Interaction of classical swine fever virus with dendritic cells

• DOI: 10.1099/vir.0.19716-0
• Publication Date: 2004-05-27T20:48:15Z
• Authors: C. P. Carrasco; R. C. Rigden; I. E. Vincent; C. Balmelli; M. Ceppi; O. Bauhofer; V. Tâche; B. Hjertner; F. McNeilly; H. G. van Gennip; K. C. McCullough; A. Summerfield
• Keywords: 0301 basic medicine; bone-marrow; double-stranded-rna; Cell Survival; Swine; pathogenesis; apoptosis; hog-cholera virus; Dendritic Cells; viral diarrhea virus; 3. Good health; 03 medical and health sciences; Classical Swine Fever Virus; immune-response; langerhans cells; Animals; Cytokines; full-length cdna; infectious rna

Functional disruption of dendritic cells (DCs) is an important strategy for viral pathogens to evade host defences. Monocytotropic viruses such as classical swine fever virus (CSFV) could employ such a mechanism, since the virus can suppress immune responses and induce apoptosis without infecting lymphocytes. Here, CSFV was shown to infect and efficiently replicate in monocyte- and in bone marrow-derived DCs. Interestingly, the infected DCs displayed neither modulated MHC nor CD80/86 expression. Stimulation of DCs with IFN-α/TNF-αor polyinosinic–polycytidylic acid (pIC) induced phenotypic maturation with increased MHC and CD80/86 expression, both with mock-treated and infected DCs. In addition, the T cell stimulatory capacity of CSFV-infected DCs was maintained both in a polyclonal T cell stimulation and in specific antigen-presentation assays, requiring antigen uptake and processing. Interestingly, similar to macrophages, CSFV did not induce IFN-αresponses in these DCs and even suppressed pIC-induced IFN-αinduction. Other cytokines including interleukin (IL)-6, IL-10, IL-12 and TNF-αwere not modulated. Taken together, these results demonstrated that CSFV can replicate in DCs and control IFN type I responses, without interfering with the immune reactivity. These results are interesting considering that DC infection with RNA viruses usually results in DC activation.