Erythrocytic inclusion body syndrome (EIBS) causes mass mortality in farmed salmonid fish, including the coho salmon, Onchorhynchus kisutchi, and chinook salmon, O. tshawytscha. The causative agent of the disease is a virus with an icosahedral virion structure, but this virus has not been characterized at the molecular level. In this study, we sequenced the genome of a virus purified from EIBS-affected coho salmon. The virus has 10 dsRNA genomic segments (L1, L2, L3, M1, M2, M3, S1, S2, S3, and S4), which closely resembles the genomic organization of piscine orthoreovirus (PRV), the causative agent of heart and skeletal inflammation (HSMI) in Atlantic salmon and HSMI-like disease in coho salmon. The genomic segments of the novel virus contain at least 10 open reading frames (ORFs): lambda 1 (λ1), λ2, λ3, mu 1 (μ1), μ2, μNS, sigma 1 (σ1), σ2, σ3, and σNS. An additional ORF encoding a 12.6-kDa protein (homologue of PRV p13) occurs in the same genomic segment as σ3. Phylogenetic analyses based on S1 and λ3 suggest that this novel virus is closely related to PRV, but distinctly different. Therefore, we designated the new virus ‘piscine orthoreovirus 2’ (PRV-2). Reverse transcription–quantitative real-time PCR revealed a significant increase in PRV-2 RNA in fish blood after the artificial infection of EIBS-naïve fish but not in that of fish that had recovered from EIBS. The degree of anemia in each fish increased as the PRV-2 RNA increased during an epizootic season of EIBS on an inland coho salmon farm. These results indicate that PRV-2 is the probable causative agent of EIBS in coho salmon, and that the host acquires immunity to reinfection with this virus. Further research is required to determine the host range of PRV species and the relationship between EIBS and HSMI in salmonid fish.

Twelve cDNA libraries from two species of catfish have been sequenced, resulting in the generation of nearly 500,000 ESTs.

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A novel Asfarvirus-like virus is proposed as the etiological agent responsible for mass mortality in abalone. The disease, called abalone amyotrophia, originally was recognized in the 1980s, but efforts to identify a causative agent were unsuccessful. We prepared a semi-purified fraction by nuclease treatment and ultracentrifugation of diseased abalone homogenate, and the existence of the etiological agent in the fraction was confirmed by a challenge test. Using next-generation sequencing and PCR-based epidemiological surveys, we obtained a partial sequence with similarity to a member of the family Asfarviridae. BLASTP analysis of the predicted proteins against a virus database resulted in 48 proteins encoded by the novel virus with top hits against proteins encoded by African swine fever virus (ASFV). Phylogenetic analyses of predicted proteins of the novel virus confirmed that ASFV represents the closest relative. Comparative genomic analysis revealed gene-order conservation between the novel virus and ASfV. In situ hybridization targeting the gene encoding the major capsid protein of the novel virus detected positive signals only in tissue from diseased abalone. The results of this study suggest that the putative causative agent should be considered a tentative new member of the family Asfarviridae, which we provisionally designate abalone asfa-like virus (AbALV). African swine fever virus (ASFV) is the causative agent of African swine fever (ASF). The virus causes a hemorrhagic fever with high mortality, with rates approaching 100% in domestic pigs 1. The virus infects domestic pigs and their relatives and ticks 2. ASF outbreaks had been recorded in Africa and Europe, but in recent years the disease has spread to China, Vietnam, Cambodia, Mongolia, Hong Kong, and Korea, becoming a threat to the swine industry worldwide 3. ASFV is a member of nucleocytoplasmic large DNA viruses (NCLDVs) with an average diameter of 200 nm. Although some related viruses, such as faustovirus 4 , kaumoebavirus 5 , and pacmanvirus 6 , have been reported, ASFV is the only member of the Asfarviridae family 7. In the present paper, we describe a virus likely to be the closest ASFV relative found to date; this novel virus was isolated as the presumptive causative agent of abalone amyotrophia. Mass mortalities of abalone have been reported since the early 1980s, during seed production in Japan. The disease was designated abalone amyotrophia because diseased abalone develop muscle atrophy in the mantle and foot 8. Diseased abalone show reduced ability to adhere to the substrate, and some diseased abalone exhibit incisions on the front margin of the shell and brown pigmentation inside of the shell 9. Histopathological evaluation has revealed the presence of abnormal cell masses that are produced extensively, primarily in the ganglion and peripheral nerve of the foot muscle 9. Cumulative mortality can reach 50% and higher 10. Abalone herpesvirus (AbHV) 11,12 and abalone shriveling syndrome-associated virus (AbSV) 13 also cause mortality ac...

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