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Herpes Simplex Virus Type-2 Paralyzes the Function of Monocyte-Derived Dendritic Cells
Linda Grosche1, Petra Mühl-Zürbes1, Barbara Ciblis1
1Department of Immune Modulation, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91052 Erlangen, Germany.
Viruses
|January 23, 2020
Summary
Herpes simplex virus type 2 (HSV-2) blocks the migration of mature dendritic cells (mDCs) by activating LFA-1 adhesion. This viral strategy hinders antiviral immunity by preventing antigen transport to lymph nodes.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Herpes simplex viruses (HSV) infect various cells, including dendritic cells (DCs).
- HSV can manipulate cellular functions to its advantage.
- Inhibiting DC migration is a strategy to impair antiviral immunity, as shown for HSV-1.
Purpose of the Study:
- To investigate if HSV-2 also affects DC biology, specifically their migration.
- To understand the mechanism by which HSV-2 impacts mature DC (mDC) migration.
Main Methods:
- Studied the effect of HSV-2 on chemokine-dependent in vitro migration of mDCs.
- Analyzed chemokine receptor expression and β2 integrin (LFA-1) mediated adhesion.
- Investigated the role of CYTIP degradation in HSV-2 induced mDC adhesion.
Main Results:
- HSV-2 significantly inhibits the in vitro migration capacity of mDCs.
- HSV-2 rapidly induces LFA-1-mediated mDC adhesion, rather than reducing chemokine receptors.
- HSV-2 triggers proteasomal degradation of CYTIP, leading to constitutive LFA-1 activation and mDC adhesion.
Conclusions:
- HSV-2 impairs mDC migration, extending findings on HSV-1.
- This mechanism involves CYTIP degradation and LFA-1 activation.
- Inhibition of mDC migration to hinder antigen transport is a conserved herpesviral strategy.
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