Equine Herpes Virus-1: Virus, Immunity and Vaccines

Abstract

Equine Herpes virus-1 (EHV-1) is one of the most common respiratory pathogens of the horse. EHV-1 induces several clinical signs of disease ranging in severity, from mild respiratory distress to abortion in pregnant mares, neonatal foal death and neuropathogenic disorders. This review details some aspects of EHV-1 biology, its life cycle and pathogenicity in the natural host. Protective immunity stimulated by natural EHV-1 infection, which is short lived and depends of both humoral and cellular immune responses, will also be treated here. Vaccination remains today one of the best options to fight EHV-1 infection and several different strategies of vaccination that have been investigated and developed over the past decades will be presented in this report.

Equine herpesvirus type 1 (EHV-1)-induced rearrangements of actin filaments in productively infected primary murine neurons

“…In its target host, it induces mild respiratory diseases, abortion, neonatal foal death, and neuropathogenic disorders. Like the other α-herpesviruses (HSV-1, BHV-1, PRV), EHV-1 infection is characterized by neurotropism and the ability to establish latent infections in trigeminal ganglion neurons [3, 16, 17, 19]. …”

Viral Equine Encephalitis, a Growing Threat to the Horse Population in Europe?

“…EHM incidence has increased in most parts of the world, in Europe and North America, as well as in Oceania, Africa, and Asia [10,11,28]. Pathogenesis and clinical disease: After primary replication in the respiratory tract, EHV-1 disseminates via cell-associated viremia in peripheral blood mononuclear cells and subsequently infects the endothelial cells of the pregnant uterus or central nervous system, leading in some cases to abortion and/or neurological disorders [34]. The incubation period of the disease is 6-8 days (before neurological signs become apparent), both in experimentally and in naturally EHV-1-infected horses [35].…”

“…Experimental infections with recombinant viruses performed by Goodman et al (2007) demonstrated that the N752 sequence variant of EHV-1 DNA Pol, when compared to the D752 variant, generated a low level of viremia in natural hosts and presented with reduced overall pathogenicity and capacity to induce neurological signs [46]. The discovery of this single polymorphism in ORF30 led to the development of a SNP-PCR (SNP-single nucleotide polymorphism) test for the detection Pathogenesis and clinical disease: After primary replication in the respiratory tract, EHV-1 disseminates via cell-associated viremia in peripheral blood mononuclear cells and subsequently infects the endothelial cells of the pregnant uterus or central nervous system, leading in some cases to abortion and/or neurological disorders [34]. The incubation period of the disease is 6-8 days (before neurological signs become apparent), both in experimentally and in naturally EHV-1-infected horses [35].…”

Avaliação da etiopagenia da encefalite causada pelo herpesvírus equino tipo 1 utilizando um modelo murino de neuroinfecção

“…Até o momento já foram identificadas 14 espécies de herpesvírus que acometem os equídeos (KLEIBOEKER et al, 2004;EHLERS et al, 2008;PAILLOT et al, 2008;OSTERRIEDER et al, 2010;KING et al, 2011) Fonte dos dados brutos: King et al (2011) Conforme já foi citado, o EHV-1 é o agente causador de diferentes formas de doença em cavalos, das quais as mais comuns são a rinopneumonite, caracterizada por manifestações respiratórias no trato superior em animais jovens; o abortamento a vírus, responsável pelo abortamento em éguas no terço final da gestação (entre o 8 o e o 11 o meses) e mortalidade perinatal em potros e a EHM, caracterizada por manifestações neurológicas em cavalos adultos. Além disso, e ainda que com menor frequência, o EHV-1 pode provocar doenças oculares e infecção pulmonar vasculotrópica.…”

“…A partir de estudos que utilizaram camundongos knockout (CCL3 / ), infectados pelo EHV-1, foi comprovado que a quimiocina CCL3 (proteína inflamatória de macrófagos 1 alfa) desempenha papel fundamental no controle da replicação viral nos pulmões por meio do desencadeamento de intensa resposta inflamatória (VAN DE WALLE et al, 2008a,b). (PAILLOT et al, 2005;PAILLOT et al, 2007;PAILLOT et al, 2008 A quimiocina CCL2 está envolvida nos mecanismos de eliminação viral atuando diretamente na permeabilidade da barreira hematoencefálica e/ou como fator quimiotático para linfócitos e macrófagos no processo inflamatório do SNC (STAMATOVIC et al, 2005;DESHMANE et al, 2009). A expressão gênica de CCL2 no tecido nervoso dos camundongos C57BL/6, CD4 / e CD8 / infectados pelo EHV-1 aumentou expressivamente, observado-se valores variando de 4 a 7 mil e 16 a 32 mil vezes maiores do que os controles no 2º e 3º dpi, respectivamente.…”