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At least 73 records · Page 4Linked to original sources

Temporal, geographic, and host distribution of avian paramyxovirus 1 (Newcastle disease virus)

Newcastle disease is caused by virulent forms of avian paramyxovirus of serotype 1 (APMV-1) and has global economic importance. The disease reached panzootic proportions within two decades after first being identified in 1926 in the United Kingdom and Indonesia and still remains endemic in many countries across the world. Here we review information on the host, temporal, and geographic distribution of APMV-1 genetic diversity based on the evolutionary systematics of the complete coding region of the fusion gene. Strains of APMV-1 are phylogenetically separated into two classes (class I and class II) and further classified into genotypes based on genetic differences. Class I viruses are genetically less diverse, generally present in wild waterfowl, and are of low virulence. Class II viruses are genetically and phenotypically more diverse, frequently isolated from poultry with occasional spillovers into wild birds, and exhibit a wider range of virulence. Waterfowl, cormorants, and pigeons are natural reservoirs of all APMV-1 pathotypes, except viscerotropic velogenic viruses for which natural reservoirs have not been identified. Genotypes I and II within class II include isolates of high and low virulence, the latter often being used as vaccines. Viruses of genotypes III and IX that emerged decades ago are now isolated rarely, but may be found in domestic and wild birds in China. Containing only virulent viruses and responsible for the majority of recent outbreaks in poultry and wild birds, viruses from genotypes V, VI, and VII, are highly mobile and have been isolated on different continents. Conversely, virulent viruses of genotypes XI (Madagascar), XIII (mainly Southwest Asia), XVI (North America) and XIV, XVII and XVIII (Africa) appear to have a more limited geographic distribution and have been isolated predominantly from poultry.

Infection, Genetics and Evolution↗

Evolutionary dynamics of Newcastle disease virus

A comprehensive dataset of NDV genome sequences was evaluated using bioinformatics to characterize the evolutionary forces affecting NDV genomes. Despite evidence of recombination in most genes, only one event in the fusion gene of genotype V viruses produced evolutionarily viable progenies. The codon-associated rate of change for the six NDV proteins revealed that the highest rate of change occurred at the fusion protein. All proteins were under strong purifying (negative) selection; the fusion protein displayed the highest number of amino acids under positive selection. Regardless of the phylogenetic grouping or the level of virulence, the cleavage site motif was highly conserved implying that mutations at this site that result in changes of virulence may not be favored. The coding sequence of the fusion gene and the genomes of viruses from wild birds displayed higher yearly rates of change in virulent viruses than in viruses of low virulence, suggesting that an increase in virulence may accelerate the rate of NDV evolution. ?? 2009 Elsevier Inc.

Virology↗

Characterization of infectious dose and lethal dose of two strains of infectious hematopoietic necrosis virus (IHNV)

The ability to infect a host is a key trait of a virus, and differences in infectivity could put one virus at an evolutionary advantage over another. In this study we have quantified the infectivity of two strains of infectious hematopoietic necrosis virus (IHNV) that are known to differ in fitness and virulence. By exposing juvenile rainbow trout ( Oncorhynchus mykiss ) hosts to a wide range of virus doses, we were able to calculate the infectious dose in terms of ID 50 values for the two genotypes. Lethal dose experiments were also conducted to confirm the virulence difference between the two virus genotypes, using a range of virus doses and holding fish either in isolation or in batch so as to calculate LD 50 values. We found that infectivity is positively correlated with virulence, with the more virulent genotype having higher infectivity. Additionally, infectivity increases more steeply over a short range of doses compared to virulence, which has a shallower increase. We also examined the data using models of virion interaction and found no evidence to suggest that virions have either an antagonistic or a synergistic effect on each other, supporting the independent action hypothesis in the process of IHNV infection of rainbow trout.

