ArticleJournal of virology1995
Genetic and structural analysis of a virulence determinant in polyomavirus VP1.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 75 citations in OpenAlex.
- Time-dependent variations in BK polyomavirus genome from kidney transplant recipients with persistent viremia.Scientific reports · 2023Article
- T cell deficiency precipitates antibody evasion and emergence of neurovirulent polyomavirus.eLife · 2022Article
- JCPyV VP1 Mutations in Progressive MultifocalLeukoencephalopathy: Altering Tropismor Mediating Immune Evasion?Viruses · 2020Review
- BK polyomavirus diversity-Why viral variation matters.Reviews in medical virology · 2020Review
- JCPyV NCCR analysis in PML patients with different risk factors: exploring common rearrangements as essential changes for neuropathogenesis.Virology journal · 2020Article
- Intra-patient viral evolution in polyomavirus-related diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- The phylogenomics of evolving virus virulence.Nature reviews. Genetics · 2018Review
- Type I Interferons Regulate the Magnitude and Functionality of Mouse Polyomavirus-Specific CD8 T Cells in a Virus Strain-Dependent Manner.Journal of virology · 2016Article
- Molecular characterization of BK virus in patients infected with human immunodeficiency virus.Medical microbiology and immunology · 2016Article
- Infectious Pancreatic Necrosis Virus Causing Clinical and Subclinical Infections in Atlantic Salmon Have Different Genetic Fingerprints.Frontiers in microbiology · 2016Article
- Structural and Functional Analysis of Murine Polyomavirus Capsid Proteins Establish the Determinants of Ligand Recognition and Pathogenicity.PLoS pathogens · 2015Article
- Ganglioside and Non-ganglioside Mediated Host Responses to the Mouse Polyomavirus.PLoS pathogens · 2015Article
- Trichodysplasia spinulosa-Associated Polyomavirus Uses a Displaced Binding Site on VP1 to Engage Sialylated Glycolipids.PLoS pathogens · 2015Article
- A mouse polyomavirus-encoded microRNA targets the cellular apoptosis pathway through Smad2 inhibition.Virology · 2014Article
- The importance of mouse models to define immunovirologic determinants of progressive multifocal leukoencephalopathy.Frontiers in immunology · 2014Review
- Article
- A cornucopia of human polyomaviruses.Nature reviews. Microbiology · 2013Review
- Stress-induced reversion to virulence of infectious pancreatic necrosis virus in naïve fry of Atlantic salmon (Salmo salar L.).PloS one · 2013Article
- Mutations in the GM1 binding site of simian virus 40 VP1 alter receptor usage and cell tropism.Journal of virology · 2012Article
- The murine coronavirus hemagglutinin-esterase receptor-binding site: a major shift in ligand specificity through modest changes in architecture.PLoS pathogens · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The LID strain of polyomavirus differs from other laboratory strains in causing a rapidly lethal infection of newborn C3H/Bi mice. This virulent behavior of LID was attenuated by dilution, yet at sublethal doses LID was able to induce tumors at a high frequency, like its parent virus PTA. By constructing and assaying LID-PTA recombinant viruses and by DNA sequencing, the determinant of virulence in LID was mapped to the major viral capsid protein, VP1. The VP1s of LID and PTA differed at two positions: at 185, LID has phenylalanine and PTA has tyrosine, and at 296, LID has alanine and PTA has valine. Results obtained with viruses constructed by site-directed mutagenesis showed that alanine at position 296 is sufficient to confer a fully virulent phenotype regardless of which amino acid is at position 185. However, with valine at position 296, an effect of phenylalanine at position 185 is apparent, as this virus possesses an intermediate level of virulence. A crystal structure of polyomavirus complexed with 3'-sialyl lactose previously indicated van der Waals contacts between the side chain of valine 296 and the sialic acid ring (T. Stehle, Y. Yan, T. L. Benjamin, and S. C. Harrison, Nature [London] 369:160-163, 1994). When this interaction was modeled with alanine, these contacts were greatly reduced. Direct confirmation that the substitutions in VP1 affected receptor binding was obtained by studying virus hemagglutination behavior. The ensemble of results are discussed in terms of the idea that a lower affinity of the virus for its receptor can result in more rapid spread and increased pathogenicity.
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.