Porcine reproductive and respiratory syndrome virus productively infects monocyte-derived dendritic cells and compromises their antigen-presenting ability - PubMed

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• PMID: 17031757
• DOI: 10.1007/s00705-006-0857-1

Porcine reproductive and respiratory syndrome virus productively infects monocyte-derived dendritic cells and compromises their antigen-presenting ability

X Wang et al. Arch Virol. 2007 Feb.

Abstract

Dendritic cells (DC) are potent antigen-presenting cells that play an important role in inducing primary antigen-specific immune responses. However, some viruses have evolved to specifically target DC to circumvent the host's immune responses for their persistence in the host. Porcine reproductive and respiratory syndrome virus (PRRSV) causes a persistent infection in susceptible animals. Although it is generally believed that the existence of PRRSV quasispecies is partly responsible for the virus persistence, other mechanisms of immune evasion or immune suppression may also exist. Here, we studied the role of DC in PRRSV persistence and immune suppression. Our results showed that PRRSV underwent a productive replication in pig monocyte-derived DC (Mo-DC) as measured by both immunofluorescence staining of viral nucleocapsid protein and virus titration assays, leading to cell death via both apoptosis and necrosis mechanisms. Additionally, PRRSV infection of Mo-DC resulted in reduced expression of MHC class I, MHC class II, CD14 and CD11b/c. This was in agreement with the impaired mixed lymphocyte reaction of PRRSV-infected Mo-DC compared to that of mock-infected Mo-DC. We also examined the cytokine profiles of PRRSV-infected Mo-DC using a quantitative ELISA method. Results indicated that no apparent change in the levels of IL-10, IL-12 and IFN-gamma was detected. Taken together, our data demonstrate that PRRSV productively infects Mo-DC and impairs the normal antigen presentation ability of Mo-DC by inducing cell death, down-regulating the expression of MHC class I, MHC class II, CD11b/c and CD14 and by inducing minimal Th1 cytokines.

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