Micro-dissecting the pathogenesis and immune response of PRRSV infection paves the way for more efficient PRRSV vaccines.

Porcine reproductive and respiratory syndrome virus (PRRSV) is the most important infectious pathogen in pigs worldwide nowadays. Due to its genetic drift and increasing power to escape from immunity, PRRSV becomes more and more difficult to control. Based on a better knowledge of PRRSV, its interaction with the host cell, the macrophage, its pathogenesis and the immunity against this virus, new vaccines can now be constructed. This research-based development of new generation vaccines will allow swine industry to face the devastating consequences of PRRSV infections in the future. The present review summarizes the present knowledge on the pathogenesis, the immune response and the research-based vaccine development.

IFN-alpha treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin.

The Arterivirus porcine reproductive and respiratory syndrome virus (PRRSV) has a specific tropism for a subset of differentiated macrophages. Porcine sialoadhesin was identified as a PRRSV internalization receptor that is, similarly to sialoadhesins from other species, only expressed on subsets of macrophages. Sialoadhesin is not expressed or only expressed at low levels on monocytes, which might explain why monocytes are largely refractory to PRRSV infection. Different molecules have been identified that regulate human, mouse, or rat sialoadhesin expression in in vitro cultivated monocytes and macrophages, but the effect of these varies greatly between species. In this study, we observed that interferon-alpha (IFN-alpha) induces sialoadhesin expression on monocytes to levels similar as those on macrophages and that it increases sialoadhesin on macrophages. IFN-alpha-induced sialoadhesin expression was shown to be functional using a red blood cell (RBC) binding assay. Furthermore, a 2 or 3 day IFN-alpha pretreatment of monocytes caused a 20-fold increase in the numbers of PRRSV-infected monocytes and increased production of infectious virus. We conclude that IFN-alpha, although it is a potent antiviral molecule, upregulated sialoadhesin infection on in vitro cultivated monocytes, which results in enhanced PRRSV infection of monocytes.