Betaarterivirus suid 1, commonly Porcine reproductive and respiratory syndrome virus (PRRSV), is a virus that causes a disease of pigs, called porcine reproductive and respiratory syndrome (PRRS), also known as blue-ear pig disease (in Chinese, zhū láněr bìng 豬藍耳病).

This economically important, panzootic disease causes reproductive failure in breeding stock and respiratory tract illness in young pigs.

In 1990-1991, a similar disease was reported in several European countries such as Germany, The Netherlands, Belgium, Denmark, France, the United Kingdom, and Spain.

[12] Phylogeographic analysis of PRRSV epidemiology suggested that the virus diversified into unique subpopulations in Russia and Belarus, approximately 110–140 years ago.

The emergence of high-density confinement management practices and adoption of artificial insemination facilitated wide expansion and diversification of PRRSV.

[17][18] Wild animals may act as a natural reservoir for PRRSV and could be considered as an additional source of viral infections in domestic pigs.

Increasing genetic diversity allows emergence of severe outbreaks characterized by an elevated abortion rate as well as mortality in growing pigs and sows.

[19] Highly pathogenic and virulent "atypical" PRRSV isolates are regularly reported in different European countries: Belarus,[20] Belgium,[21] Hungary,[22] Austria[23] and others.

Immunization programs of swine herds worldwide with attenuated vaccines made of both PRRSV genotypes provided initially optimistic results in the 1990s.

The European and North American PRRSV strains cause similar clinical symptoms, but represent two distinct viral genotypes whose genomes diverge by approximately 40%, thus creating a veil of mystery about the origin of this virus.

Similarly, maintaining diagnostic PCR detection assays is difficult due to the high mutation rate of this virus.

[38] It was shown that pigs could be infected with PRRS virus by several routes of exposure: intranasal, intramuscular, peroral, intrauterine, and vaginal.

Subsequently, depending on the immune status of the pigs, the acute infection may be continued with a persistent stage with viral replication localized in lymphoid organs, including tonsils, spleen and lymph nodes.

The mechanism of persistence may be based on the high mutation rate of the PRRSV RNA genome allowing an escape from the host immune surveillance.

[43][44][45] After an extensive viremia, the virus reaches macrophages in different internal organs (e.g. lymphoid tissues and maternal endometrium) resulting in disorders, such as reproductive failure in sows.

[42] Depending on the viral strain and immune status of the host, PRRSV may cause both subclinical and severe reproductive and/or respiratory disease.

[20][49] Infected pigs display a range of respiratory (dyspnea, sneezing, coughing) and systemic clinical signs (a long-lasting high fever of over +41 °C, depression, anorexia, discoloration of the skin and the ears), conjunctivitis.

[52] The common lesions at necropsy may include inflammation of lungs and lymph nodes, fibrinous pleuropneumonia and pericarditis, peritonitis.

[59][60][61] The great genetic diversity of PRRSV and the absence of clear immunological parameters correlating with the protection are substantial barriers to new PRRS vaccine development.