Throughout a 20-year biosurveillance period, viral hemorrhagic septicemia virus was isolated in low titers from only 6 / 7,355 opportunistically sampled adult Pacific herring, reflecting the typical endemic phase of the disease when the virus persists covertly. However, more focused surveillance efforts identified the presence of disease hot spots occurring among juvenile life history stages from certain nearshore habitats. These outbreaks sometimes recurred annually in the same temporal and spatial patterns and were characterized by infection prevalence as high as 96%. Longitudinal sampling indicated that some epizootics were relatively transient, represented by positive samples on a single sampling date, and others were more protracted, with positive samples occurring throughout the first 10 weeks of the juvenile life history phase. Sampling and biological data associated with these surveillances are presented in this dataset.

Viral hemorrhagic septicemia virus (VHSV) is an aquatic rhabdovirus causing severe disease in numerous freshwater and saltwater fish species. Initially the virus was been found to cause disease in European fish populations starting around 1938 and was first detected in North America in the late 1980s. Of the four VHSV genotypes (I, II, III, and IV), the North American subtype IVb isolates have a broad host range. To determine whether endangered pallid sturgeon Scaphirhynchus albus, are susceptible to VHSV-IVb infection, juvenile pallid sturgeon and two pallid sturgeon cell lines derived from skin and spleen tissue were tested. Detection of viable virus via a plaque assay and molecular detection of the virus results by a RT-PCR (reverse transcription-polymerase chain reaction) confirmed VHSV-IVb in vitro replication in pallid sturgeon cell lines. Pallid sturgeon were also susceptible to VHSV-IVb infection when exposed to the virus by immersion at concentration of 5 X 10e5 plaque forming units per milliliter (pfu/ml) and by injection at a dose of 1 X 10e6 plaque forming units per fish (pfu/fish) during 28-day long challenge experiments. However, after widespread mortality occurred in all treatment groups, including control fish, it was determined that the pallid sturgeon stock fish were infected with Missouri River Sturgeon Iridovirus (MRSIV) prior to experimental challenge. Nevertheless, VHSV-exposed fish suffered equal or higher mortalities (38 – 48%) than mock treated (MRSIV-infected) fish (29 – 38%) and histopathology samples showed reduced hematopoietic cells in spleen and kidney tissues and hemorrhage in the gastrointestinal organs only in VHSV-treated fish. These results suggest that pallid sturgeon are susceptible to VHSV-IVb infection, but the degree of pathogenicity was confounded by the underlying MRSIV infection. Our data also suggest that pallid sturgeon may serve as carriers of VHSV because the virus was isolated from surviving fish that showed no clinical signs, yet were positive for both VHSV and MRSIV. Research comparing susceptibility of pathogen-free and MRSIV-infected fish to VHSV-IVb is needed to accurately assess the vulnerability of pallid sturgeon to VHSV-IVb.

Viral hemorrhagic septicemia virus (VHSV) is an aquatic rhabdovirus causing severe disease in numerous freshwater and saltwater fish species. Initially the virus was been found to cause disease in European fish populations starting around 1938 and was first detected in North America in the late 1980s. Of the four VHSV genotypes (I, II, III, and IV), the North American subtype IVb isolates have a broad host range. To determine whether endangered pallid sturgeon Scaphirhynchus albus, are susceptible to VHSV-IVb infection, juvenile pallid sturgeon and two pallid sturgeon cell lines derived from skin and spleen tissue were tested. Detection of viable virus via a plaque assay and molecular detection of the virus results by a RT-PCR (reverse transcription-polymerase chain reaction) confirmed VHSV-IVb in vitro replication in pallid sturgeon cell lines. Pallid sturgeon were also susceptible to VHSV-IVb infection when exposed to the virus by immersion at concentration of 5 X 10e5 plaque forming units per milliliter (pfu/ml) and by injection at a dose of 1 X 10e6 plaque forming units per fish (pfu/fish) during 28-day long challenge experiments. However, after widespread mortality occurred in all treatment groups, including control fish, it was determined that the pallid sturgeon stock fish were infected with Missouri River Sturgeon Iridovirus (MRSIV) prior to experimental challenge. Nevertheless, VHSV-exposed fish suffered equal or higher mortalities (38 – 48%) than mock treated (MRSIV-infected) fish (29 – 38%) and histopathology samples showed reduced hematopoietic cells in spleen and kidney tissues and hemorrhage in the gastrointestinal organs only in VHSV-treated fish. These results suggest that pallid sturgeon are susceptible to VHSV-IVb infection, but the degree of pathogenicity was confounded by the underlying MRSIV infection. Our data also suggest that pallid sturgeon may serve as carriers of VHSV because the virus was isolated from surviving fish that showed no clinical signs, yet were positive for both VHSV and MRSIV. Research comparing susceptibility of pathogen-free and MRSIV-infected fish to VHSV-IVb is needed to accurately assess the vulnerability of pallid sturgeon to VHSV-IVb.

