|Kehrli Jr, Marcus|
Submitted to: Clinical and Vaccine Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/1/2012
Publication Date: N/A
Citation: N/A Interpretive Summary: In this study, pigs were given a harmless adenovirus that was engineered to deliver interferon, an antiviral substance that the body naturally produces, and simultaneously challenged with porcine reproductive and respiratory syndrome virus (PRRSV). The presence of the interferon decreased viral load and delayed the detection of virus in pigs challenged with PRRSV as compared to pigs not given the adenovirus and challenged with PRRSV. There was also an increase in a cell-mediated immune response and the profile of several cytokines was altered. These results indicate that interferon can have protective effects if present during the time of infection with PRRSV.
Technical Abstract: Porcine reproductive and respiratory syndrome (PRRS) is one of the most devastating and costly diseases to the swine industry world-wide. Overall, the adaptive immune response to PRRS virus (PRRSV) is weak and results in delayed elimination of virus from the host and inferior vaccine protection. PRRSV has been shown to induce a meager interferon (IFN)-alpha response, and in a previous study by our group, pigs that were injected with a nonreplicating human adenovirus type 5 vector expressing porcine interferon-alpha (Ad5-pIFN-alpha) and then challenged one day later with PRRSV had delayed viral replication and diminished disease severity. In this study, we followed the immune response in swine given Ad5-pIFN-alpha and challenged with PRRSV simultaneously. Not only was viremia delayed, but there was a decrease in viral load in the sera of pigs administered the Ad5-pIFN-alpha. Although seroconversion was slightly delayed in pigs receiving IFN-alpha, probably due to the delay in viremia, little difference was seen in the overall or neutralizing antibody response. However, there was an increase in virus-specific IFN-gamma secreting cells detected in the pigs receiving IFN-alpha, as well as an altered cytokine profile in the lung 14 days post infection, indicating that the presence of IFN-alpha at the time of infection can alter the innate and adaptive immune response to PRRSV.