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Entry of equid herpesvirus 1 into CD172a+ monocytic cells

Kathlyn Laval (UGent) , Herman Favoreel (UGent) , Jolien Van Cleemput (UGent) , Katrien Poelaert (UGent) , Ivy Brown, Bruno Verhasselt (UGent) and Hans Nauwynck (UGent)
(2016) JOURNAL OF GENERAL VIROLOGY. 97(3). p.733-746
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Abstract
Equid herpesvirus 1 (EHV-1) causes respiratory disease, abortion and neurological disorders in horses. Cells from the myeloid lineage (CD172a(+)) are one of the main target cells of EHV-1 during primary infection. Recently, we showed that EHV-1 restricts and delays its replication in CD172a(+) cells as part of an immune-evasive strategy to disseminate to target organs. Here, we hypothesize that a low efficiency of EHV-1 binding to and entry in CD172a(+) cells is responsible for this restriction. Thus, we characterized EHV-1 binding and entry into CD172a(+) cells, and showed that EHV-1 only bound to 15-20 % of CD172a(+) cells compared with 70 % of RK-13 control cells. Enzymic removal of heparan sulphate did not reduce EHV-1 infection, suggesting that EHV-1 does not use heparan sulphate to bind and enter CD172a(+) cells. In contrast, we found that treatment of cells with neuraminidase (NA) reduced infection by 85-100 % compared with untreated cells, whilst NA treatment of virus had no effect on infection. This shows that sialic acid residues present on CD172a(+) cells are essential in the initiation of EHV-1 infection. We found that alpha(V)beta(3) integrins are involved in the post-binding stage of CD172a(+) cell infection. Using pharmacological inhibitors, we showed that EHV-1 does not enter CD172a(+) cells via a clathrin- or caveolae-dependent endocytic pathway, nor by macropinocytosis, but requires cholesterol, tyrosine kinase, actin, dynamin and endosomal acidification, pointing towards a phagocytic mechanism. Overall, these results show that the narrow tropism of EHV-1 amongst CD172a(+) cells is determined by the presence of specific cellular receptors.
Keywords
HERPES-SIMPLEX-VIRUS, DEPENDENT ENDOCYTIC PATHWAY, RECEPTOR-BINDING PROPERTIES, RAFT-MEDIATED ENDOCYTOSIS, HEPARAN-SULFATE, SIALIC-ACID, GLYCOPROTEIN C, INFLUENZA HEMAGGLUTININ, HUMAN CYTOMEGALOVIRUS, INFECTION REQUIRES

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Chicago
Laval, Kathlyn, Herman Favoreel, Jolien Van Cleemput, Katrien Poelaert, Ivy Brown, Bruno Verhasselt, and Hans Nauwynck. 2016. “Entry of Equid Herpesvirus 1 into CD172a+ Monocytic Cells.” Journal of General Virology 97 (3): 733–746.
APA
Laval, K., Favoreel, H., Van Cleemput, J., Poelaert, K., Brown, I., Verhasselt, B., & Nauwynck, H. (2016). Entry of equid herpesvirus 1 into CD172a+ monocytic cells. JOURNAL OF GENERAL VIROLOGY, 97(3), 733–746.
Vancouver
1.
Laval K, Favoreel H, Van Cleemput J, Poelaert K, Brown I, Verhasselt B, et al. Entry of equid herpesvirus 1 into CD172a+ monocytic cells. JOURNAL OF GENERAL VIROLOGY. 2016;97(3):733–46.
MLA
Laval, Kathlyn, Herman Favoreel, Jolien Van Cleemput, et al. “Entry of Equid Herpesvirus 1 into CD172a+ Monocytic Cells.” JOURNAL OF GENERAL VIROLOGY 97.3 (2016): 733–746. Print.
@article{8506076,
  abstract     = {Equid herpesvirus 1 (EHV-1) causes respiratory disease, abortion and neurological disorders in horses. Cells from the myeloid lineage (CD172a(+)) are one of the main target cells of EHV-1 during primary infection. Recently, we showed that EHV-1 restricts and delays its replication in CD172a(+) cells as part of an immune-evasive strategy to disseminate to target organs. Here, we hypothesize that a low efficiency of EHV-1 binding to and entry in CD172a(+) cells is responsible for this restriction. Thus, we characterized EHV-1 binding and entry into CD172a(+) cells, and showed that EHV-1 only bound to 15-20 \% of CD172a(+) cells compared with 70 \% of RK-13 control cells. Enzymic removal of heparan sulphate did not reduce EHV-1 infection, suggesting that EHV-1 does not use heparan sulphate to bind and enter CD172a(+) cells. In contrast, we found that treatment of cells with neuraminidase (NA) reduced infection by 85-100 \% compared with untreated cells, whilst NA treatment of virus had no effect on infection. This shows that sialic acid residues present on CD172a(+) cells are essential in the initiation of EHV-1 infection. We found that alpha(V)beta(3) integrins are involved in the post-binding stage of CD172a(+) cell infection. Using pharmacological inhibitors, we showed that EHV-1 does not enter CD172a(+) cells via a clathrin- or caveolae-dependent endocytic pathway, nor by macropinocytosis, but requires cholesterol, tyrosine kinase, actin, dynamin and endosomal acidification, pointing towards a phagocytic mechanism. Overall, these results show that the narrow tropism of EHV-1 amongst CD172a(+) cells is determined by the presence of specific cellular receptors.},
  author       = {Laval, Kathlyn and Favoreel, Herman and Van Cleemput, Jolien and Poelaert, Katrien and Brown, Ivy and Verhasselt, Bruno and Nauwynck, Hans},
  issn         = {0022-1317},
  journal      = {JOURNAL OF GENERAL VIROLOGY},
  keyword      = {HERPES-SIMPLEX-VIRUS,DEPENDENT ENDOCYTIC PATHWAY,RECEPTOR-BINDING PROPERTIES,RAFT-MEDIATED ENDOCYTOSIS,HEPARAN-SULFATE,SIALIC-ACID,GLYCOPROTEIN C,INFLUENZA HEMAGGLUTININ,HUMAN CYTOMEGALOVIRUS,INFECTION REQUIRES},
  language     = {eng},
  number       = {3},
  pages        = {733--746},
  title        = {Entry of equid herpesvirus 1 into CD172a+ monocytic cells},
  url          = {http://dx.doi.org/10.1099/jgv.0.000375},
  volume       = {97},
  year         = {2016},
}

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