Regulation and evasion of antiviral immune responses by porcine reproductive and respiratory syndrome virus

• Five PRRSV viral proteins are shown to inhibit type I IFN induction and signaling by targeting different intracellular signaling intermediates.
• PRRSV regulates the expression of IL-10 and TNFα.
• PRRSV modulates apoptosis during infection.
• MicroRNAs might play significant roles in subverting immunity for PRRSV.
• PRRSV escapes from adaptive immunity by impairing antigen presentation, activating Tregs, and ADE.

Virus infection of mammalian cells triggers host innate immune responses to restrict viral replication and induces adaptive immunity for viral elimination. In order to survive and propagate, viruses have evolved sophisticated mechanisms to subvert host defense system by encoding proteins that target key components of the immune signaling pathways. Porcine reproductive and respiratory syndrome virus (PRRSV), a RNA virus, impairs several processes of host immune responses including interfering with interferon production and signaling, modulating cytokine expression, manipulating apoptotic responses and regulating adaptive immunity. In this review, we highlight the molecular mechanisms of how PRRSV interferes with the different steps of initial antiviral host responses to establish persistent infection in pigs. Dissection of the PRRSV–host interaction is the key in understanding PRRSV pathogenesis and will provide a basis for the rational design of vaccines.