Impact of virus-induced gill disease caused by carp edema virus (CEV) on the immunological status of fish

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Gill diseases seriously affect fish health and have a high negative impact on aquaculture, mainly because of the multifunctional properties of gills in fish physiology. Studies on pathogen related gill diseases are largely hampered by the lack of infection models, which exclusively affect gills. Carp edema virus (CEV), a fish-infecting pox virus, infects predominantly the gills of common carp (Cyprinus carpio). It induces a severe gill disease known as koi sleepy disease (KSD) and is fatal for the majority of infected fish. Due to its severe effect on gills, the CEV infection causes physiological distress to infected fish and also seems to induce an impairment of the immunity. Interestingly, different strains of common carp show high (Amur wild carp - AS strain) or low (koi strain) resistance to this virus. Our working hypotheses propose that: (i) differential stress response/stress sensitivity might affect the outcome of KSD in koi and AS strains of carp and (ii) severe impairment of the immune response during KSD may have an impact on susceptibility to secondary infections and the general immunological status of the survivors after CEV infection. In the present project, we will study the mechanisms underlying the differences in the resistance to CEV between AS and koi carp strains. We will also study how a CEV-induced impairment of immune response influences the susceptibility of carp to other pathogens such as the bacterium Flavobacterium branchiophilum or the viruses cyprinid herpesvirus 3 (CyHV-3) and spring viraemia of carp virus (SVCV). To study the mechanisms of the immunity diminishing we will use a “salt rescue model” which is based on the supplementation of salt (NaCl) into the tank water, which abolishes the impairment of physiology and immune responses in CEV infected fish. The results of this project will allow us to identify the interplay of stress and immune responses in fish affected by a viral gill disease and its importance for resistance/susceptibility of fish to clinical disease. Finally, the results will allow us to expand our knowledge on important and phylogenetically conserved mechanisms regulating anti-viral immune response. In future, in-depth knowledge of such interactions will help to develop novel strategies for preventing and combating pathogen-induced gill diseases.