Virus Research↗

Genetic characterization of Hawaiian isolates of Plasmodium relictum reveals mixed-genotype infections

Background: The relatively recent introduction of a highly efficient mosquito vector and an avian pathogen (Plasmodium relictum) to an isolated island ecosystem with nai??ve, highly susceptible avian hosts provides a unique opportunity to investigate evolution of virulence in a natural system. Mixed infections can significantly contribute to the uncertainty in host-pathogen dynamics with direct impacts on virulence. Toward further understanding of how host-parasite and parasite-parasite relationships may impact virulence, this study characterizes within-host diversity of malaria parasite populations based on genetic analysis of the trap (thrombospondin-related anonymous protein) gene in isolates originating from Hawaii, Maui and Kauai Islands. Methods: A total of 397 clones were produced by nested PCR amplification and cloning of a 1664 bp fragment of the trap gene from two malarial isolates, K1 (Kauai) and KV115 (Hawaii) that have been used for experimental studies, and from additional isolates from wild birds on Kauai, Maui and Hawaii Islands. Diversity of clones was evaluated initially by RFLP-based screening, followed by complete sequencing of 33 selected clones. Results: RFLP analysis of trap revealed a minimum of 28 distinct RFLP haplotypes among the 397 clones from 18 birds. Multiple trap haplotypes were detected in every bird evaluated, with an average of 5.9 haplotypes per bird. Overall diversity did not differ between the experimental isolates, however, a greater number of unique haplotypes were detected in K1 than in KV115. We detected high levels of clonal diversity with clear delineation between isolates K1 and KV115 in a haplotype network. The patterns of within-host haplotype clustering are consistent with the possibility of a clonal genetic structure and rapid within-host mutation after infection. Conclusion: Avian malaria (P. relictum) and Avipoxvirus are the significant infectious diseases currently affecting the native Hawaiian avifauna. This study shows that clonal diversity of Hawaiian isolates of P. relictum is much higher than previously recognized. Mixed infections can significantly contribute to the uncertainty in host-pathogen dynamics with direct implications for host demographics, disease management strategies, and evolution of virulence. The results of this study indicate a widespread presence of multiple-genotype malaria infections with high clonal diversity in native birds of Hawaii, which when coupled with concurrent infection with Avipoxvirus, may significantly influence evolution of virulence. ?? 2008 Jarvi et al; licensee BioMed Central Ltd.

Biology Direct↗

Host specificity and ecology of infectious hematopoietic necrosis virus (IHNV) in Pacific salmonids

Some circumstances IHNV infection can cause acute disease with mortality ranging from 5-90% in host populations. Genetic typing of IHNV field isolates has shown that three major genetic groups of the virus occur in North America. These groups are designated the U, M, and L virus genogroups because they occur in the upper, middle, and lower portions of the geographic range of IHNV in western North America. Among field isolates there is some indication of host specificity: most IHNV isolated from sockeye salmon ( Oncorhynchus nerka ) is in the U genogroup, and most IHNV isolated from rainbow and steelhead trout ( Oncorhynchus mykiss ) is in the M genogroup. Experimental challenges confirm that U isolates are highly virulent for sockeye salmon, but not rainbow trout. In contrast, M isolates are virulent in rainbow trout but not in sockeye salmon. Studies comparing U and M virus infections show that virulence is associated with more rapid virus replication in the first few days after infection. In addition, high virulence isolates persist at higher viral loads in the host, while low virulence isolates do not persist. These host-specific aspects of the different IHNV genogroups are important for understanding the ecology of IHNV emergence events in the field. The recent emergence of U IHNV in Russian sockeye salmon of the Kamchatka Peninsula, and the emergence of M IHNV in steelhead trout on the Olympic Peninsula in the U.S.A, serve as examples of the relevance of IHNV host specificity.

