ArticleJournal of virology2012
Protruding domain of capsid protein is necessary and sufficient to determine murine norovirus replication and pathogenesis in vivo.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
84 citing papers in PubMed, 109 citations in OpenAlex.
- Diverse infections transcriptionally reprogram the intestinal epithelium and epithelial-immune cell interactions.Nature immunology · 2026Article
- Article
- IgA is necessary and sufficient to prevent norovirus infection in mice.Science translational medicine · 2026Article
- A single amino acid mutation in norovirus NS4 promotes viral spread.Journal of 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
- Trim7 does not have a role in the restriction of murine norovirus infectionJournal of virology · 2025Article
- Norovirus co-opts NINJ1 for selective protein secretion.Science advances · 2025Article
- Conformational Flexibility in Capsids Encoded by theViruses · 2024Review
- Evaluating diurnal rhythms of host responses to enteric norovirus infection in mouse models.Immunometabolism (Cobham, Surrey) · 2024Article
- HDAC3 integrates TGF-β and microbial cues to program tuft cell biogenesis and diurnal rhythms in mucosal immune surveillance.Science immunology · 2024Article
- HOIL1 mediates MDA5 activation through ubiquitination of LGP2.bioRxiv : the preprint server for biology · 2024Article
- Oxidative Stress Markers and Histopathological Changes in Selected Organs of Mice Infected with Murine Norovirus 1 (MNV-1).International journal of molecular sciences · 2024Article
- Intestinal tuft cell immune privilege enables norovirus persistence.Science immunology · 2024Article
- Amino acid substitutions in norovirus VP1 dictate host dissemination via variations in cellular attachment.Journal of virology · 2023Article
- IFN-λ derived from nonsusceptible enterocytes acts on tuft cells to limit persistent norovirus.Science advances · 2023Article
- Infection of neonatal mice with the murine norovirus strain WU23 is a robust model to study norovirus pathogenesis.Lab animal · 2023Article
- Age-associated features of norovirus infection analysed in mice.Nature microbiology · 2023Article
- Genetic mapping revealsScience immunology · 2023Article
- Recent insights into reverse genetics of norovirus.Virus research · 2023Review
24 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 2 institutions in 1 country.
Funding
Abstract
Human noroviruses (HuNoVs) are the major cause of epidemic, nonbacterial gastroenteritis worldwide. Due to the lack of a tractable model system and the inability to grow HuNoVs in cell culture, factors required for the norovirus (NoV) life cycle and pathogenesis in the host remain largely unknown. The discovery of murine norovirus (MNV) and the development of reverse-genetics systems for this virus provide an opportunity to study these aspects of NoV infection in vitro and in vivo. Previous studies identified a single amino acid at residue 296 in the protruding (P) domain of the capsid protein that is responsible for determining the virulence of the MNV clone MNV1.CW1 in 12956/SvEv background STAT1-deficient (STAT1(-/-)) mice. In this report, we identified and characterized another determinant of lethality in the P domain that is necessary and sufficient to determine the replication and pathogenesis of the MNV clones MNV1.CW3 and CR6.STL1 in C57BL/6 background STAT1(-/-) mice. Furthermore, we describe how the role of residue 296 in MNV virulence differs between STAT1(-/-) mouse strains. We also describe potential interactions between subdomains of the P domain, as well as between other virus elements, which facilitate recovery of MNV using a reverse-genetics system.
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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.