Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: December 8, 2004
Publication Date: April 2, 2005
Citation: Loving, C.L., Brockmeier, S., Sacco, R.E. 2005. Prrs virus productively infects monocyte-derived dendritic cells and induces production of innate antiviral mediators. Federation of American Societies for Experimental Biology Conference. 19:A404.
Infection with porcine reproductive and respiratory syndrome virus (PRRSV), a member of the Arteriviridae family, results in prolonged viremia and persistent infection of lymphoid tissues. The adaptive immune response has been characterized as weak and delayed, because neutralizing antibody and antigen-specific T-cells are not generated until approximately 4-weeks post-infection. Also, alveolar macrophages, the primary cell for PRRSV replication, exhibit a weak innate response to infection. The activation of dendritic cells to infection is critical in initiating an adaptive immune response. The effect of PRRSV on dendritic cells has not been elucidated and is important for understanding mechanisms of viral immune modulation. We show PRRSV is capable of replicating in porcine monocyte-derived dendritic cells (MD-DC's) to extremely high titers (>109CCID50 /ml) within 24 hours of infection. Although there is an apparent cytocidal effect on MD-DCís by PRRSV, there is an increase in the production of host antiviral mediators. IFN-alpha mRNA, measured by real-time PCR, increased 60-fold at 24-hours post-infection. Mx-1 and TNF-alpha mRNA increased 4-fold and 6-fold, respectively. Little change was detected for IL-1beta or IL-8 up to 72-hours post-infection. Overall, this data indicates that although PRRSV is capable of replicating in MD-DCís these cells respond with the production of innate antiviral mediators.