Evidence map›Paper›PMID 27349677›Full record

ArticleScientific reports2016

Herpes simplex virus 1 induces egress channels through marginalized host chromatin.

Markko Myllys, Visa Ruokolainen, Vesa Aho, Elizabeth A Smith, Satu Hakanen, Piritta Peri, Anna Salvetti, Jussi Timonen, Veijo Hukkanen, Carolyn A Larabell and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

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  15. Imaging cell morphology and physiology using X-rays.Biochemical Society transactions · 2019
    Review
  16. Article
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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

11 authors.

Markko MyllysUniversity of Jyvaskyla, Department of Physics and Nanoscience Center, Jyvaskyla, FI-40500, Finland.
Visa RuokolainenUniversity of Jyvaskyla, Department of Biological and Environmental Science and Nanoscience Center, Jyvaskyla, FI-40500, Finland.
Vesa AhoUniversity of Jyvaskyla, Department of Physics and Nanoscience Center, Jyvaskyla, FI-40500, Finland.
Elizabeth A SmithDepartment of Anatomy, University of California San Francisco, San Francisco, CA, 94158, USA.
Satu HakanenUniversity of Jyvaskyla, Department of Biological and Environmental Science and Nanoscience Center, Jyvaskyla, FI-40500, Finland.
Piritta PeriUniversity of Turku, Turku, Finland.
Anna SalvettiInternational Center for Research in Infectiology (CIRI), INSERM U1111, CNRS UMR5308, Lyon, F-69007, France.
Jussi TimonenUniversity of Jyvaskyla, Department of Physics and Nanoscience Center, Jyvaskyla, FI-40500, Finland.
Veijo HukkanenUniversity of Turku, Turku, Finland.
Carolyn A LarabellDepartment of Anatomy, University of California San Francisco, San Francisco, CA, 94158, USA.
Maija Vihinen-RantaUniversity of Jyvaskyla, Department of Biological and Environmental Science and Nanoscience Center, Jyvaskyla, FI-40500, Finland.

Funding

TrainingP41GM103445 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LARABELL, CAROLYN A · 2012 to 2019
$8.2M
NIGMS NIH HHS P41 GM103445
6 · The paper itself

Abstract

Lytic infection with herpes simplex virus type 1 (HSV-1) induces profound modification of the cell nucleus including formation of a viral replication compartment and chromatin marginalization into the nuclear periphery. We used three-dimensional soft X-ray tomography, combined with cryogenic fluorescence, confocal and electron microscopy, to analyse the transformation of peripheral chromatin during HSV-1 infection. Our data showed an increased presence of low-density gaps in the marginalized chromatin at late infection. Advanced data analysis indicated the formation of virus-nucleocapsid-sized (or wider) channels extending through the compacted chromatin of the host. Importantly, confocal and electron microscopy analysis showed that these gaps frequently contained viral nucleocapsids. These results demonstrated that HSV-1 infection induces the formation of channels penetrating the compacted layer of cellular chromatin and allowing for the passage of progeny viruses to the nuclear envelope, their site of nuclear egress.

Indexed as

AnimalsB-LymphocytesCell LineChromatinHerpesvirus 1, HumanHost-Pathogen InteractionsHumansMiceMicroscopy, ConfocalMicroscopy, Electron, TransmissionTime-Lapse ImagingTomography, X-RayVirionVirus ReplicationChromatin

Identifiers

PMID27349677
PMCPMC5378911

What OpenQuestion holds

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LicenceCC BY
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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.