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

Authors
  • Laval, Kathlyn1
  • Favoreel, Herman W1
  • Nauwynck, Hans J2
  • 1 Department of Virology, Parasitology and Immunology, Faculty of Veterinary Medecine, Ghent University, Salisburylaan 133, B-9820 Merelbeke, Belgium. , (Belgium)
  • 2 Department of Virology, Parasitology and Immunology, Faculty of Veterinary Medecine, Ghent University, Salisburylaan 133, B-9820 Merelbeke, Belgium [email protected] , (Belgium)
Type
Published Article
Journal
Journal of General Virology
Publisher
Microbiology Society
Publication Date
Jan 01, 2015
Volume
96
Issue
Pt 1
Pages
118–130
Identifiers
DOI: 10.1099/vir.0.067363-0
PMID: 25239765
Source
Medline
License
Unknown

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.

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