Effect Of Prrsv Infection On Immune Suppression And Porcine FcγRs MRNA Expression

Porcine reproductive and respiratory syndrome (PRRS), which is caused by PRRSV, is an infectious disease characterized by abortion of pregnant sow and breathing obstacle of piglets. PRRSV, one of the most important pathogenic microorganisms, is endemic in the many provinces of China. Immunosuppression, which may due to serious effecte on immune response, happen after the PRRSV infection.FcγRs play a critical role in immune regulation by providing a link between the humoral and cellular immune responses. Three classes of porcine FcγR, named FcγRI, FcγRII and FcγIII, was characterized. FcγRII is the inhibitory Fc receptor, as an ITIM motif was found in intracellular domain. While porcine FcγRI and FcγIII function as activation receptors. Moreover, by regulating DC activity, FcγRs control whether an immunogenic or tolerogenic response is initiated after the recognition of antigenic peptides. Thus, it can be speculated that there may be a correlation between the changes of cellular immunity and humoral immune and the expression of Fc receptor after infection by different PRRSV strains.In this study, the relationship between immune suppression and dynamic expression of porcine activation and inhibitory FcγRs after infection with PRRSV isolates was investigated. 2-month-old piglets were inoculated with PRRSV variant strain HN07-01 and classical strain BJ-4 respectively. The clinical symptoms was observed and the peripheral blood immune cells were detected. Using real-time PCR, the activating and inhibitory Fc receptor transcription dynamic in porcine peripheral blood was investigated after infection with isolated PRRSV. Peripheral blood immune cells in PRRSV variant infected piglets decreased significantly than in BJ-4 strain. The expression of activation receptors, FcγRI and FcγRIII, was found to be rapidly reduced, and the inhibitory Fc receptor, poFcγRII, was slight increased after infection, and there is a significantly distinctive between different PRRSV strains. PRRSV infection can rapidly induce high levels of PRRSV-specific antibodies, but the immune effector cells were not to be activated by antibody and antigen-antibody complex as the decreased expression of activating FcγRs. This may be the molecular basis of immunosuppression after PRRSV infection.