Interplay between Interferon-Mediated Innate Immunity and Porcine Reproductive and Respiratory Syndrome Virus

Viruses

Yan Sun¹  Mingyuan Han¹  Chiyong Kim¹  Jay G. Calvert² 

[1] Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61802, USA;Pfizer Animal Health, Kalamazoo, MI 49007, USA;

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

DOI  :  10.3390/v4040424

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2012 by the authors; licensee MDPI, Basel, Switzerland.