Evidence map›Paper›PMID 28835716›Full record

ArticleScientific reports2017

The ERK-1 function is required for HSV-1-mediated G1/S progression in HEP-2 cells and contributes to virus growth.

Ivana Colao, Rosamaria Pennisi, Assunta Venuti, Michaela Nygårdas, Outi Heikkilä, Veijo Hukkanen, Maria Teresa Sciortino

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

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  15. Article
  16. Host-Directed Antiviral Therapy.Clinical microbiology reviews · 2020
    Review
  17. Article
  18. Article
  19. Human DNA Virus Exploitation of the MAPK-ERK Cascade.International journal of molecular sciences · 2019
    Review
  20. Article
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.

Ivana ColaoDepartment of Biological and Environmental Sciences, University of Messina, Viale F. Stagno d'Alcontres 31, 98166, Messina, Italy.
Rosamaria PennisiDepartment of Biological and Environmental Sciences, University of Messina, Viale F. Stagno d'Alcontres 31, 98166, Messina, Italy.
Assunta VenutiDivision of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy.
Michaela NygårdasDepartment of Virology, University of Turku, Turku, Finland.
Outi HeikkiläDepartment of Virology, University of Turku, Turku, Finland.
Veijo HukkanenDepartment of Virology, University of Turku, Turku, Finland.
Maria Teresa SciortinoDepartment of Biological and Environmental Sciences, University of Messina, Viale F. Stagno d'Alcontres 31, 98166, Messina, Italy. mtsciortino@unime.it.ORCID 0000-0002-8519-7724
University of Messina · ITUniversity of Turku · FIVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The herpes simplex virus 1 is able to readdress different cellular pathways including cell cycle to facilitate its replication and spread. During infection, the progression of the cell cycle from G1 to S phase makes the cellular replication machinery accessible to viral DNA replication. In this work we established that HSV-1, in asynchronized HEp-2 cells, strictly controls cell cycle progression increasing S-phase population from 9 hours post infection until the end of HSV-1 replication. The G1/S phases progression depends on two important proteins, cyclin E and CDK2. We demonstrate that their phosphorylated status and then their activity during the infection is strongly correlated to viral replication events. In addition, HSV-1 is able to recruit and distribute ERK1/2 proteins in a spatio-temporal fashion, highlighting its downstream regulatory effects on cellular processes. According with this data, using chemical inhibitor U0126 and ERK dominant negative cells we found that the lack of ERK1 activity affects cyclin E protein accumulation, viral gene transcription and percentage of the cells in S phase, during the viral replication. These data suggested a complex interaction between ERK, cell cycle progression and HSV-1 replication.

Indexed as

G1 PhaseS PhaseVirus ReplicationCell CycleCell LineCells, CulturedCyclin-Dependent Kinase 2Herpes SimplexHerpesvirus 1, HumanHumansMitogen-Activated Protein Kinase 3CDK2 protein, humanCyclin-Dependent Kinase 2MAPK3 protein, humanMitogen-Activated Protein Kinase 3

Identifiers

PMID28835716
PMCPMC5569015
OpenAlexW2746390445

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.