Arteriviruses, formerly classified as members of the family Togaviridae, have been assigned to the family Arteriviridae which contains a single genus, Arterivirus. The name of the genus derives from the disease, equine arteritis, which is caused by the type species. Arteriviruses are spherical, 50 to 74 nm in diameter and possess a lipid-containing envelope which has small surface projections. The icosahedral nucleocapsid contains a molecule of linear, positive-sense, single-stranded RNA. Replication takes place in the cytoplasm of infected cells. Arteriviruses, which are relatively labile, are sensitive to heat, low pH, lipid solvents, detergent treatment, UV irradiation and many disinfectants.
Members of the genus are host-specific. Infections have been described in horses, pigs, mice and monkeys. The primary target cells are macrophages. These viruses, which frequently persist in infected animals, can be spread horizontally by aerosols, by biting and also by venereal transmission.
Although infection with equine arteritis virus occurs worldwide, outbreaks of clinical disease are comparatively rare. Conjunctivitis, upper respiratory tract infection, ventral oedema and abortion are prominent clinical features. Close contact facilitates spread of infection. Virus is usually eliminated from mares and geldings within one to two months but may persist in about 35% of infected stallions. Carrier stallions are asymptomatic and shed virus continuously in semen. Mares infected venereally may spread virus horizontally to in-contact susceptible animals. Abortion or infection of the foal may occur when pregnant mares are infected.
Diagnosis requires laboratory confirmation. Virus isolation should be carried out in appropriate cell lines such as rabbit or equine kidney cells. Viral RNA can be detected in semen and other specimens using RT-PCR. Acute and convalescent blood samples should be submitted for serology. Seropositive stallions should be tested for virus in their semen and the breeding activities of carrier stallions confined to seropositive or vaccinated mares. In order to reduce the risk of colt foals becoming carriers, vaccination at six to twelve months of age is recommended.
This economically important condition is characterized by reproductive failure in sows and pneumonia in young pigs. The syndrome was first described in the USA in 1987. Despite attempts at controlling spread, the disease is now endemic in many countries. Natural infection occurs in pigs and wild boars. Significant antigenic and genomic differences between European and American isolates of the virus are evident, referred to as type 1 and type 2 genotypes, respectively. A variant of type 2 has been the cause of severe disease in China and south-east Asia. Nose-to-nose contact is considered to be the most likely route of transmission. Introduction of virus to a breeding herd is usually followed by reproductive failure. In some cases, cyanosis of the ears and vulva along with erythematous plaques on the skin (‘blue-ear disease’) have been described. Respiratory distress and increased pre-weaning mortality are important features of the disease in neonatal pigs. Severe outbreaks of other infections such as enzootic pneumonia or Streptococcus suis meningitis are frequently reported in infected herds. Subclinical infection occurs in some herds.
Serology is the most widely used diagnostic method. However, these tests do not distinguish carrier from vaccinated animals. The presence of PRRSV may be demonstrated by virus isolation, immunohistochemical staining or RT-PCR. Vaccination, combined with effective hygiene and health management are important measures for preventing disease transmission.