Evidence map›Paper›PMID 31963276›Full record

ArticleViruses2020

Herpes Simplex Virus Type-2 Paralyzes the Function of Monocyte-Derived Dendritic Cells.

Linda Grosche, Petra Mühl-Zürbes, Barbara Ciblis, Adalbert Krawczyk, Christine Kuhnt, Lisa Kamm, Alexander Steinkasserer, Christiane Silke Heilingloh

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Review
  7. Review
  8. 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

8 authors at 2 institutions in 1 country.

Linda GroscheDepartment of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Petra Mühl-ZürbesDepartment of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Barbara CiblisDepartment of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Adalbert KrawczykDepartment of Infectious Diseases, University Hospital Essen, University of Duisburg-Essen, D-45147 Essen, Germany.ORCID 0000-0001-9502-9903
Christine KuhntDepartment of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Lisa KammDepartment of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Alexander SteinkassererDepartment of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Christiane Silke HeilinglohDepartment of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of Duisburg-Essen · DE

Funding

Deutsche Forschungsgemeinschaft STE 432/11-1
6 · The paper itself

Abstract

Herpes simplex viruses not only infect a variety of different cell types, including dendritic cells (DCs), but also modulate important cellular functions in benefit of the virus. Given the relevance of directed immune cell migration during the initiation of potent antiviral immune responses, interference with DC migration constitutes a sophisticated strategy to hamper antiviral immunity. Notably, recent reports revealed that HSV-1 significantly inhibits DC migration in vitro. Thus, we aimed to investigate whether HSV-2 also modulates distinct hallmarks of DC biology. Here, we demonstrate that HSV-2 negatively interferes with chemokine-dependent in vitro migration capacity of mature DCs (mDCs). Interestingly, rather than mediating the reduction of the cognate chemokine receptor expression early during infection, HSV-2 rapidly induces β2 integrin (LFA-1)-mediated mDC adhesion and thereby blocks mDC migration. Mechanistically, HSV-2 triggers the proteasomal degradation of the negative regulator of β2 integrin activity, CYTIP, which causes the constitutive activation of LFA-1 and thus mDC adhesion. In conclusion, our data extend and strengthen recent findings reporting the reduction of mDC migration in the context of a herpesviral infection. We thus hypothesize that hampering antigen delivery to secondary lymphoid organs by inhibition of mDC migration is an evolutionary conserved strategy among distinct members of Herpesviridae.

Indexed as

Cell MovementCell AdhesionCells, CulturedDendritic CellsGuanine Nucleotide Exchange FactorsHerpesvirus 2, HumanHumansLymphocyte Function-Associated Antigen-1Receptors, ChemokineTranscription FactorsViral ProteinsCYTIP protein, humancytohesin-1Guanine Nucleotide Exchange FactorsLymphocyte Function-Associated Antigen-1Receptors, ChemokineTranscription FactorsViral ProteinsadhesionCYTIPcytohesin-1dendritic cellsHSV-1HSV-2LFA-1migration

Identifiers

PMID31963276
PMCPMC7019625
OpenAlexW2998804182

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.