Seventeen percent of aquaculture Atlantic salmon in Norway die after transfer from freshwater to seawater facilities, many from infectious disease. The degree to which these deaths are attributable to unseen weakness in smolt preparation is therefore an important concern. Strong evidence in mammals and supporting evidence in other teleosts show that the light environment shapes the immune response via entrainment of the circadian clock. These data are alarming as most smoltification protocols use constant light, which does not entrain the circadian clock and is associated with negative survival outcomes to disease challenge in other species. The goal of our study was to establish how different light environments affected the anti-viral immunity of Atlantic salmon smolts. To achieve this goal, we measured the transcriptional response of select type I and type II interferons and major histocompatibility complexes in the heart and head kidney following an intraperitoneal SAV3 viral challenge delivered under different lighting conditions. We began with two hypotheses. First, that compared with a regular light-dark cycle (long photoperiod; LP), Atlantic salmon smolts kept at constant light (LL) would have a weaker resistance to viral challenge. Second, that Atlantic salmon smolts kept in a regular light-dark cycle would have altered immune sensitivity between the light and dark phases. To test our first hypothesis, we photostimulated smoltification in parr through exposure to either LP or LL conditions for 6 weeks then challenged them by SAV3 infection. LP and LL groups showed indistinguishable measurements in classical smolt characteristics and comparable levels of SAV3 mRNA in the heart after 8 and 14 days post infection. They also showed comparable transcriptional responses of select type I interferons (IFNa, IFNb, IFNc) and class II major histocompatibility complexes (MHC II) in both heart and head kidney tissue. MHCI induction in the heart was, however, lower in the LL group compared to the LP group after 8 days, and IFNγ induction in the heart was marked higher in the LL compared to the LP group after 14 days. While this data suggests a heightened sensitivity of the LL group to SAV3 challenge after 14 days, the consistent induction of MHC II, a key target gene of IFNγ signaling, to SAV3 infection in both LL and LP groups indicates that photoperiod may only have a minor impact on interferon regulation, rather than a more general influence on the viral immune response. To test our second hypothesis, we compared the transcriptomic response in the heart to SAV3 infection delivered either at the mid-light or mid-dark phase in the LP group. Both mid-light and mid-dark groups showed an upregulation of immune related genes and down-regulation of structural genes of mitochondria, but an analysis of the interaction between infection and time of day identified no differentially regulated genes. This second experiment suggests that, unlike in mammals, daily timing of viral infection may not play a major role in the immune response of Atlantic salmon.
