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Equine herpesvirus type 1 replication is delayed in CD172a⁺ monocytic cells and controlled by histone deacetylases

Kathlyn Laval (UGent) , Herman Favoreel (UGent) and Hans Nauwynck (UGent)
(2015) JOURNAL OF GENERAL VIROLOGY. 96(1). p.118-130
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Abstract
Equine herpesvirus type 1 (EHV-1) replicates in the epithelial cells of the upper respiratory tract and disseminates through the body via a cell-associated viraemia in monocytic cells, despite the presence of neutralizing antibodies. However, the mechanism by which EHV-1 hijacks immune cells and uses them as 'Trojan horses' in order to disseminate inside its host is still unclear. Here, we hypothesize that EHV-1 delays its replication in monocytic cells in order to avoid recognition by the immune system. We compared replication kinetics in vitro of EHV-1 in RK-13, a cell line fully susceptible to EHV-1 infection, and primary horse cells from the myeloid lineage (CD172a(+)). We found that EHV-1 replication was restricted to 4% of CD172a(+) cells compared with 100% in RK-13 cells. In susceptible CD172a(+) cells, the expression of immediate-early (IEP) and early (EICP22) proteins was delayed in the cell nuclei by 2-3 h post-infection (p.i.) compared with RK-13, and the formation of replicative compartments by 15 h p.i. Virus production in CD172a(+) cells was significantly lower (from 10(1.7) to 10(3.1) TCID50 per 10(5) inoculated cells) than in RK-13 (from 10(5) to 10(5.7) TCID50 per 10(5) inoculated cells). Less than 0.02% of inoculated CD172a(+) cells produced and transmitted infectious virus to neighbouring cells. Pre-treatment of CD172a(+) cells with inhibitors of histone deacetylase activity increased and accelerated viral protein expression at very early times of infection and induced productive infection in CD172a(+) cells. Our results demonstrated that the restriction and delay of EHV-1 replication in CD172a(+) cells are part of an immune evasive strategy and involve silencing of EHV-1 gene expression associated with histone deacetylases.
Keywords
INFECTION, BLOOD MONONUCLEAR-CELLS, ACID, NASAL MUCOSAL EXPLANTS, HUMAN CYTOMEGALOVIRUS, GENE-EXPRESSION, IMMUNE EVASION, VIRUS, EHV-1, PROTEIN

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Chicago
Laval, Kathlyn, Herman Favoreel, and Hans Nauwynck. 2015. “Equine Herpesvirus Type 1 Replication Is Delayed in CD172a+ Monocytic Cells and Controlled by Histone Deacetylases.” Journal of General Virology 96 (1): 118–130.
APA
Laval, K., Favoreel, H., & Nauwynck, H. (2015). Equine herpesvirus type 1 replication is delayed in CD172a+ monocytic cells and controlled by histone deacetylases. JOURNAL OF GENERAL VIROLOGY, 96(1), 118–130.
Vancouver
1.
Laval K, Favoreel H, Nauwynck H. Equine herpesvirus type 1 replication is delayed in CD172a+ monocytic cells and controlled by histone deacetylases. JOURNAL OF GENERAL VIROLOGY. 2015;96(1):118–30.
MLA
Laval, Kathlyn, Herman Favoreel, and Hans Nauwynck. “Equine Herpesvirus Type 1 Replication Is Delayed in CD172a+ Monocytic Cells and Controlled by Histone Deacetylases.” JOURNAL OF GENERAL VIROLOGY 96.1 (2015): 118–130. Print.
@article{6847417,
  abstract     = {Equine herpesvirus type 1 (EHV-1) replicates in the epithelial cells of the upper respiratory tract and disseminates through the body via a cell-associated viraemia in monocytic cells, despite the presence of neutralizing antibodies. However, the mechanism by which EHV-1 hijacks immune cells and uses them as 'Trojan horses' in order to disseminate inside its host is still unclear. Here, we hypothesize that EHV-1 delays its replication in monocytic cells in order to avoid recognition by the immune system. We compared replication kinetics in vitro of EHV-1 in RK-13, a cell line fully susceptible to EHV-1 infection, and primary horse cells from the myeloid lineage (CD172a(+)). We found that EHV-1 replication was restricted to 4\% of CD172a(+) cells compared with 100\% in RK-13 cells. In susceptible CD172a(+) cells, the expression of immediate-early (IEP) and early (EICP22) proteins was delayed in the cell nuclei by 2-3 h post-infection (p.i.) compared with RK-13, and the formation of replicative compartments by 15 h p.i. Virus production in CD172a(+) cells was significantly lower (from 10(1.7) to 10(3.1) TCID50 per 10(5) inoculated cells) than in RK-13 (from 10(5) to 10(5.7) TCID50 per 10(5) inoculated cells). Less than 0.02\% of inoculated CD172a(+) cells produced and transmitted infectious virus to neighbouring cells. Pre-treatment of CD172a(+) cells with inhibitors of histone deacetylase activity increased and accelerated viral protein expression at very early times of infection and induced productive infection in CD172a(+) cells. Our results demonstrated that the restriction and delay of EHV-1 replication in CD172a(+) cells are part of an immune evasive strategy and involve silencing of EHV-1 gene expression associated with histone deacetylases.},
  author       = {Laval, Kathlyn and Favoreel, Herman and Nauwynck, Hans},
  issn         = {0022-1317},
  journal      = {JOURNAL OF GENERAL VIROLOGY},
  keyword      = {INFECTION,BLOOD MONONUCLEAR-CELLS,ACID,NASAL MUCOSAL EXPLANTS,HUMAN CYTOMEGALOVIRUS,GENE-EXPRESSION,IMMUNE EVASION,VIRUS,EHV-1,PROTEIN},
  language     = {eng},
  number       = {1},
  pages        = {118--130},
  title        = {Equine herpesvirus type 1 replication is delayed in CD172a\unmatched{207a} monocytic cells and controlled by histone deacetylases},
  url          = {http://dx.doi.org/10.1099/vir.0.067363-0},
  volume       = {96},
  year         = {2015},
}

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