin, which interferes with ubiquitin pathways in cells. Previously, it has been reported that ISG15 expression inhibited the E3 ubiquitin ligase, Nedd4, and prevented association of the ESCRT-I protein Tsg101 with human immunodeficiency virus type 1 (HIV-1) Gag. The budding of avian sarcoma leukosis virus and HIV-1 Gag virus-like particles containing L-domain mutations can be rescued by fusion to ESCRT proteins, which cause entry into the budding pathway beyond these early steps. The release of these fusions from cells was susceptible to inhibition by ISG15, indicating that there was a block late in the budding process. We now demonstrate that the Vps4 protein does not associate with the avian sarcoma leukosis virus or the HIV-1 budding complexes when ISG15 is expressed. This is caused by a loss in interaction between Vps4 with its coactivator protein LIP5 needed to promote the formation of the ESCRT-III-Vps4 double-hexamer complex required for membrane scission and virus release. The inability of LIP5 to interact with Vps4 is the probable result of ISG15 conjugation to the ESCRT-III protein, CHMP5, which regulates the availability of LIP5. Thus, there appear to be multiple levels of ISG15-induced inhibition acting at different stages of the virus release process.
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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.