TLR22 occurs exclusively in aquatic animals and its role is unknown. Herein we show that the fugu (Takifugu rubripes) (fg)TLR3 and fgTLR22 link the IFN-inducing pathway via the fg Toll-IL-1R homology domain-containing adaptor protein 1(fgTICAM-1, or TRIF) adaptor in fish cells. fgTLR3 resides in endoplasmic reticulum and recognizes relatively short-sized dsRNA, whereas fgTLR22 recognizes long-sized dsRNA on the cell surface. On poly(I:C)-stimulated fish cells, both recruit fgTICAM-1, which in turn moves from the TLR to a cytoplasmic signalosome region. Thus, fgTICAM-1 acts as a shuttling platform for IFN signaling. When fish cells expressing fgTLR22 are exposed to dsRNA or aquatic dsRNA viruses, cells induce IFN responses to acquire resistance to virus infection. Thus, fish have a novel TICAM-1-coupling TLR that is distinct from the mammalian TLR3 in cellular localization, ligand selection, and tissue distribution. TLR22 may be a functional substitute of human cell-surface TLR3 and serve as a surveillant for infection with dsRNA virus to alert the immune system for antiviral protection in fish.

Aquabirnaviruses, represented by Infectious pancreatic necrosis virus (IPNV), have been isolated from epizootics in salmonids and a variety of aquatic animals in the world; six genogroups of aquabirnaviruses have been identified. In comparisons of nucleotide sequences of the VP2/NS junction region, maximum nucleotide diversities of 30?8 % were observed among 93 worldwide aquabirnavirus isolates. A phylogenetic tree revealed the existence of a new genogroup, VII, for Japanese aquabirnavirus isolates from marine fish and molluscan shellfish. Nucleotide diversities between genogroups VII and I-VI were 18?7 % or greater. At the nucleotide level, Japanese IPNV isolates from epizootics in salmonids were nearly identical to a genogroup I strain from the USA or Canada. It is suggested that Japanese IPNV isolates belonging to genogroup I were originally introduced from North American sources, whereas Japanese aquabirnavirus isolates of genogroup VII were from marine aquatic animals indigenous to Japan.

Skin tumours of fish are easily recognizable lesions, some of which have been known for centuries. Causes of fish tumour formation are varied and are often proposed to be multifactorial. In more than half of all cases examined by electron rnicroscopy and virological methods, virus or virus-hke particles were found in tumour tissues. So far, oncogenicity has been clearly demonstrated only for herpesviruses isolated from benign tumours. Classification of fish skin tumours, tumour-associated and turnour-inducing viruses, and the possible reasons for seasonal variation in slun tumour prevalence, are revlewed. It is postulated that fundamental principles determne the role of viruses in the induction of skin tumours of fish within a framework of different biological and environmental parameters.

Infectious hematopoietic necrosis virus (IHNV), a member of the genus Novirhabdovirus, causes a highly lethal disease of salmonid fish. In the present study, G gene nucleotide sequences of 9 Japanese IHNV isolates obtained from 1971 to 1996 were analyzed to evaluate the genetic diversity and compared with IHNV isolates from North America and Europe. A radial phylogenetic tree revealed 5 major clusters including 3 genogroups (U, M and L) for North American isolates and 1 genogroup for European isolates. Five Japanese isolates from 1971 to 1982 appeared in the cluster for genogroup U, while the remaining Japanese isolates from 1980 to 1996 formed a new genogroup, JRt (Japanese rainbow trout). Maximum nucleotide diversity among the Japanese isolates was 4.5%, which was greater than that within the North American isolates (3.6%), and the degree of nucleotide diversity within Japanese isolates was increased by inclusion of the genogroup JRt isolates. It was concluded that Japanese isolates shared a common source with the genogroup U of the North American isolates and that there were large divergences between Japanese isolates before and after the 1980s.

Barfin flounder nervous necrosis virus (BFNNV), the causative agent of viral nervous necrosis (VNN) of barfin flounder, is vertically transmitted from spawners to larvae. In the present study, an ELISA with a recombinant protein of BFNNV was performed for the detection of antibodies against BFNNV and applied for the selection of brood fish in order to prevent viral vertical transmissions. Brood stocks were divided into 4 groups based on ELISA antibody titers (<10, 20, 40 and >40), and the BFNNV status of the brood stocks was determined by PCR. BFNNV was detected from the brood fish in the group with an antibody titer of >40 but not from those with titers 210, 20 and 40. The offspring obtained from PCRnegative brood fish pairs in each group of ELISA antibody titers were subsequently reared for observation of VNN occurrence. VNN occurred in juveniles from 2 of 9 pairs of spawners with an antibody titer 240, but did not occur in spawners with an antibody titer of 510. Therefore, it was concluded that selection of brood fish using both the PCR test and ELISA antibody titers could help prevent vertical transmission of BFNNV in larval production of barfin flounder.