ArticleJournal of virology2018
Cleavage of the C-Terminal Fragment of Reovirus μ1 Is Required for Optimal Infectivity.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 13 citations in OpenAlex.
- Spatiotemporal coordination of reovirus peripheral core replication to perinuclear whole virus assembly.PLoS pathogens · 2025Article
- The M2 Gene Is a Determinant of Reovirus-Induced Myocarditis.Journal of virology · 2022Article
- Selection and Characterization of a Reovirus Mutant with Increased Thermostability.Journal of virology · 2019Article
- Components of the Reovirus Capsid Differentially Contribute to Stability.Journal of virology · 2019Article
- Protein Mismatches Caused by Reassortment Influence Functions of the Reovirus Capsid.Journal of virology · 2018Article
- Molecular and Antigenic Characterization of Piscine orthoreovirus (PRV) from Rainbow Trout (Oncorhynchus mykiss).Viruses · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The mammalian orthoreovirus (reovirus) outer capsid, which is composed of 200 μ1/σ3 heterohexamers and a maximum of 12 σ1 trimers, contains all of the proteins that are necessary for attaching to and entering host cells. Following attachment, reovirus is internalized by receptor-mediated endocytosis and acid-dependent cathepsin proteases degrade the σ3 protein. This process generates a metastable intermediate, called infectious subviral particle (ISVP), in which the μ1 membrane penetration protein is exposed. ISVPs undergo a second structural rearrangement to deposit the genome-containing core into the host cytoplasm. The conformationally altered particle is called ISVP*. ISVP-to-ISVP* conversion culminates in the release of μ1 N- and C-terminal fragments, μ1N and Φ, respectively. Released μ1N is thought to facilitate core delivery by generating size-selective pores within the endosomal membrane, whereas the precise role of Φ, particularly in the context of viral entry, is undefined. In this report, we characterize a recombinant reovirus that fails to cleave Φ from μ1
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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.