Dataset for the publication 'Molecular testing of adult Pacific salmon and trout (Oncorhynchus spp.) for several RNA viruses demonstrates widespread distribution of piscine orthoreovirus (PRV) in Alaska and Washington'. This research was initiated in conjunction with a systematic, multi-agency surveillance effort in the United States (U.S.) in response to reported findings of infectious salmon anemia virus (ISAV) RNA in British Columbia, Canada. In the systematic surveillance study reported in a companion paper, tissues from various salmonids taken from Washington and Alaska were surveyed for ISAV RNA using the U.S. approved diagnostic method and samples were released for use in this present study only after testing negative. Here we tested a subset of these samples for ISAV RNA with three additional published molecular assays, as well as for RNA from salmonid alphavirus (SAV), piscine myocarditis virus (PMCV) and piscine orthoreovirus (PRV). All samples (n=2252; 121 stock cohorts) tested negative for RNA from ISAV, PMCV, and SAV. In contrast, there were 25 stock cohorts from Washington and Alaska that had one or more individuals test positive for PRV RNA. Findings of PRV RNA were most common in coho (Oncorhynchus kisutch Walbaum) and Chinook (O. tshawytscha Walbaum) salmon. The disease associated with PRV in Atlantic salmon, heart skeletal muscle inflammation (HSMI), has not been reported in Pacific salmon.

Piscine orthoreovirus genotype one (PRV-1) is the causative agent of heart and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon (Salmo salar L.). The virus has also been found in Pacific salmonids in western North America, raising concerns about the risk to native salmon and trout. Here, we report the results of laboratory challenges using juvenile Chinook salmon, coho salmon, and rainbow trout injected with tissue homogenates from Atlantic salmon testing positive for PRV-1 or with control material. Fish were sampled at intervals to assess viral RNA transcript levels, hematocrit, erythrocytic inclusions, and histopathology. While PRV-1 replicated to high loads in all species, there was negligible mortality in any group. We observed a few erythrocytic inclusion bodies in fish from PRV-1 infected groups. At a few time points, hematocrits were significantly lower in the PRV-1 infected groups relative to controls but in no case was anemia noted. The most common histopathological finding was mild, focal myocarditis in both the non-infected controls and PRV-1 infected fish. All cardiac lesions were judged mild and none were consistent with those of HSMI. Together, these results suggest all three species are relatively susceptible to PRV-1 infection, but in no case did infection cause notable disease in these experiments.

Piscine orthoreovirus genotype one (PRV-1) is the causative agent of heart and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon (Salmo salar L.). The virus has also been found in Pacific salmonids in western North America, raising concerns about the risk to native salmon and trout. Here, we report the results of laboratory challenges using juvenile Chinook salmon, coho salmon, and rainbow trout injected with tissue homogenates from Atlantic salmon testing positive for PRV-1 or with control material. Fish were sampled at intervals to assess viral RNA transcript levels, hematocrit, erythrocytic inclusions, and histopathology. While PRV-1 replicated to high loads in all species, there was negligible mortality in any group. We observed a few erythrocytic inclusion bodies in fish from PRV-1 infected groups. At a few time points, hematocrits were significantly lower in the PRV-1 infected groups relative to controls but in no case was anemia noted. The most common histopathological finding was mild, focal myocarditis in both the non-infected controls and PRV-1 infected fish. All cardiac lesions were judged mild and none were consistent with those of HSMI. Together, these results suggest all three species are relatively susceptible to PRV-1 infection, but in no case did infection cause notable disease in these experiments.

This investigation sought to characterize the shedding of infectious hematopoietic necrosis virus (IHNV) in two populations of Columbia River Basin (CRB) Chinook salmon (Oncorhynchus tshawytscha). Juvenile spring- and fall-run Chinook salmon were exposed by immersion to each of three IHN virus strains from the UC, MD, and L subgroups, and then monitored for viral shedding from individual fish for 30 days. Detectable quantities of UC, MD and L IHN virus were shed by a subset of fish from each host population (1–9 out of 10 fish total in each treatment group). Viral shedding kinetics were consistent, with a rapid onset of shedding, peak shedding by 2–3 days, and then a rapid decline to below detectable levels by 7 days’ post-exposure to IHNV. Intraspecies variation was observed as spring Chinook salmon shed more UC virus than fall fish: spring Chinook salmon shed UC virus in greater numbers of fish, with 22-fold higher mean peak shedding magnitude, 33-fold higher mean total virus shed per fish, and 900-fold higher total virus shed per treatment group. The L and MD viruses had comparable shedding at intermediate levels in each host population. All viral shedding occurred well before host mortality began, and shedding magnitude did not correlate with virulence differences. Overall, the greater shedding of UC virus from spring Chinook salmon, combined with low virulence, indicates a uniquely high transmission potential that may explain the predominance of UC viruses in CRB Chinook salmon. This also suggests that spring-run fish may contribute more to the ecology of IHNV in the CRB than fall-run Chinook salmon.

