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Deletion of gE in herpes simplex virus 1 leads to increased extracellular virus production and augmented interferon alpha production by peripheral blood mononuclear cells

Manon Claeys (UGent) , Jonas Delva (UGent) , Cedric Jacqmotte (UGent) , Cliff Van Waesberghe (UGent) and Herman Favoreel (UGent)
(2024) PATHOGENS. 13(12).
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Abstract
Herpes simplex virus (HSV) in humans and pseudorabies virus (PRV) in pigs are both alphaherpesviruses. Plasmacytoid dendritic cells (pDCs) make part of the peripheral blood mononuclear cells (PBMCs) and are specialized in producing large amounts of antiviral type I interferon (IFN-I). IFN-I production by PBMCs in response to both HSV-1 and PRV can be virtually exclusively attributed to pDCs. Recently, we discovered that cells infected with gEnull PRV trigger increased production of IFNalpha by porcine PBMCs/pDCs compared with cells infected with wild-type (WT) PRV. This increased IFNalpha response correlates with increased extracellular virus production triggered by gEnull PRV compared with WT PRV. The gE protein and some of its currently described functions are conserved in different alphaherpesviruses, including PRV and HSV-1. In the current study, we report that cells infected with gEnull HSV-1 trigger increased IFNalpha production by human PBMCs and increased extracellular virus production compared with WT HSV-1. Hence, these recently described functions of PRV gE are conserved in HSV-1 gE. Since the increased extracellular virus production and IFNalpha response have also been reported for successful (gEnull) PRV vaccines, the current findings may have important consequences for the rational design of HSV vaccines.
Keywords
HSV-1, glycoprotein E, type I interferon, peripheral blood mononuclear cells, plasmacytoid dendritic cell, PLASMACYTOID DENDRITIC CELLS, VIRAL GLYCOPROTEINS, TYPE-1, MATURATION, PROTEIN, SPREAD, DRIVE

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Citation

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MLA
Claeys, Manon, et al. “Deletion of GE in Herpes Simplex Virus 1 Leads to Increased Extracellular Virus Production and Augmented Interferon Alpha Production by Peripheral Blood Mononuclear Cells.” PATHOGENS, vol. 13, no. 12, 2024, doi:10.3390/pathogens13121138.
APA
Claeys, M., Delva, J., Jacqmotte, C., Van Waesberghe, C., & Favoreel, H. (2024). Deletion of gE in herpes simplex virus 1 leads to increased extracellular virus production and augmented interferon alpha production by peripheral blood mononuclear cells. PATHOGENS, 13(12). https://doi.org/10.3390/pathogens13121138
Chicago author-date
Claeys, Manon, Jonas Delva, Cedric Jacqmotte, Cliff Van Waesberghe, and Herman Favoreel. 2024. “Deletion of GE in Herpes Simplex Virus 1 Leads to Increased Extracellular Virus Production and Augmented Interferon Alpha Production by Peripheral Blood Mononuclear Cells.” PATHOGENS 13 (12). https://doi.org/10.3390/pathogens13121138.
Chicago author-date (all authors)
Claeys, Manon, Jonas Delva, Cedric Jacqmotte, Cliff Van Waesberghe, and Herman Favoreel. 2024. “Deletion of GE in Herpes Simplex Virus 1 Leads to Increased Extracellular Virus Production and Augmented Interferon Alpha Production by Peripheral Blood Mononuclear Cells.” PATHOGENS 13 (12). doi:10.3390/pathogens13121138.
Vancouver
1.
Claeys M, Delva J, Jacqmotte C, Van Waesberghe C, Favoreel H. Deletion of gE in herpes simplex virus 1 leads to increased extracellular virus production and augmented interferon alpha production by peripheral blood mononuclear cells. PATHOGENS. 2024;13(12).
IEEE
[1]
M. Claeys, J. Delva, C. Jacqmotte, C. Van Waesberghe, and H. Favoreel, “Deletion of gE in herpes simplex virus 1 leads to increased extracellular virus production and augmented interferon alpha production by peripheral blood mononuclear cells,” PATHOGENS, vol. 13, no. 12, 2024.
@article{01JJKNM917VMQ8SWX00AF3Z1YN,
  abstract     = {{Herpes simplex virus (HSV) in humans and pseudorabies virus (PRV) in pigs are both alphaherpesviruses. Plasmacytoid dendritic cells (pDCs) make part of the peripheral blood mononuclear cells (PBMCs) and are specialized in producing large amounts of antiviral type I interferon (IFN-I). IFN-I production by PBMCs in response to both HSV-1 and PRV can be virtually exclusively attributed to pDCs. Recently, we discovered that cells infected with gEnull PRV trigger increased production of IFNalpha by porcine PBMCs/pDCs compared with cells infected with wild-type (WT) PRV. This increased IFNalpha response correlates with increased extracellular virus production triggered by gEnull PRV compared with WT PRV. The gE protein and some of its currently described functions are conserved in different alphaherpesviruses, including PRV and HSV-1. In the current study, we report that cells infected with gEnull HSV-1 trigger increased IFNalpha production by human PBMCs and increased extracellular virus production compared with WT HSV-1. Hence, these recently described functions of PRV gE are conserved in HSV-1 gE. Since the increased extracellular virus production and IFNalpha response have also been reported for successful (gEnull) PRV vaccines, the current findings may have important consequences for the rational design of HSV vaccines.}},
  articleno    = {{1138}},
  author       = {{Claeys, Manon and Delva, Jonas and Jacqmotte, Cedric and Van Waesberghe, Cliff and Favoreel, Herman}},
  issn         = {{2076-0817}},
  journal      = {{PATHOGENS}},
  keywords     = {{HSV-1,glycoprotein E,type I interferon,peripheral blood mononuclear cells,plasmacytoid dendritic cell,PLASMACYTOID DENDRITIC CELLS,VIRAL GLYCOPROTEINS,TYPE-1,MATURATION,PROTEIN,SPREAD,DRIVE}},
  language     = {{eng}},
  number       = {{12}},
  pages        = {{11}},
  title        = {{Deletion of gE in herpes simplex virus 1 leads to increased extracellular virus production and augmented interferon alpha production by peripheral blood mononuclear cells}},
  url          = {{http://doi.org/10.3390/pathogens13121138}},
  volume       = {{13}},
  year         = {{2024}},
}
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