This virus has many potential hosts. So far, it has been isolated from more than 50 different species. The virus was first demonstrated in a marine environment in 1979. An article by Marty and collaborators (2003) concludes that VHS-virus is the most important pathogen of pacific herring, and that the virus may play a population size regulatory role Atlantic herring and Atlantic cod are important species in Norwegian fisheries, and as this virus may play a role in wild populations it is necessary to investigate the presence of VHS-virus in these species.
VHS-virus can cause the disease Viral Haemorragic Septicaemia. It has been reported that at least 50 species of fresh water and marine fish may be carriers of different variants (genotypes) of the virus. The mortality varies with species, and the variant (genotype) of the virus. In rainbow trout fry, mortality may be up to 80-100%, whereas mortality of older and larger rainbow trout often is lower. The same applies to turbot. VHS has not been demonstrated at higher temperatures than 18°C, and outbreaks typically occur during spring at variable and rapidly increasing temperatures.
The background of the present project is the outbreak of VHS in farmed rainbow trout in Storfjorden, Sunnmøre, autumn 2007. This was the first demonstrated outbreak of VHS in Norwegian waters since 1974. Before this, the disease had been detected in different rainbow trout farms in a decade from 1964. Norway has had international status as free from VHS since 1994. With exception of Storfjorden, this is still the case. However, the management of the disease is disputed, and the need for increased knowledge is large. Although Norway did not experience outbreaks of the disease for more than 30 years, VHS is a well-known problem elsewhere in Europe and USA. In many countries, the disease may cause large economic losses for farmers of rainbow trout.
The unique finding from the Storfjorden outbreak was the genotype of the VHS-virus that was isolated. Genotype III has never ever been demonstrated in rainbow trout. Challenge experiments previously performed have given indications that rainbow trout was not susceptible for this type of VHS-virus. This indicates that the outbreak in Storfjorden is unique. Genotype III has earlier been demonstrated associated with disease of turbot (in Scotland), and from a range of marine species in Skagerrak and waters surrounding U.K.
So far, VHSV has not been investigated in northern coastal waters, but we intend to do this during the present project.
We wish to achieve increased understanding of the distribution of VHSV in wild fish stocks and in cultured fish, which genotypes are present in different geographical areas, and which that infect and cause disease to different speces. We know that there are reservoirs in wild marine fish stocks, but we do not know the degree to which thes may constitute a threat to cultured fish. We know that the virus may proliferate in cultured rainbow trout, but not to which degree such proliferation may cause a threat to wild fish stocks. Therefore, we will also test the susceptibility to the virus of different important fish species in laboratory experiments. This knowledge will be greatly needed in order to develop future management strategies for aquaculture and fisheries.