Viral erythrocytic necrosis (VEN) is a disease of marine and anadromous fishes, which is poorly understood, largely because its causative iridovirus, erythrocytic necrosis virus (ENV), is intractable to cell culture. Natural VEN epizootics and observations studies in wild populations suggest that temperature may be an important disease cofactor. Here, a controlled laboratory exposure study provides evidence for a direct relationship between temperature and the progression of viral erythrocytic necrosis (VEN) in Pacific herring. Waterborne exposure of Pacific herring to kidney homogenates containing ENV resulted in the establishment of infections, characterized by high infection prevalence (89%; 40/45) and mean viral loads (5.5 log10- gene copies / ug DNA) in kidney tissues at 44 d post exposure. Viral loads were higher in herring from the ambient (9.0 °C) and warm (13.5 °C) treatments (6.1 - 6.2 log10- gene copies / total DNA) than from the cool (6.9 °C) treatment (4.3 log10- gene copies / total DNA). Similarly, the peak proportion of diseased fish was directly related to temperature (P 0.001), with cytoplasmic inclusion bodies detected in 21% of herring from the cool, 52% from the ambient, and 60% from the warm treatments. The mean disease load in each fish (enumerated as the percent of erythrocytes with cytoplasmic inclusions), increased with temperature from 15% in the cool, 36% in the ambient, and 32% in the warm treatments at 44 days post exposure. Transcriptional analysis indicated that the number of differentially expressed genes among ENV-exposed herring increased with temperature, time post exposure, and viral load. Correlation network analysis of transcriptomic data showed robust activation of interferon and viral immune responses in hepatic tissue of infected individuals independent of other experimental variables.

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.

Viral nervous necrosis is a neurologic disease that causes vacuolating lesions in the brain and retina of a broad range of marine fish species. The viral agent responsible is nervous necrosis virus (NNV), a Betanodavirus within the family Nodaviridae. Based on genetic characterization of the viral genome, at least four species of NNV are known to exist, though this diversity is likely under appreciated. The virus poses a threat to marine fisheries and aquaculture throughout its range, though limited data exists on its presence in the mid-Atlantic region of the United States. Black sea bass, a serranid marine fish, were collected from artificial reefs along the New Jersey coast between 2020 and 2022 to screen for NNV using molecular methods. Prevalence of detection and genetic sequencing of the virus was completed to determine viral prevalence and to characterize the viral genotypes in this region.

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.

Spring viremia of carp virus (SVCV) is a rhabdovirus that primarily infects cyprinid finfishes and causes a disease notifiable to the World Organization for Animal Health. Amphibians, which are sympatric with cyprinids in freshwater ecosystems, are considered non-permissive hosts of rhabdoviruses. The potential host range expansion of SVCV in an atypical host species was evaluated by testing the susceptibility of amphibians native to the Pacific Northwest. Larval long-toed salamanders Ambystoma macrodactylum and Pacific tree frog Pseudacris regilla tad-poles were exposed to SVCV strains from genotypes Ia, Ib, Ic or Id by either intraperitoneal injection, immersion, or cohabitation with virus-infected koi Cyprinus rubrofuscus. Cumulative mortality was 100% for salamanders injected with SVCV, 98-100% for tadpoles exposed to virus via immersion, and 0 – 100% for tadpoles cohabited with SVCV-infected koi. Many of the animals that died exhibited clinical signs of disease and SVCV RNA was found by in situ hybridization in tissue sections of immersion-exposed tadpoles, particularly in the cells of the gastrointestinal tract and liver. SVCV was also detected by plaque assay and RT-qPCR testing in both amphibian species regardless of the virus exposure method, and viable virus was detected up to 28 days after initial exposure. Recovery of infectious virus from naïve tadpoles cohabited with SVCV-infected koi further demonstrated that SVCV transmission can occur between classes of ectothermic vertebrates. Collectively, these results indicated that SVCV, a fish rhabdovirus, can be transmitted to and cause lethal disease in two amphibian species. Therefore members of all five of the major vertebrate groups (mammals, birds, reptiles, fish, and amphibians) appear to be vulnerable to rhabdovirus infections.

Spring viremia of carp virus (SVCV) is a rhabdovirus that primarily infects cyprinid finfishes and causes a disease notifiable to the World Organization for Animal Health. Amphibians, which are sympatric with cyprinids in freshwater ecosystems, are considered non-permissive hosts of rhabdoviruses. The potential host range expansion of SVCV in an atypical host species was evaluated by testing the susceptibility of amphibians native to the Pacific Northwest. Larval long-toed salamanders Ambystoma macrodactylum and Pacific tree frog Pseudacris regilla tad-poles were exposed to SVCV strains from genotypes Ia, Ib, Ic or Id by either intraperitoneal injection, immersion, or cohabitation with virus-infected koi Cyprinus rubrofuscus. Cumulative mortality was 100% for salamanders injected with SVCV, 98-100% for tadpoles exposed to virus via immersion, and 0 – 100% for tadpoles cohabited with SVCV-infected koi. Many of the animals that died exhibited clinical signs of disease and SVCV RNA was found by in situ hybridization in tissue sections of immersion-exposed tadpoles, particularly in the cells of the gastrointestinal tract and liver. SVCV was also detected by plaque assay and RT-qPCR testing in both amphibian species regardless of the virus exposure method, and viable virus was detected up to 28 days after initial exposure. Recovery of infectious virus from naïve tadpoles cohabited with SVCV-infected koi further demonstrated that SVCV transmission can occur between classes of ectothermic vertebrates. Collectively, these results indicated that SVCV, a fish rhabdovirus, can be transmitted to and cause lethal disease in two amphibian species. Therefore members of all five of the major vertebrate groups (mammals, birds, reptiles, fish, and amphibians) appear to be vulnerable to rhabdovirus infections.