Equine arteritis virus (EAV), the causative agent of equine viral arteritis (EVA), was rst isolated from the lung of an aborted fetus following an extensive outbreak of respiratory disease among horses on a Standardbred breeding farm in Bucyrus, Ohio, in 1953.1,2 EAV is the prototype virus in the family Arteriviridae (genus Arterivirus), order Nidovirales, which also includes porcine reproductive and respiratory syndrome virus, simian hemorrhagic fever virus, lactate dehydrogenase-elevating virus of mice, and recently identied wobbly possum disease virus of free-ranging Australian brushtail possums (Trichosurus vulpecula) in New Zealand.3,4 All members of the order Nidovirales are enveloped viruses with linear, positive-sense, single-stranded ribonucleic acid (RNA) genomes. Furthermore, the genome organization and replication strategy of EAV strikingly resemble those of corona-and toroviruses, including the production of a 3′-coterminal nested set of subgenomic mRNAs (sg mRNAs), and key domains of the arterivirus replicase are homologs of domains found in corona-and torovirus replicases.5 However, EAV and other arteriviruses differ considerably in their genetic complexity and virion architecture from the other nidoviruses.