Herpes Simplex Virus Type-2 Paralyzes the Function of Monocyte-Derived Dendritic Cells.
Cell Adhesion
Cell Movement
Cells, Cultured
Dendritic Cells
/ pathology
Guanine Nucleotide Exchange Factors
/ genetics
Herpesvirus 2, Human
/ immunology
Humans
Lymphocyte Function-Associated Antigen-1
/ immunology
Receptors, Chemokine
/ genetics
Transcription Factors
/ genetics
Viral Proteins
/ genetics
CYTIP
HSV-1
HSV-2
LFA-1
adhesion
cytohesin-1
dendritic cells
migration
Journal
Viruses
ISSN: 1999-4915
Titre abrégé: Viruses
Pays: Switzerland
ID NLM: 101509722
Informations de publication
Date de publication:
16 01 2020
16 01 2020
Historique:
received:
11
12
2019
revised:
09
01
2020
accepted:
14
01
2020
entrez:
23
1
2020
pubmed:
23
1
2020
medline:
18
2
2021
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 31963276
pii: v12010112
doi: 10.3390/v12010112
pmc: PMC7019625
pii:
doi:
Substances chimiques
CYTIP protein, human
0
Guanine Nucleotide Exchange Factors
0
Lymphocyte Function-Associated Antigen-1
0
Receptors, Chemokine
0
Transcription Factors
0
Viral Proteins
0
cytohesin-1
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : STE 432/11-1
Pays : International
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