Evidence map›Paper›PMID 29257050›Full record

ArticleViruses2017

Mutations in HPV18 E1^E4 Impact Virus Capsid Assembly, Infectivity Competence, and Maturation.

Jennifer Biryukov, Jocelyn C Myers, Margaret E McLaughlin-Drubin, Heather M Griffin, Janice Milici, John Doorbar, Craig Meyers

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Jennifer BiryukovDepartment of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. jenbiryukov@gmail.com.
Jocelyn C MyersDepartment of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. jcmyers81@gmail.com.
Margaret E McLaughlin-DrubinDepartment of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Heather M GriffinDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK. hgriffi@nimr.mrc.ac.uk.
Janice MiliciDepartment of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. jem10@psu.edu.
John DoorbarDepartment of Pathology, University of Cambridge, Cambridge CB2 1QP, UK. jd121@cam.ac.uk.
Craig MeyersDepartment of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. cmm10@psu.edu.
Pennsylvania State University · USUniversity of Cambridge · GBBrigham and Women's Hospital · US

Funding

Medical Research Council MC_PC_13050
6 · The paper itself

Abstract

The most highly expressed protein during the productive phase of the human papillomavirus (HPV) life cycle is E1^E4. Its full role during infection remains to be established. HPV E1^E4 is expressed during both the early and late stages of the virus life cycle and contributes to viral genome amplification. In an attempt to further outline the functions of E1^E4, and determine whether it plays a role in viral capsid assembly and viral infectivity, we examined wild-type E1^E4 as well as four E1^E4 truncation mutants. Our study revealed that HPV18 genomes containing the shortest truncated form of E1^E4, the 17/18 mutant, produced viral titers that were similar to wild-type virus and significantly higher compared to virions containing the three longer E1^E4 mutants. Additionally, the infectivity of virus containing the shortest E1^E4 mutation was equivalent to wild-type and significantly higher than the other three mutants. In contrast, infectivity was completely abrogated for virus containing the longer E1^E4 mutants, regardless of virion maturity. Taken together, our results indicate for the first time that HPV18 E1^E4 impacts capsid assembly and viral infectivity as well as virus maturation.

Indexed as

MutationVirus AssemblyCapsidCells, CulturedFibroblastsHuman papillomavirus 18HumansMicrobial ViabilityOncogene Proteins, FusionOncogene Proteins, ViralViral LoadOncogene Proteins, FusionOncogene Proteins, ViralE1^E4HPV18Human Papillomavirus (HPV)infectionviral titervirion maturation

Identifiers

PMID29257050
PMCPMC5744159
OpenAlexW2778128256

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.