Conference Paper↗

Successful mitigation of viral disease based on a delayed exposure rearing strategy at a large-scale steelhead trout conservation hatchery

In 2009, the largest steelhead trout conservation hatchery in the state of Idaho, Dworshak National Fish Hatchery (NFH), lost over 50% of the juvenile steelhead trout ( Oncorhynchus mykiss ) population being reared for release. The causative agent of this high mortality was the viral pathogen infectious hematopoietic necrosis virus (IHNV). This was neither the first nor the worst epidemic of IHNV to occur at the hatchery, but it was the worst in over a decade. Genetic analysis of IHNV isolates taken from juveniles suffering epidemic IHN disease in 2009 revealed that the virus was of the M group of IHNV viruses, known to have high virulence for trout. The water supply for steelhead trout rearing at Dworshak NFH is untreated water taken directly from the Clearwater River. Further genetic analysis of IHNV isolates from adults spawned in 2009 indicated that adult steelhead trout in the river (in the hatchery water supply) were the most probable transmission source for the epidemic IHN disease in the juvenile fish. Previously, Dworshak NFH had been able to gain access to reservoir water from behind the Dworshak Dam for nursery egg incubation and the earliest stage of fry rearing, which nearly eliminated incidence of IHN disease in that stage of rearing. Additionally, the nearby Clearwater State Fish Hatchery (SFH), which operates entirely with reservoir water, has never had a case of IHN disease in juvenile steelhead trout. Therefore, staff at Dworshak NFH sought and obtained access to a limited supply of reservoir water for the first few months of outdoor rearing of juvenile steelhead trout, beginning in 2010. This strategy delayed the exposure of juvenile steelhead trout to river water for several months. The effects of this program change were: drastic reduction in IHN disease in juvenile steelhead trout; interruption in the transmission of highly virulent M group IHNV from adult steelhead trout; no interruption in the transmission of low virulent U group IHNV from adult Chinook salmon; and a shift of IHNV types in adult fish spawned at Dworshak NFH in subsequent years from M to U group viruses. While juvenile steelhead trout may still be infected via exposure to IHNV in river water, the disruption of virulent M group IHNV has been successful in dramatically reducing IHN disease in steelhead trout every year since 2010.

Idaho↗

Attenuation of monkeypox virus by deletion of genomic regions

Monkeypox virus (MPXV) is an emerging pathogen from Africa that causes disease similar to smallpox. Two clades with different geographic distributions and virulence have been described. Here, we utilized bioinformatic tools to identify genomic regions in MPXV containing multiple virulence genes and explored their roles in pathogenicity; two selected regions were then deleted singularly or in combination. In vitro and in vivo studies indicated that these regions play a significant role in MPXV replication, tissue spread, and mortality in mice. Interestingly, while deletion of either region led to decreased virulence in mice, one region had no effect on in vitro replication. Deletion of both regions simultaneously also reduced cell culture replication and significantly increased the attenuation in vivo over either single deletion. Attenuated MPXV with genomic deletions present a safe and efficacious tool in the study of MPX pathogenesis and in the identification of genetic factors associated with virulence.

Virology↗

Characterization and isolation of an extracellular serine protease from the tomato pathogen Colletotrichum coccodes, and it's role in pathogenicity

Extracellular enzymes play an important role in the pathogenicity and virulence of phytopathogenic fungi. Several isolates of Colletotrichum coccodes, causal agent of anthracnose on tomato, were screened to determine the relationship between protease activity and virulence. A direct relationship was observed between extracellular protease activity and the induction of disease symptoms of fruit and mortality in plants. Isolate Cc155 exhibited the highest protease activity after five days of growth in protease induction medium and produced an extracellular serine protease (sp78) that was 78 kDa, auto-degradative, glucose repressible, and non-glycosylated. To determine the role of sp78 in pathogenicity, a uv-induced extracellular protease deficient mutant (np155) was generated from the wildtype isolate Cc155. Np155 maintained growth rates comparable to Cc155 and produced wildtype levels of extracellular cellulase but did not produce extracellular protease. Unlike Cc155, np155 caused no disease symptoms on tomato fruit and 0% mortality on tomato seedlings. These results suggest that extracellular protease activity is required for pathogenicity and virulence of C. coccodes, and that the elimination of protease activity transforms a virulent pathogen to a non-pathogenic endophyte.

