Immune Responses Against Classical Swine Fever Virus: Between Ignorance and Lunacy.

Artur Summerfield,Nicolas Ruggli

doi:10.3389/fvets.2015.00010

Abstract

Classical swine fever virus infection of pigs causes disease courses from life-threatening to asymptomatic, depending on the virulence of the virus strain and the immunocompetence of the host. The virus targets immune cells, which are central in orchestrating innate and adaptive immune responses such as macrophages and conventional and plasmacytoid dendritic cells. Here, we review current knowledge and concepts aiming to explain the immunopathogenesis of the disease at both the host and the cellular level. We propose that the interferon type I system and in particular the interaction of the virus with plasmacytoid dendritic cells and macrophages is crucial to understand elements governing the induction of protective rather than pathogenic immune responses. The review also concludes that despite the knowledge available many aspects of classical swine fever immunopathogenesis are still puzzling.

Highlights

Classical swine fever (CSF) is a highly contagious disease of pigs caused by the classical swine fever virus (CSFV), which is a member of the genus pestivirus within the Flaviviridae family
A particular affinity of the virus for the reticuloendothelial cell system has been noted with macrophages (MΦ), dendritic cells (DC), and endothelial cells (EDC) being primary targets [2,3,4,5,6,7,8,9,10]
We propose that the large quantities of IFN-α produced by plasmacytoid DC (pDC) play a central role in the innate immune response to CSFV

Summary

Introduction

Classical swine fever (CSF) is a highly contagious disease of pigs caused by the classical swine fever virus (CSFV), which is a member of the genus pestivirus within the Flaviviridae family. CSFV probably passes through the epithelial cells and M-cells of the tonsilar crypts, the primary target tissue for virus replication. A particular affinity of the virus for the reticuloendothelial cell system has been noted with macrophages (MΦ), dendritic cells (DC), and endothelial cells (EDC) being primary targets [2,3,4,5,6,7,8,9,10] From these primary sites of replication, the virus spreads to other lymphoid organs. More recent investigations using quantitative RT-PCR confirmed these older studies, demonstrating a wider tissue distribution with longer durations of infection [12] This is reflected at the level of cell tropism. In the skin, efficient infection of keratinocytes, hair follicle epithelial cells, and mesenchymal cells in the dermis was demonstrated at later time points after infection [14]

Highly Virulent Strains Induce a Disastrous Infection for the Immune System

Proposed Mechanisms Leading to Control

Findings

Conclusion and Future Research