This investigation sought to characterize the shedding of infectious hematopoietic necrosis virus (IHNV) in two populations of Columbia River Basin (CRB) Chinook salmon (Oncorhynchus tshawytscha). Juvenile spring- and fall-run Chinook salmon were exposed by immersion to each of three IHN virus strains from the UC, MD, and L subgroups, and then monitored for viral shedding from individual fish for 30 days. Detectable quantities of UC, MD and L IHN virus were shed by a subset of fish from each host population (1–9 out of 10 fish total in each treatment group). Viral shedding kinetics were consistent, with a rapid onset of shedding, peak shedding by 2–3 days, and then a rapid decline to below detectable levels by 7 days’ post-exposure to IHNV. Intraspecies variation was observed as spring Chinook salmon shed more UC virus than fall fish: spring Chinook salmon shed UC virus in greater numbers of fish, with 22-fold higher mean peak shedding magnitude, 33-fold higher mean total virus shed per fish, and 900-fold higher total virus shed per treatment group. The L and MD viruses had comparable shedding at intermediate levels in each host population. All viral shedding occurred well before host mortality began, and shedding magnitude did not correlate with virulence differences. Overall, the greater shedding of UC virus from spring Chinook salmon, combined with low virulence, indicates a uniquely high transmission potential that may explain the predominance of UC viruses in CRB Chinook salmon. This also suggests that spring-run fish may contribute more to the ecology of IHNV in the CRB than fall-run Chinook salmon.

국립수산물품질관리원 검역검사과에서 검역동향_해외(베트남, 프랑스, 대만 등) 수산생물 질병발생에 대해 월별로 정리한 동향 보고서

Infectious hematopoietic necrosis virus (IHNV) represents one of the most critical challenges for salmonids in the Pacific Northwest. There are three genogroups of IHNV, designated U, M, and L; the U is further delineated into two subgroups, UC and UP, and the M is further delineated into four subgroups (MA – MD). The UP, UC and MD subgroups co-occur in the Columbia River Basin where the host species sockeye salmon, Chinook salmon, and steelhead trout spawn and rear. Field prevalence data shows that UC viruses exhibit a generalist strategy in Chinook, and steelhead, while two other virus lineages, MD and UP, are more consistent with being specialists in steelhead or sockeye salmon, respectively. The L is found in Northern California and is considered a specialist of Chinook salmon. This study sought to understand early entry and replication of the specialist and generalist IHNV strains in three salmonid hosts. Chinook, steelhead and sockeye were exposed by immersion to their specialist viruses (L, MD and UP, respectively) and to the generalist UC virus. As controls, these hosts were also exposed to buffer (mock control) and IHNV variants that were not specialist for their species (non-specialists). Mortality was monitored throughout the experiments. Fish were sampled at early timepoints post-infection (2, 5, and 8 days post-exposure). Kidney and fin tissues were taken to represent external and internal tissues, respectively. Viral load was assessed by reverse transcriptase quantitative PCR (RT-qPCR) targeting the nucleocapsid (N) gene of IHNV. Additional fish from each experimental group were sampled for histopathology but only a subset were processed and analyzed.

Infectious hematopoietic necrosis virus (IHNV) represents one of the most critical challenges for salmonids in the Pacific Northwest. There are three genogroups of IHNV, designated U, M, and L; the U is further delineated into two subgroups, UC and UP, and the M is further delineated into four subgroups (MA – MD). The UP, UC and MD subgroups co-occur in the Columbia River Basin where the host species sockeye salmon, Chinook salmon, and steelhead trout spawn and rear. Field prevalence data shows that UC viruses exhibit a generalist strategy in Chinook, and steelhead, while two other virus lineages, MD and UP, are more consistent with being specialists in steelhead or sockeye salmon, respectively. The L is found in Northern California and is considered a specialist of Chinook salmon. This study sought to understand early entry and replication of the specialist and generalist IHNV strains in three salmonid hosts. Chinook, steelhead and sockeye were exposed by immersion to their specialist viruses (L, MD and UP, respectively) and to the generalist UC virus. As controls, these hosts were also exposed to buffer (mock control) and IHNV variants that were not specialist for their species (non-specialists). Mortality was monitored throughout the experiments. Fish were sampled at early timepoints post-infection (2, 5, and 8 days post-exposure). Kidney and fin tissues were taken to represent external and internal tissues, respectively. Viral load was assessed by reverse transcriptase quantitative PCR (RT-qPCR) targeting the nucleocapsid (N) gene of IHNV. Additional fish from each experimental group were sampled for histopathology but only a subset were processed and analyzed.