Mycological Research↗

Atlantic salmon, Salmo salar L. are broadly susceptible to isolates representing the North American genogroups of infectious hematopoietic necrosis virus

Beginning in 1992, three epidemic waves of infectious hematopoietic necrosis, often with high mortality, occurred in farmed Atlantic salmon Salmo salar L. on the west coast of North America. We compared the virulence of eleven strains of infectious hematopoietic necrosis virus (IHNV), representing the U, M and L genogroups, in experimental challenges of juvenile Atlantic salmon in freshwater. All strains caused mortality and there was wide variation within genogroups: cumulative mortality for five U-group strains ranged from 20 to 100%, four M-group strains ranged 30-63% and two L-group strains varied from 41 to 81%. Thus, unlike Pacific salmonids, there was no apparent correlation of virulence in a particular host species with virus genogroup. The mortality patterns indicated two different phenotypes in terms of kinetics of disease progression and final per cent mortality, with nine strains having moderate virulence and two strains (from the U and L genogroups) having high virulence. These phenotypes were investigated by histopathology and immunohistochemistry to describe the variation in the course of IHNV disease in Atlantic salmon. The results from this study demonstrate that IHNV may become a major threat to farmed Atlantic salmon in other regions of the world where the virus has been, or may be, introduced.

Journal of Fish Diseases↗

Trichomoniasis

Avian trichomoniasis is caused by a single celled protozoan, Trichomonas gallinae. Avirulent T. gallinae strains that do not cause disease and highly virulent strains are found in nature and circulate within bird populations. The factors that make a strain virulent are not known, but they are thought to be controlled genetically within the parasite. Similarly, the reasons why an avirulent or a virulent form of the parasite is found within a bird population at any period of time also remain unknown. Virulent strains of T. gallinae have caused major mortality events or epizootics in doves and pigeons in addition to less visible, chronic losses (Table 25.1). Infection typically involves the upper digestive tract of doves and pigeons but other species have also been infected (Fig. 25.1).

Information and Technology Report↗

Cotton farming pesticides affect ileal microbiota activity expressions of virulome but not resistome or metabolic pathways in a sedentary wild passerine

The increased use of agrochemicals to enhance crop production has had detrimental environmental effects including implication in the sharp decline of North American farmland-breeding birds. Here, using a combination of deep shotgun metatranscriptomics and pesticide exposure data, we sought to assess whether exposure to cotton ( Gossypium spp.) production had a differential effect on ileum multi-kingdom microbial activity, metabolism, anti-microbial resistance, and virulence factors of sedentary northern mockingbirds ( Mimus polyglottos ) sampled from two cotton-producing areas (16 birds in total) and one uncultivated area (7 birds) in Texas, USA. Both Shannon Index values (Adj. r 2 = 0.174, F (1,21) = 5.633, p = 0.027) and a Mantel test (Spearman ρ = 0.184, p = 0.013) supported a relationship between metabolically active microbiota Bray–Curtis dissimilarities and differences in pesticide mixtures among study areas. Virulence factor richness (Adj. r 2 = 0.182, F (1,21) = 5.890, p = 0.024), Shannon Index (Adj. r 2 = 0.231, F (1,21) = 7.612, p = 0.012), and load (sum of virulence factor abundances; Adj. r 2 = 0.160, F (1,21) = 5.194, p = 0.033) were related to total pesticide load (total quantity of pesticides). We found no pesticide effects on expression of either antimicrobial resistance genes or metabolic pathways.

