ArticleThe Journal of cell biology2022
Viral protein engagement of GBF1 induces host cell vulnerability through synthetic lethality.
Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Breaking barriers: Respiratory viral strategies targeting the host's nuclear pore complex and nuclear transport pathways.Molecular biology of the cell · 2026Review
- Exploiting host kinases to combat dengue virus infection and disease.Antiviral research · 2025Review
- Predicting host-based, synthetic lethal antiviral targets from omics data.NAR molecular medicine · 2024Article
- Predicting host-based, synthetic lethal antiviral targets from omics data.bioRxiv : the preprint server for biology · 2023Article
- Discovery of host-directed modulators of virus infection by probing the SARS-CoV-2-host protein-protein interaction network.Briefings in bioinformatics · 2022Article
- Article
- Synthetic lethality-based prediction of anti-SARS-CoV-2 targets.bioRxiv : the preprint server for biology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Viruses co-opt host proteins to carry out their lifecycle. Repurposed host proteins may thus become functionally compromised; a situation analogous to a loss-of-function mutation. We term such host proteins as viral-induced hypomorphs. Cells bearing cancer driver loss-of-function mutations have successfully been targeted with drugs perturbing proteins encoded by the synthetic lethal (SL) partners of cancer-specific mutations. Similarly, SL interactions of viral-induced hypomorphs can potentially be targeted as host-based antiviral therapeutics. Here, we use GBF1, which supports the infection of many RNA viruses, as a proof-of-concept. GBF1 becomes a hypomorph upon interaction with the poliovirus protein 3A. Screening for SL partners of GBF1 revealed ARF1 as the top hit, disruption of which selectively killed cells that synthesize 3A alone or in the context of a poliovirus replicon. Thus, viral protein interactions can induce hypomorphs that render host cells selectively vulnerable to perturbations that leave uninfected cells otherwise unscathed. Exploiting viral-induced vulnerabilities could lead to broad-spectrum antivirals for many viruses, including SARS-CoV-2.
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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.