ArticleRetrovirology2018
A CRISPR screen for factors regulating SAMHD1 degradation identifies IFITMs as potent inhibitors of lentiviral particle delivery.
Article in Retrovirology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
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- Progress in Pseudotyping Lentiviral Vectors Towards Cell-Specific Gene Delivery In Vivo.Viruses · 2025Review
- Genome-aware annotation of CRISPR guides validates targets in variant cell lines and enhances discovery in screens.Genome medicine · 2024Article
- Human trophoblast stem cells restrict human cytomegalovirus replication.Journal of virology · 2024Article
- Interferon inhibits a model RNA virus via a limited set of inducible effector genes.EMBO reports · 2023Article
- Pseudotyped lentiviral vectors: Ready for translation into targeted cancer gene therapy?Genes & diseases · 2023Review
- A modular CRISPR screen identifies individual and combination pathways contributing to HIV-1 latency.PLoS pathogens · 2023Article
- Identification of DAXX as a restriction factor of SARS-CoV-2 through a CRISPR/Cas9 screen.Nature communications · 2022Article
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- Grouper Interferon-Induced Transmembrane Protein 1 Inhibits Iridovirus and Nodavirus Replication by Regulating Virus Entry and Host Lipid Metabolism.Frontiers in immunology · 2021Article
- Review
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- Analysis of IFITM-IFITM Interactions by a Flow Cytometry-Based FRET Assay.International journal of molecular sciences · 2019Article
- A virus-packageable CRISPR screen identifies host factors mediating interferon inhibition of HIV.eLife · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The InterFeron Induced TransMembrane (IFITM) proteins are interferon stimulated genes that restrict many viruses, including HIV-1. SAMHD1 is another restriction factor blocking replication of HIV-1 and other viruses. Some lentiviruses evolved Vpx/Vpr proteins to degrade SAMHD1. However, this viral antagonism can be perturbed by host mechanisms: a recent study showed that in interferon (IFN) treated THP1 cells, Vpx is unable to degrade SAMHD1. In the present work, we designed an Interferon Stimulated Genes (ISGs)-targeted CRISPR knockout screen in order to identify ISGs regulating this phenotype. We found that IFITM proteins contribute to the IFNα-mediated protection of SAMHD1 by blocking VSV-G-mediated entry of the lentiviral particles delivering Vpx. Consistent with this, IFNα treatment and IFITM expression had no effect when the A-MLV envelope was used for pseudotyping. Using an assay measuring viral entry, we show that IFNα and IFITMs directly block the delivery of Vpx into cells by inhibiting VSV-G viral fusion. Strikingly, the VSV-G envelope was significantly more sensitive to this IFNα entry block and to IFITMs than HIV-1's natural envelope. This highlights important differences between VSV-G pseudotyped and wild-type HIV-1, in particular relative to the pathways they use for viral entry, suggesting that HIV-1 may have evolved to escape restriction factors blocking entry.
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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.