Texas↗

The aerosphere as a network connector of organisms and their diseases

Aeroecological processes, especially powered flight of animals, can rapidly connect biological communities across the globe. This can have profound consequences for evolutionary diversification, energy and nutrient transfers, and the spread of infectious diseases. The latter is of particular consequence for human populations, since migratory birds are known to host diseases which have a history of transmission into domestic poultry or even jumping to human hosts. In this chapter, we present a scenario under which a highly pathogenic avian influenza (HPAI) strain enters North America from East Asia via post-molting waterfowl migration. We use an agent-based model (ABM) to simulate the movement and disease transmission among 10 6 generalized waterfowl agents originating from ten molting locations in eastern Siberia, with the HPAI seeded in only ~10 2 agents at one of these locations. Our ABM tracked the disease dynamics across a very large grid of sites as well as individual agents, allowing us to examine the spatiotemporal patterns of change in virulence of the HPAI infection as well as waterfowl host susceptibility to the disease. We concurrently simulated a 12-station disease monitoring network in the northwest USA and Canada in order to assess the potential efficacy of these sites to detect and confirm the arrival of HPAI. Our findings indicated that HPAI spread was initially facilitated but eventually subdued by the migration of host agents. Yet, during the 90-day simulation, selective pressures appeared to have distilled the HPAI strain to its most virulent form (i.e., through natural selection), which was counterbalanced by the host susceptibility being conversely reduced (i.e., through genetic predisposition and acquired immunity). The monitoring network demonstrated wide variation in the utility of sites; some were clearly better at providing early warnings of HPAI arrival, while sites further from the disease origin exposed the selective dynamics which slowed the spread of the disease albeit with the result of passing highly virulent strains into southern wintering locales (where human impacts are more likely). Though the ABM presented had generalized waterfowl migration and HPAI disease dynamics, this exercise demonstrates the power of such simulations to examine the extremely large and complex processes which comprise aeroecology. We offer insights into how such models could be further parameterized to represent HPAI transmission risks as well as how ABMs could be applied to other aeroecological questions pertaining to individual-based connectivity.

Book chapter↗

Genetic diversity and mutation of avian paramyxovirus serotype 1 (Newcastle disease virus) in wild birds and evidence for intercontinental spread

Avian paramyxovirus serotype 1 (APMV-1), or Newcastle disease virus, is the causative agent of Newcastle disease, one of the most economically important diseases for poultry production worldwide and a cause of periodic epizootics in wild birds in North America. In this study, we examined the genetic diversity of APMV-1 isolated from migratory birds sampled in Alaska, Japan, and Russia and assessed the evidence for intercontinental virus spread using phylogenetic methods. Additionally, we predicted viral virulence using deduced amino acid residues for the fusion protein cleavage site and estimated mutation rates for the fusion gene of class I and class II migratory bird isolates. All 73 isolates sequenced as part of this study were most closely related to virus genotypes previously reported for wild birds; however, five class II genotype I isolates formed a monophyletic clade exhibiting previously unreported genetic diversity, which met criteria for the designation of a new sub-genotype. Phylogenetic analysis of wild-bird isolates provided evidence for intercontinental virus spread, specifically viral lineages of APMV-1 class II genotype I sub-genotypes Ib and Ic. This result supports migratory bird movement as a possible mechanism for the redistribution of APMV-1. None of the predicted deduced amino acid motifs for the fusion protein cleavage site of APMV-1 strains isolated from migratory birds in Alaska, Japan, and Russia were consistent with those of previously identified virulent viruses. These data therefore provide no support for these strains contributing to the emergence of avian pathogens. The estimated mutation rates for fusion genes of class I and class II wild-bird isolates were faster than those reported previously for non-virulent APMV-1 strains. Collectively, these findings provide new insight into the diversity, spread, and evolution of APMV-1 in wild birds.

Archives of Virology↗

Serological comparison of selected isolates of Aeromonas salmonicida ssp. Salmonicida

Eight isolates of Acronionus salmonicida ssp. salmonicida were collected during furunculosis epizootics in North American Pacific coast states and provinces. Both virulent and avirulent forms of each isolate, confirmed by challenge and electron microscopy, were examined. Serological comparisons by cross-absorption agglutination tests revealed no serological differences between isolates. Using the double diffusion precipitin test, a single band was observed when antigen from a sonicated virulent strain was reacted with antiserum against a sonicated, virulent strain absorbed with homologous, avirulent strain. The presence of the single band was eliminated by excess sonication.

