Arteriviridae ~ ViralZone

Host-virus interaction

Apoptosis modulation

The equine arteritis virus and PRRSV induce apoptosis via host caspases activation (caspase-8 and mitochondria-dependent caspase-9)

Autophagy modulation

PRRSV induces autophagy to promote virus replication .

Innate immune response inhibition

PRRSV clearly inhibits the type-I IFN response and down-regulates TLR3, TLR7, and TLR8 expression.
At least three non-structural proteins (Nsp1, Nsp2, and Nsp11) play roles in the IFN suppression and NF-κB pathways :

Nsp1α subunit inhibits the IκB phosphorylation in the cytoplasm and therefore the activation of NF-κB.

Nsp1β inhibits phosphorylation of STAT1 and nuclear translocation of ISGF3 complex (composed of STAT1, STAT2 and IRF9). Nsp1β prevents IRF3 activation, thereby interfering with the RIG-I signaling pathway .

Nsp2 inhibits IFN production by blocking the ubiquitinylation of phosphorylated IκB and phosphorylation of IRF3 through the OTU domain. Nsp2 has the potential to deconjugate ISGylation.

Nsp11 suppresses IFN-β production through degradation of IPS-1 mRNA. For the second wave of IFN signaling, PRRSV Nsp1β blocks the phosphorylation of STATs and inhibits the nuclear translocation of ISGF3 complex (composed of STAT1, STAT2 and IRF9).