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Viruses. 2012 Apr;4(4):424-46. doi: 10.3390/v4040424. Epub 2012 Apr 2.

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

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Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61802, USA.


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/β) 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.


JAK-STAT; MDA5; NF-κB; Nsp; PRRS; PRRSV; RIG-I; arterivirus; interferon; non-structural proteins; nucleocapsid

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