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Modulation of CD112 by the alphaherpesvirus gD protein suppresses DNAM-1-dependent NK cell-mediated lysis of infected cells

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Abstract
Natural killer (NK) cells are key players in the innate response to viruses, including herpesviruses. In particular, the variety of viral strategies to modulate the recognition of certain herpesviruses witnesses the importance of NK cells in the control of this group of viruses. Still, NK evasion strategies have remained largely elusive for the largest herpesvirus subfamily, the alphaherpesviruses. Here, we report that the gD glycoprotein of the alphaherpesviruses pseudorabies virus (PRV) and herpes simplex virus 2 (HSV-2) displays previously uncharacterized immune evasion properties toward NK cells. Expression of gD during infection or transfection led to degradation and consequent down-regulation of CD112, a ligand for the activating NK receptor DNAX accessory molecule 1 (DNAM-1). CD112 downregulation resulted in a reduced ability of DNAM-1 to bind to the surface of both virus-infected and gDtransfected cells. Consequently, expression of gD suppressed NK cell degranulation and NK cell-mediated lysis of PRV- or HSV-2–infected cells. These data identify an alphaherpesvirus evasion strategy from NK cells and point out that interactions between viral envelope proteins and host cell receptors can have biological consequences that stretch beyond virus entry.
Keywords
CD112, pseudorabies, Herpes, NK, DNAM-1, HERPES-SIMPLEX-VIRUS, NATURAL-KILLER-CELLS, DNA-DAMAGE RESPONSE, HUMAN CYTOMEGALOVIRUS UL141, CYTOTOXICITY RECEPTORS, POLIOVIRUS RECEPTOR, DOWN-REGULATION, PSEUDORABIES VIRUS, LIGAND EXPRESSION, NECTIN-2 CD112

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Citation

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MLA
Grauwet, Korneel, et al. “Modulation of CD112 by the Alphaherpesvirus GD Protein Suppresses DNAM-1-Dependent NK Cell-Mediated Lysis of Infected Cells.” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, vol. 111, no. 45, 2014, pp. 16118–23, doi:10.1073/pnas.1409485111.
APA
Grauwet, K., Cantoni, C., Parodi, M., De Maria, A., Devriendt, B., Pende, D., … Favoreel, H. (2014). Modulation of CD112 by the alphaherpesvirus gD protein suppresses DNAM-1-dependent NK cell-mediated lysis of infected cells. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 111(45), 16118–16123. https://doi.org/10.1073/pnas.1409485111
Chicago author-date
Grauwet, Korneel, Claudia Cantoni, Monica Parodi, Andrea De Maria, Bert Devriendt, Daniela Pende, Lorenzo Moretta, Massimo Vitale, and Herman Favoreel. 2014. “Modulation of CD112 by the Alphaherpesvirus GD Protein Suppresses DNAM-1-Dependent NK Cell-Mediated Lysis of Infected Cells.” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 111 (45): 16118–23. https://doi.org/10.1073/pnas.1409485111.
Chicago author-date (all authors)
Grauwet, Korneel, Claudia Cantoni, Monica Parodi, Andrea De Maria, Bert Devriendt, Daniela Pende, Lorenzo Moretta, Massimo Vitale, and Herman Favoreel. 2014. “Modulation of CD112 by the Alphaherpesvirus GD Protein Suppresses DNAM-1-Dependent NK Cell-Mediated Lysis of Infected Cells.” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 111 (45): 16118–16123. doi:10.1073/pnas.1409485111.
Vancouver
1.
Grauwet K, Cantoni C, Parodi M, De Maria A, Devriendt B, Pende D, et al. Modulation of CD112 by the alphaherpesvirus gD protein suppresses DNAM-1-dependent NK cell-mediated lysis of infected cells. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2014;111(45):16118–23.
IEEE
[1]
K. Grauwet et al., “Modulation of CD112 by the alphaherpesvirus gD protein suppresses DNAM-1-dependent NK cell-mediated lysis of infected cells,” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, vol. 111, no. 45, pp. 16118–16123, 2014.
@article{5758197,
  abstract     = {{Natural killer (NK) cells are key players in the innate response to viruses, including herpesviruses. In particular, the variety of viral strategies to modulate the recognition of certain herpesviruses witnesses the importance of NK cells in the control of this group of viruses. Still, NK evasion strategies have remained largely elusive for the largest herpesvirus subfamily, the alphaherpesviruses. Here, we report that the gD glycoprotein of the alphaherpesviruses pseudorabies virus (PRV) and herpes simplex virus 2 (HSV-2) displays previously uncharacterized immune evasion properties toward NK cells. Expression of gD during infection or transfection led to degradation and consequent down-regulation of CD112, a ligand for the activating NK receptor DNAX accessory molecule 1 (DNAM-1). CD112 downregulation resulted in a reduced ability of DNAM-1 to bind to the surface of both virus-infected and gDtransfected cells. Consequently, expression of gD suppressed NK cell degranulation and NK cell-mediated lysis of PRV- or HSV-2–infected cells. These data identify an alphaherpesvirus evasion strategy from NK cells and point out that interactions between viral envelope proteins and host cell receptors can have biological consequences that stretch beyond virus entry.}},
  author       = {{Grauwet, Korneel and Cantoni, Claudia and Parodi, Monica and De Maria, Andrea and Devriendt, Bert and Pende, Daniela and Moretta, Lorenzo and Vitale, Massimo and Favoreel, Herman}},
  issn         = {{0027-8424}},
  journal      = {{PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA}},
  keywords     = {{CD112,pseudorabies,Herpes,NK,DNAM-1,HERPES-SIMPLEX-VIRUS,NATURAL-KILLER-CELLS,DNA-DAMAGE RESPONSE,HUMAN CYTOMEGALOVIRUS UL141,CYTOTOXICITY RECEPTORS,POLIOVIRUS RECEPTOR,DOWN-REGULATION,PSEUDORABIES VIRUS,LIGAND EXPRESSION,NECTIN-2 CD112}},
  language     = {{eng}},
  number       = {{45}},
  pages        = {{16118--16123}},
  title        = {{Modulation of CD112 by the alphaherpesvirus gD protein suppresses DNAM-1-dependent NK cell-mediated lysis of infected cells}},
  url          = {{http://doi.org/10.1073/pnas.1409485111}},
  volume       = {{111}},
  year         = {{2014}},
}

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