The Alphaarterivirus equid (equine arteritis virus [EAV]) causes equine viral arteritis (EVA), a respiratory and reproductive disease that affects horses, donkeys, mules, and zebras, with limited evidence suggesting that the host range may also extend to camelids (i.e., alpacas and llamas). The virus was first isolated from the lung of an aborted fetus during a respiratory disease and abortion outbreak on a Standardbred breeding farm near Bucyrus, Ohio, in 1953. Since then, EVA outbreaks have been reported in many countries. This disease can lead to economic loss in the equine industry due to abortions in pregnant mares, neonatal mortality, and the establishment of the long-term carrier state in stallions that shed the virus in semen. The persistently infected stallions play a pivotal role in maintaining and perpetuating the virus in nature. During the carrier state in stallions, EAV is exclusively localized in the reproductive tract of carrier stallions, and it has been shown that the ampulla of the vas deferens is the primary site of EAV persistence. Furthermore, in vitro susceptibility of equine CD3+ T lymphocytes to EAV strongly correlates with the establishment of persistent infection in the stallion. Equine CXCL16 (EqCXCL16) was identified as a critical cellular protein associated with the EAV carrier state in stallions, and a genotyping assay was developed to identify colts and stallions that carry the susceptible genotype. The control, elimination of infection or disease, and ultimately eradication of EVA can be achieved by combining genetic screening of colts/stallions for selective breeding and targeted vaccination, serological screening of stallions and mares before breeding and movement, vaccination, and improved biosecurity and management practices.