ArticlePLoS pathogens2019
Caspase-mediated cleavage of murine norovirus NS1/2 potentiates apoptosis and is required for persistent infection of intestinal epithelial cells.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Astroviruses use mucus secretion as a novel form of viral egress.PLoS pathogens · 2026Article
- Virus-Induced Intestinal Barrier Injury: Mechanisms and Therapeutic Perspectives.Veterinary sciences · 2026Review
- The MNV-1 protease-polymerase precursor cleaves a novel site in the NS1-2 protein.The Journal of general virology · 2026Article
- Type I and III interferons synergize with TNF to promote virally-triggered damage to the intestinal epithelium.bioRxiv : the preprint server for biology · 2026Article
- TRIM47 inhibits murine norovirus replication in a strain-dependent manner.Journal of virology · 2025Article
- Norovirus co-opts NINJ1 for selective protein secretion.Science advances · 2025Article
- Norovirus-mediated translation repression promotes macrophage cell death.PLoS pathogens · 2024Article
- The Disorderly Nature of Caliciviruses.Viruses · 2024Review
- Interferon regulatory factor 6 (IRF6) determines intestinal epithelial cell development and immunity.Mucosal immunology · 2024Article
- Norovirus NS1/2 protein increases glutaminolysis for efficient viral replication.PLoS pathogens · 2024Article
- Intestinal tuft cell immune privilege enables norovirus persistence.Science immunology · 2024Article
- Thrombin cleavage of the hepatitis E virus polyprotein at multiple conserved locations is required for genome replication.PLoS pathogens · 2023Article
- Article
- Recent insights into reverse genetics of norovirus.Virus research · 2023Review
- Tuft-cell-intrinsic and -extrinsic mediators of norovirus tropism regulate viral immunity.Cell reports · 2022Article
- Environmentally-triggered contraction of the norovirus virion determines diarrheagenic potential.Frontiers in immunology · 2022Article
- Lagovirus Non-structural Protein p23: A Putative Viroporin That Interacts With Heat Shock Proteins and Uses a Disulfide Bond for Dimerization.Frontiers in microbiology · 2022Article
- Interferon responses to norovirus infections: current and future perspectives.The Journal of general virology · 2021Review
- Egress of non-enveloped enteric RNA viruses.The Journal of general virology · 2021Review
- CD300lf Conditional Knockout Mouse Reveals Strain-Specific Cellular Tropism of Murine Norovirus.Journal of virology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Human norovirus (HNoV) is the leading cause of acute gastroenteritis and is spread by fecal shedding that can often persist for weeks to months after the resolution of symptoms. Elimination of persistent viral reservoirs has the potential to prevent outbreaks. Similar to HNoV, murine norovirus (MNV) is spread by persistent shedding in the feces and provides a tractable model to study molecular mechanisms of enteric persistence. Previous studies have identified non-structural protein 1 (NS1) from the persistent MNV strain CR6 as critical for persistent infection in intestinal epithelial cells (IECs), but its mechanism of action remains unclear. We now find that the function of CR6 NS1 is regulated by apoptotic caspase cleavage. Following induction of apoptosis in infected cells, caspases cleave the precursor NS1/2 protein, and this cleavage is prevented by mutation of caspase target motifs. These mutations profoundly compromise CR6 infection of IECs and persistence in the intestine. Conversely, NS1/2 cleavage is not strictly required for acute replication in extra-intestinal tissues or in cultured myeloid cells, suggesting an IEC-centric role. Intriguingly, we find that caspase cleavage of CR6 NS1/2 reciprocally promotes caspase activity, potentiates cell death, and amplifies spread among cultured IEC monolayers. Together, these data indicate that the function of CR6 NS1 is regulated by apoptotic caspases, and suggest that apoptotic cell death enables epithelial spread and persistent shedding.
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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.