Only one virus, Avipox, has been documented in wild birds in Hawaii. Here, using immunohistochemistry and PCR, we found that two native threatened Hawaiian geese, one with multicentric histiocytoma and another with toxoplasmosis and one Laysan albatross with avian pox were infected with reticuloendotheliosis virus (REV). The virus was isolated from one of the geese by cell culture. PCR surveys of other Hawaiian geese with various pathologies, avian pox cases, and pox viral isolates failed to reveal REV suggesting the virus is uncommon, at least in samples examined. The full genome of the Gag, Pol, and Env genes were sequenced for all three infected birds and revealed geographic divergence of the Pol gene suggesting it to be under strong selective pressure. Our finding of REV in Hawaii makes this only the second virus documented in native Hawaiian birds associated with pathology. Moreover, the presence of REV in a pelagic seabird is unusual. Future surveys should seek the reservoir of the virus in efforts to trace its origins.

In summer 2020, SARS-CoV-2 was detected on mink farms in Utah. An interagency One Health response was initiated to assess the extent of the outbreak and included sampling animals from or near affected mink farms and testing them for SARS-CoV-2 and non-SARS coronaviruses. Among the 365 animals sampled, including domestic cats, mink, rodents, raccoons, and skunks, 261 (72%) of the animals harbored at least one coronavirus at the time. Among the samples which could be further characterized, 126 alphacoronaviruses and 88 betacoronaviruses (including 74 detections of SARS-CoV-2) were identified. Moreover, at least 10% (n=27) of the corona-virus-positive animals were found to be co-infected with more than one coronavirus. Our findings indicate an unexpectedly high prevalence of coronavirus among the domestic and wild animals tested on mink farms and raise the possibility that commercial animal husbandry operations could be potential hot spots for future trans-species viral spillover and the emergence of new pandemic coronaviruses. Figure 1. Phylogenetic relationships of the identified coronaviruses from mink and other animals from mink farms in Utah. The four genera of coronaviruses are highlighted in different colors. AlphaCoV, alkphacoronavirus; BetaCoV, betacoronavirus; DeltaCoV, deltacoronaviruses; and GammaCoV, gammacoronavirus. Type species for the currently recognized subgenera are annotated according to the nomenclature scheme used in this manuscript with the addition of the ICTV subgenus. Additional viruses, including the closest GenBank entry as identified by the BLAST tool, were included to help delineate relationship. Red circles are viruses identified in this study. Panel A. Full phylogenetic tree (A full-size image is included in Supplementary Figure 1). Red arrows designate the group of nearly identical Utah mink coronavirus strains collapsed into the colored triangle in Panel B. Table 1. Coronavirus distribution among species tested. The species are listed by their common names; Total, the total number of animals of each species tested; Negative, number of each species with no coronavirus detected among the tissues tested; Positive, number of animals positive for coronavirus in at least one tissue; % Pos, percentage of coronavirus positives in each species. Table 2. Detailed tissue panel tested for SARS-CoV-2. The distribution of SARS-CoV-2 RNA detection in the first 96 animals is listed. Tissue, tissue or tissue pools received; Total, total number tested in each category; Negative, number of N1 RT-PCR negatives; Posi-tives, number of N1 RT-PCR positives; % Pos, percentage of tissues positive for corona-virus. Table 3. Summary of coronaviruses identified. The distribution of coronaviruses detected and characterized according to their host is listed. Species, common name of animal species tested; AlphaCoV, number of alphacoronaviruses identified; BetaCoV, number of betacoronaviruses identified; Sequenced, number of viruses identified by sequencing, Unchar, number of coronavirus-positive samples not further characterized. Table 4. SARS-CoV-2 coinfections identified in Utah mammals. The individual animals that are both SARS-CoV-2 positive and infected with a second coronavirus are listed. Animal ID, Unique animal identification number; Common name, common name of animal; Scientific name, scientific name of animal; Sex, F, female, M, male. Unk, un-known; Age, A adult, J juvenile, Unk, unknown; SARS-CoV-2, Neg-N1 RT-PCR nega-tive, Pos-N1 RT-PCR positive, Second strain, genus and common name of the coronavirus, Pan-CoV RT-PCR Equivocal, sample is PCR positive but not further characterized. Supplementary Figure 1. Phylogenetic relationships of the identified coronaviruses from mink farms in Utah. The four genera of coronaviruses are highlighted in different colors. AlphaCoV, alkphacoronavirus; BetaCoV, betacoronavirus; DeltaCoV, deltacoronaviruses; and GammaCoV, gammacoronavirus. Type species for the currently recognized