Submitted to: Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/13/2006
Publication Date: 11/20/2006
Citation: Loving, C.L., Brockmeier, S., Sacco, R.E. 2006. Differential type I interferon activation and susceptibility of dendritic cell populations to porcine arterivirus. Immunology. 120:217-229.
Interpretive Summary: Porcine reproductive and respiratory syndrome virus (PRRSV) causes significant economic losses to the swine industry each year. One problem is the ability of the virus to persist in pigs. We determined whether PRRSV could infect certain types of white blood cells isolated from pig lungs and what effect this infection would have on the cells. One of the two could be infected by PRRSV but the functions of both were modified. These lung cells while not infected could serve as a transport vessel of the virus to other parts of the body. Therefore, they may play a role in the virus' persistence in swine.
Technical Abstract: Dendritic cells play a role in antiviral immunity by providing early innate protection against viral replication and by presenting antigen to T-cells for initiation of the adaptive immune response. Studies show the adaptive response to porcine reproductive and respiratory syndrome virus (PRRSV) is ineffective for complete viral elimination. Other studies describe the kinetics of the adaptive response to PRRSV, but have not investigated the early response by dendritic cells (DC's). We hypothesize that there is an eberrant activation of DC's early in PRRSV infection; consequently, the adaptive response is inadequately triggered. The current study characterized a subtype of porcine lung DC's (L-DC's) and investigated the ability of PRRSV to infect and replicate in L-DC's and monocyte-derived DC's (MDDC's). Furthermore, the type I interferon antiviral response to PRRSV with and without the addition of recombinant porcine IFN-a (rplFN-a), an important cytokine that signals for antiviral mediator activation, was analyzed. Results show that PRRSV replicated in MDDC's but not L-DC's, providing evidence these cells have followed distinct differentiation pathways. Although both cell types responded to PRRSV with an induction of IFN-B mRNA, the magnitude and duration of the response differed between cell types. The addition of rplFN-a was protective in MDDC's, and mRNA synthesis of Mx and PKR was observed in both cell types after rplFN-a addition. Overall, PRRSV replicated in MDDC's but not L-DC's, and rplFN-a was required for the transcription of protective antiviral mediators. DC response to PRRSV was limited to IFN-B transcription, which may be inadequate in triggering the adaptive immune response.