Equid herpesvirus-1 Distribution in Equine Lymphoid and Neural Tissues 70 Days Post Infection.

Susanna Samoilowa,Allison Allum,Matti Kiupel,Kim S Giessler,Robert Fux,Lutz S Goehring,Kaspar Matiasek,Gisela Soboll Hussey,Carlos E Medina Torres,Dodd G Sledge,Christin Jerke

doi:10.3390/pathogens10060707

Abstract

Equid herpesvirus-1 (EHV-1) causes respiratory disease, abortion and myeloencephalopathy in horses worldwide. As member of the Alphaherpesvirinae, latency is key to EHV-1 epidemiology. EHV-1 latent infection has been detected in the trigeminal ganglion (TG), respiratory associated lymphoid tissue (RALT) and peripheral blood mononuclear cells (PBMC) but additional locations are likely. The aim of this study was to investigate the distribution of viral DNA throughout the equine body. Twenty-five horses divided into three groups were experimentally infected via intranasal instillation with one of three EHV-1 viruses and euthanized on Day 70, post infection. During necropsy, TG, various sympathetic/parasympathetic ganglia of head, neck, thorax and abdomen, spinal cord dorsal root ganglia, RALT, mesenteric lymph nodes, spleen and PBMC of each horse were collected. Genomic viral loads and L-(late) gene transcriptional activity in each tissue and PBMC were measured using qPCR. In addition, immunohistochemistry (IHC) was applied on neural parenchyma tissue sections. EHV-1 DNA was detected in many neural and lymphoid tissue sections, but not in PBMC. L-gene transcriptional activity was not detected in any sample, and translational activity was not apparent on IHC. Tissue tropism differed between the Ab4 wild type and the two mutant viruses.

Highlights

Equid herpesvirus-1 (EHV-1), a member of the Alphaherpesvirinae subfamily, causes respiratory disease, abortion, equid herpesvirus-associated myeloencephalopathy (EHM), chorioretinopathy, and infection of gonads of the intact male following a cell-associated viremia in peripheral blood mononuclear cells (PBMC) [1]
Ab4 N752 infected horses showed the most severe signs of respiratory disease followed by Ab4 WT infected horses
Our results suggest that EHV-1 is present at multiple sites throughout the body, in an arrested and very restricted, quiet phase of infection

Summary

Introduction

Equid herpesvirus-1 (EHV-1), a member of the Alphaherpesvirinae subfamily, causes respiratory disease, abortion, equid herpesvirus-associated myeloencephalopathy (EHM), chorioretinopathy, and infection of gonads of the intact male following a cell-associated viremia in peripheral blood mononuclear cells (PBMC) [1]. EHV-1 is typically spread by direct nose-to-nose contact followed by viral replication in the upper respiratory tract epithelium. This active lytic infection includes viremia and spread to the vascular endothelia of secondary sites of infection. After or even during the lytic phase, EHV-1 prepares for its characteristic chronic-persistent phase. This likely life-long infection phase is known as latent infection. In contrast to lytic infection, where transcriptional activity of the entire viral genome is fully upregulated, transcriptional activity during latency is likely limited to a single region known as the immediate early gene (IE) [2]. Current thoughts are that a latent infection is established early in life during first-time respiratory tract infection with EHV-1

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