Interplay between interferon-mediated innate immunity and porcine reproductive and respiratory syndrome virus.

Innate immunity is the first line of defense against viral infection, and in turn, viruses have evolved to evade host immune surveillance. As a result, viruses may persist in host and develop chronic infections. Type I interferons (IFN-α/ß) are among the most potent antiviral cytokines triggered by viral infections. Porcine reproductive and respiratory syndrome (PRRS) is a disease of pigs that is characterized by negligible induction of type I IFNs and viral persistence for an extended period. For IFN production, RIG-I/MDA5 and JAK-STAT pathways are two major signaling pathways, and recent studies indicate that PRRS virus is armed to modulate type I IFN responses during infection. This review describes the viral strategies for modulation of type I IFN responses. At least three non-structural proteins (Nsp1, Nsp2, and Nsp11) and a structural protein (N nucleocapsid protein) have been identified and characterized to play roles in the IFN suppression and NF-κB pathways. Nsp's are early proteins while N is a late protein, suggesting that additional signaling pathways may be involved in addition to the IFN pathway. The understanding of molecular bases for virus-mediated modulation of host innate immune signaling will help us design new generation vaccines and control PRRS.

Comparison of Torque Teno Sus Virus (TTSuV) viral load in Porcine Circovirus Type 2 vaccinated and non-vaccinated pig herds.

Torque Teno Sus Virus (TTSuV) viral load in accordance with the Porcine Circovirus Type 2 (PCV2) infection and age of two pig herds was determined. A total of 100 and 155 piglets from two farms were divided into two groups. Half of the piglets from each farm were given a commercial vaccine against PCV2 (vaccinated group), and the remaining piglets were used as a control group (non-vaccinated group). An early onset and a chronic viremic state of TTSuV genogroups were present regardless of the PCV2 infection, and there were no significant differences in the dynamics of TTSuV genogroups.