Since the disease emerged on swine farms, the PRRS virus (PRRSV) has spread worldwide, gained genetic diversity and, in particular cases, increased its virulence. The basis for the virulence, however, remains unknown, despite being investigated with a variety of different approaches.
Porcine Reproductive and Respiratory Syndrome (PRRS) is characterized by reproductive and respiratory symptoms, a decrease in growth performance, and increased mortality in young pigs. The etiological agent, PRRSV belongs to the genus Artevirus within the family Arteriviridae, and its strains are divided into major genotypes. Type 1 viruses are related to the early European isolates (prototype Lelystad virus), whilst Type 2 genotype viruses are related to the North American strains (prototype VR-2332) isolated on swine farms.
It is now widely accepted that significant genetic variability can occur not only between but also within genotypes. This genetic variability of the PRRSV may correspond to the wide range of symptoms also observed on swine farms, extending from lack of clinical signs to fatal disease (highly virulent PRRSV). Multiple genomic regions may be responsible for the immunological behaviour and the virulence of the PRRSV. However, a link between specific molecular sequences and the degree of clinical severity among PRRS virus isolates on swine farms has not yet been identified. At the present time, molecular and antigenic characterization of isolates is used as an epidemiological tool rather than a virulence determinant or vaccine selection tool.
Although the most pathogenic outbreaks reported up to now have always been related to Type 2 isolates, highly virulent PRRSV strains of both genotypes have been isolated from severe clinical cases on swine farms all over the world. Some examples of virulent strains are described below:
Europe (Type 1; Subtype III): Karniychuk et al. (2010) investigated the pathogenesis and antigenic characteristics of type 1 Lena strain, which was isolated from a Belarusian farm with reproductive and respiratory clinical signs. The main conclusion of the study was that the Lena strain is a highly pathogenic PRRS virus strain belonging to subtype III (type 1).
North-America (Type 2): Numerous severe PRRS outbreaks have been reported from North-American farms, mainly in the U.S.A. In the last twenty years, three outbreaks have been particularly significant:
Isolates 142 (1996). Atypical PRRS clinical outbreaks known as swine abortion and mortality syndrome. It was mainly characterised by mid- or late-term abortions of 10-50% of the sows in a period of a few weeks. Sows and gilts had fever and were anorexic. Mortality was from 5% to 10% of the breeding herd. An increase in preweaning mortality and a decrease in nursery pig performance were also observed. The wild-type isolates involved were known as 142, because of their RFLP patterns.
Isolates 184 (2001 and 2006). RFLP 1-8-4 or Strain MN184. This caused high morbidity (50%) and mortality (20%) rates. ORF5 nucleotide sequence analysis and comparison with other type 2 PRRS virus strains demonstrated that MN184 were significantly different to previous strains. Three quite variable regions were identified, corresponding to nsp1β, nsp2 and ORF5. Nsp2 shared only 66-70% amino acid similarity to other North-American PRRS virus nsp2 proteins.
Asia (Type 2; Highly-pathogenic PRRS virus – HP-PRRSV): In June 2006, a very severe disease called porcine high fever syndrome emerged in Jiangxi province (People’s Republic of China) and rapidly spread throughout the country. By the end of that year, the disease had already been detected in 16 provinces affecting over 2 million pigs with about 400,000 fatal cases. Subsequent analysis demonstrated that the disease was caused by an atypical highly virulent strain of the PRRS virus. Since then, highly-pathogenic PRRS virus (HP-PRRSV) has been isolated around the East, South and North of Asia, including China, Vietnam, Bhutan, Cambodia, Indonesia, Laos, Malaysia, Myanmar, the Philippines, Russia, Singapore, etc. Nowadays, it has become endemic in some of these countries and continues to have a devastating economic impact in all of them.
According to ORF5 phylogenetic analysis, it seems that HP-PRRSV might have evolved from strains previously detected in China. Although the basis for HP-PRRSV virulence remains unknown, some authors have claimed that Nsp2, Nsp9 and/or Nsp10 may be involved in the fatal virulence of HP-PRRSV. Other studies have concluded that aberrant immune responses triggered by HP-PRRSV infection could be closely related to acute lung injury.
The risk of a new highly-pathogenic PRRS virus emerging and/or its worldwide spread is a real threat.