ArticleJournal of virology2018
Reovirus Neurotropism and Virulence Are Dictated by Sequences in the Head Domain of the Viral Attachment Protein.
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 22 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
22 citing papers in PubMed, 31 citations in OpenAlex.
- Comparative evaluation of oncolytic viruses reveals opposing preferences for glioblastoma subtypes.Molecular therapy. Oncology · 2026Article
- Article
- Enhancing Oncolytic Virus Therapy with Nanomedicine: A Review of Progress, Challenges, and Future Directions in a New Frontier of Cancer Treatment.International journal of nanomedicine · 2026Review
- Review
- Sialic acid and PirB are not required for targeting of neural circuits by neurotropic mammalian orthoreovirus.mSphere · 2024Article
- Ependymal cells: roles in central nervous system infections and therapeutic application.Journal of neuroinflammation · 2024Review
- Multiciliated ependymal cells: an update on biology and pathology in the adult brain.Acta neuropathologica · 2024Review
- Sequence polymorphisms in the reovirus σ1 attachment protein modulate encapsidation efficiency and replication in mice.Journal of virology · 2024Article
- NRP1 is a receptor for mammalian orthoreovirus engaged by distinct capsid subunits.Cell host & microbe · 2024Article
- Mammalian orthoreovirus can exit cells in extracellular vesicles.PLoS pathogens · 2024Article
- NgR1 binding to reovirus reveals an unusual bivalent interaction and a new viral attachment protein.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Reovirus σ1 Attachment Protein Influences the Stability of Its Entry Intermediate.Journal of virology · 2023Article
- Paired immunoglobulin-like receptor B is an entry receptor for mammalian orthoreovirus.Nature communications · 2023Article
- Neural-Cell-Intrinsic NF-κB Signaling Enhances Reovirus Virulence.Journal of virology · 2023Article
- Reovirus Activated Cell Death Pathways.Cells · 2022Review
- The Murine Neuronal Receptor NgR1 Is Dispensable for Reovirus Pathogenesis.Journal of virology · 2022Article
- The multi-functional reovirus σ3 protein is a virulence factor that suppresses stress granule formation and is associated with myocardial injury.PLoS pathogens · 2021Article
- Enteric viruses evoke broad host immune responses resembling those elicited by the bacterial microbiome.Cell host & microbe · 2021Article
- Reovirus directly engages integrin to recruit clathrin for entry into host cells.Nature communications · 2021Article
- Ins and Outs of Reovirus: Vesicular Trafficking in Viral Entry and Egress.Trends in microbiology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Viral capsid components that bind cellular receptors mediate critical functions in viral tropism and disease pathogenesis. Mammalian orthoreoviruses (reoviruses) spread systemically in newborn mice to cause serotype-specific disease in the central nervous system (CNS). Serotype 1 (T1) reovirus infects ependymal cells to cause nonlethal hydrocephalus, whereas serotype 3 (T3) reovirus infects neurons to cause fulminant and lethal encephalitis. This serotype-dependent difference in tropism and concomitant disease is attributed to the σ1 viral attachment protein, which is composed of head, body, and tail domains. To identify σ1 sequences that contribute to tropism for specific cell types in the CNS, we engineered a panel of viruses expressing chimeric σ1 proteins in which discrete σ1 domains have been reciprocally exchanged. Parental and chimeric σ1 viruses were compared for replication, tropism, and disease induction following intracranial inoculation of newborn mice. Viruses expressing T1 σ1 head sequences infect the ependyma, produce relatively lower titers in the brain, and do not cause significant disease. In contrast, viruses expressing T3 σ1 head sequences efficiently infect neurons, replicate to relatively higher titers in the brain, and cause a lethal encephalitis. Additionally, T3 σ1 head-expressing viruses display enhanced infectivity of cultured primary cortical neurons compared with T1 σ1 head-expressing viruses. These results indicate that T3 σ1 head domain sequences promote infection of neurons, likely by interaction with a neuron-specific receptor, and dictate tropism in the CNS and induction of encephalitis.
Indexed as
Identifiers
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.