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Equid herpesvirus type 1 (EHV1) is an ubiquitous alphaherpesvirus that will infect most horses during their life time,sometimes resulting in serous clinical signs with a considerable negative impact on horse welfare and economics.EHV-1 is capable of causing a respiratory disease (rhinopneumonitis) and nervous system damage (myeloencephalopathy) in horses worldwide.Affected equines show a variety of clinical symptoms,including anorexia,fever,and ocular discharge,and nasal discharge,ataxia of varying severity,paralysis,abortion and neonatalfoal death.During EHV1 pathogenesis,the virus is able to infect several cell types and tissues such as the respiratory epithelium and underlying connective tissues (primary replication).It can also cause a cell-associated viremia followed by infection of the endothelium of the pregnant uterus and the central nervous system (secondary replication).EHV-1 serves as a model for studying aspects of alpha herpesviruses,such as productive and persistent infection,gene regulation and immune responses against these infections with members of this subfamily.The genome of EHV-1 harbours at least 76 genes,including one known as UL24.This gene is evolutionarily conserved among many members of the family Herpesviridae and is considered as a core gene for herpesviruses.The UL24 of herpes simplex virus 1 (HSV-1) exerts some effects on the subcellular distribution of viral glycoproteins associated with fusion.It plays an important role in dispersing nucleolin.In addition,it is associated with nervous pathogenicity.Transcriptional regulation performs an important role in the pathogenicity of herpesviruses as well as in keeping a cascaded expression of viral genes in the temporal order of immediate-early (α),early (β) and late (γ) upon viral infection.The late pattern is further divided into two types: leaky-late (γ1),whose expression begins prior to viral genome replication and subsequently reaches maximal levels after the onset of viral DNA replication and true-late(γ2),whose expression is strictly dependent on replication of the viral genome.