Betaarterivirus suid 2 is a species of enveloped, positive-strand RNA viruses which infect domestic pigs.
[6] As a member of the family Arteriviridae, PRRSV has an in vivo and in vitro tropism for cells like macrophages or monocytes.
These can then be identified by the expression of sialoadhesin[7] PRRSV type 2 has been historically classified according to RFLP (restriction fragment length polymorphism) patterns.
These are characterized by displaying a cut pattern of three different enzymes (MluI, HincII and SacII) in the ORF5 portion of the PRRSV genome.
Criticism to this way of classifying the virus range from the multitude of possible combinations of different cut pattern of the three enzymes (leading to tens of thousands of different PRRSV RFLP patterns, with unknown epidemiological significance)[8] to the quick change in RFLP types of a single virus in as few as 10 animal passages.
[9] Because of those limitations, PRRSV type 2 has been recently classified according to phylogenetic characteristics of the ORF5 portion of the viral genome, which aggregates isolates into phylogenetic lineages based on the ancestral relationships and genetic distance among isolates.
The other lineages had what is assumed introductions into other geographic locations such as Thailand, Canada, China and Italy.
There has been the introduction of the MN184-related cluster, acute PRRS/abortion storm, and highly pathogenic Chinese strains.
[8] Canada and the United States have shown the highest degree of continued diversity.
[3] Currently, inactivated and live attenuated viruses are used to try to eliminate porcine reproductive and respiratory syndrome (PRRS).
The live attenuated vaccine works through an unknown mechanism and only helps clinical symptoms; it does not prevent infection.
Researchers are currently trying to identify neutralizing antibodies that will provide true immunity against type 2 PRRSV.
The N protein is composed of 123 amino acids, produces an immune response within the cell, and is thought to be multifunctional.
[14] Infection by PRRSV can be completely blocked using monoclonal antibodies that precipitate the 210- kDa protein out of solution.
[4] Despite the genetic variation that occurs in type 2 PRRSV, a conserved stem loop in the genome has been identified.
It has been shown that mutations within the leader transcription regulating sequence (TRS) of the type 2 PRRSV genome may inhibit proper sgmRNA translation.
PRSSV uses different non-conical (non-structural) body translation regulating sequences (TRS-B) to produce different sg mRNA species.
It is thought that this apoptosis of the host cell plays a significant role in the pathogenesis of the type 2 PRRSV infection.
[20] One main way that Type 2 PRSSV modulates the host cell is through the activation of the inflammatory response.
This pro-inflammatory response in host cells oftentimes most visibly results in interstitial pneumonia of the infected swine.
It has now been found that type 2 PRRSV increases the NF - KB-driven inflammatory cytokine response.
When researchers knocked out DHX36, the activation of NF-κB signaling by PRSSV and nucleocapsid (N) protein was inhibited.