ArticlePLoS pathogens2022
ISG15 deficiency restricts HIV-1 infection.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 26 citations in OpenAlex.
- Hijacking the Host: Post-Translational Modifications as Molecular Switches in HIV Persistence and Immune Evasion.Journal of medical virology · 2026Review
- Three immunoregulatory signatures define non-productive HIV infection in stem cell memory CD4Nature communications · 2026Article
- Three immunoregulatory signatures define non-productive HIV infection in CD4bioRxiv : the preprint server for biology · 2026Article
- Interferon-induced protein ISG15 in the central nervous system, quo vadis?FEBS letters · 2025Review
- Aberrant DNA methylation of genes regulating CD4+ T cell HIV-1 reservoir in women with HIV.Clinical and translational medicine · 2025Article
- Review
- The intestinal interferon system and specialized enterocytes as putative drivers of HIV latency.Frontiers in immunology · 2025Review
- A multi-trait epigenome-wide association study identified DNA methylation signature of inflammation among men with HIV.Clinical epigenetics · 2024Article
- Current State of Therapeutics for HTLV-1.Viruses · 2024Review
- NKG2C and NKG2A coexpression defines a highly functional antiviral NK population in spontaneous HIV control.JCI insight · 2024Article
- Foot-and-mouth disease virus VP1 degrades YTHDF2 through autophagy to regulate IRF3 activity for viral replication.Autophagy · 2024Article
- A multi-trait epigenome-wide association study identified DNA methylation signature of inflammation among people with HIV.Research square · 2024Article
- Review
- Deep analysis of CD4 T cells in the rhesus CNS during SIV infection.PLoS pathogens · 2023Article
- ISG15: its roles in SARS-CoV-2 and other viral infections.Trends in microbiology · 2023Review
- NOG1 downregulates type I interferon production by targeting phosphorylated interferon regulatory factor 3.PLoS pathogens · 2023Article
- FEZ1 Plays Dual Roles in Early HIV-1 Infection by Independently Regulating Capsid Transport and Host Interferon-Stimulated Gene Expression.Journal of virology · 2023Article
- The emerging role of E3 ubiquitin ligase RNF213 as an antimicrobial host determinant.Frontiers in cellular and infection microbiology · 2023Review
- Genetic polymorphisms in thePeerJ · 2023Article
- Targeted Nanocarrier Delivery of RNA Therapeutics to Control HIV Infection.Pharmaceutics · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Type I interferons (IFN-Is) are a group of potent inflammatory and antiviral cytokines. They induce IFN stimulated genes (ISGs), which act as proinflammatory mediators, antiviral effectors, and negative regulators of the IFN-I signaling cascade itself. One such regulator is interferon stimulated gene 15 (ISG15). Humans with complete ISG15 deficiency express persistently elevated levels of ISGs, and consequently, exhibit broad spectrum resistance to viral infection. Here, we demonstrate that IFN-I primed fibroblasts derived from ISG15-deficient individuals are more resistant to infection with single-cycle HIV-1 compared to healthy control fibroblasts. Complementation with both wild-type (WT) ISG15 and ISG15ΔGG (incapable of ISGylation while retaining negative regulation activity) was sufficient to reverse this phenotype, restoring susceptibility to infection to levels comparable to WT cells. Furthermore, CRISPR-edited ISG15ko primary CD4+ T cells were less susceptible to HIV-1 infection compared to cells treated with non-targeting controls. Transcriptome analysis of these CRISPR-edited ISG15ko primary CD4+ T cells recapitulated the ISG signatures of ISG15 deficient patients. Taken together, we document that the increased broad-spectrum viral resistance in ISG15-deficiency also extends to HIV-1 and is driven by a combination of T-cell-specific ISGs, with both known and unknown functions, predicted to target HIV-1 replication at multiple steps.
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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.