The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1.

Kathlyn Laval,Hossein B Baghi,Eline Van Crombrugge,Jing Zhao,Annick C Gryspeerdt,Hans J Nauwynck,Haileleul N Dubale,Katrien C K Poelaert,Barbara Garré,Annelies P Vandekerckhove,Ines Zarak,Jolien Van Cleemput,Karen Van Der Meulen

doi:10.3389/fmicb.2021.662686

Abstract

Equine herpesvirus type 1 (EHV-1) is an alphaherpesvirus related to pseudorabies virus (PRV) and varicella-zoster virus (VZV). This virus is one of the major pathogens affecting horses worldwide. EHV-1 is responsible for respiratory disorders, abortion, neonatal foal death and equine herpes myeloencephalopathy (EHM). Over the last decade, EHV-1 has received growing attention due to the frequent outbreaks of abortions and/or EHM causing serious economical losses to the horse industry worldwide. To date, there are no effective antiviral drugs and current vaccines do not provide full protection against EHV-1-associated diseases. Therefore, there is an urgent need to gain a better understanding of the pathogenesis of EHV-1 in order to develop effective therapies. The main objective of this review is to provide state-of-the-art information on the pathogenesis of EHV-1. We also highlight recent findings on EHV-1 immune evasive strategies at the level of the upper respiratory tract, blood circulation and endothelium of target organs allowing the virus to disseminate undetected in the host. Finally, we discuss novel approaches for drug development based on our current knowledge of the pathogenesis of EHV-1.

Highlights

EHV-1 is a highly contagious pathogen and is usually transmitted via direct contact with infectious secretions or via inhalation of infectious aerosols (Patel et al, 1982)
Single infected epithelial cells were visible at 12 h post-inoculation and EHV-1-induced plaques were observed in the epithelium of equine nasal and nasopharyngeal explants starting from 24 hpi (Vandekerckhove et al, 2010; Negussie et al, 2016)
The authors demonstrated that the replication of EHV-1 is highly restricted in these cells with less than 10% infected compared to fully susceptible rabbit kidney (RK-13) cells (Laval et al, 2015a, 2017)

Summary

Introduction

EHV-1 is a highly contagious pathogen and is usually transmitted via direct contact with infectious secretions (saliva, nasal discharge) or via inhalation of infectious aerosols (Patel et al, 1982). EHV1-induced plaques were observed in the epithelium of the nasal mucosa starting from 2 to 7 days post-inoculation (dpi) (Gryspeerdt et al, 2010). Single infected epithelial cells were visible at 12 h post-inoculation (hpi) and EHV-1-induced plaques were observed in the epithelium of equine nasal and nasopharyngeal explants starting from 24 hpi (Vandekerckhove et al, 2010; Negussie et al, 2016). Primary EHV-1 infection of several tissues of the URT results in the destruction and erosion of the epithelium and in nasal shedding starting from 1 to 14 dpi (Gibson et al, 1992; Gryspeerdt et al, 2010; Figure 1.1b). The nasal discharge can become mucopurulent, due to secondary bacterial infections, and contribute to the development of rhinopneumonitis (Thomson et al, 1979; McGavin and Zachary, 2007)

Objectives

Findings

Conclusion