Journal of Fish Diseases↗

In vitro infection of salmonid epidermal tissues by infectious hematopoietic necrosis virus and viral hemorrhagic septicemia virus

The ability of two rhabdoviruses, infectious hematopoietic necrosis virus (IHNV) and viral hemorrhagic septicemia virus (VHSV), to infect fish skin was investigated by in vitro infection of excised tissues. Virus replication was determined by plaque assay of homogenized tissue extracts, and the virus antigen was detected by immunohistology of tissue sections. Gill, fin, and ventral abdominal skin tissues of rainbow trout Oncorhynchus mykiss that had been infected in vitro with a virulent strain of IHNV (193–110) produced substantial increases in virus titer within 24 h. Titers continued to increase up until day 3 of incubation; by this time, virus had increased 1,000-fold or more. This increase in IHNV titer occurred in epidermal tissues of fingerlings and of older fish. In another experiment, IHNV replicated in excised rainbow trout tissues whether the fish had been subject to prior infection with a virulent strain of IHNV (Western Regional Aquaculture Consortium isolate) or whether the fish had been infected previously with an attenuated strain of the virus (Nan Scott Lake, with 100 passes in culture). A virulent strain of VHSV (23/75) replicated effectively in excised gill tissues and epidermal tissues of rainbow trout and chinook salmon O. tshawytscha ; however, the avirulent North American strain of VHSV (Makah) replicated poorly or not at all.

Journal of Aquatic Animal Health↗

Analytical validation of two RT-qPCR tests and detection of spring viremia of carp virus (SVCV) in persistently infected koi Cyprinus carpio

Spring viremia of carp virus (SVCV) ia a carp sprivivirus and a member of the genus Sprivivirus within the family Rhabdoviridae . The virus is the etiological agent of spring viremia of carp, a disease of cyprinid species including koi Cyprinus carpio L. and notifiable to the World Organisation for Animal Health. The goal of this study was to explore hypotheses regarding inter-genogroup (Ia to Id) SVCV infection dynamics in juvenile koi and contemporaneously create new reverse-transcription quantitative PCR (RT-qPCR) assays and validate their analytical sensitivity, specificity (ASp) and repeatability for diagnostic detection of SVCV. RT-qPCR diagnostic tests targeting the SVCV nucleoprotein (Q2N) or glycoprotein (Q1G) nucleotides were pan-specific for isolates typed to SVCV genogroups Ia to Id. The Q2N test had broader ASp than Q1G because Q1G did not detect SVCV isolate 20120450 and Q2N displayed occasional detection of pike fry sprivivirus isolate V76. Neither test cross-reacted with other rhabdoviruses, infectious pancreatic necrosis virus or co-localizing cyprinid herpesvirus 3. Both tests were sensitive with observed 50% limits of detection of 3 plasmid copies and high repeatability. Test analysis of koi immersed in SVCV showed that the virus could be detected for at least 167 d following exposure and that titer, prevalence, replicative rate and persistence in koi were correlated significantly with virus virulence. In this context, high virulence SVCV isolates were more prevalent, reached higher titers quicker and persisted in koi for longer periods of time relative to moderate and low virulence isolates.

Diseases of Aquatic Organisms↗

Characterization of Pasteurella multocida isolates from wetland ecosystems during 1996 to 1999

We cultured 126 Pasteurella multocida isolates, 92 from water and 34 from sediment samples collected from wetlands in the Pacific and Central flyways of the United States between 1996 and 1999. Most (121) of the isolates were P. multocida serotype 1, but serotypes 3, 3/4, 10, and 11 were also found. Many (82) of the isolates were further characterized by DNA fingerprinting procedures and tested in Pekin ducks for virulence. Almost all the serotype 1 isolates we tested caused mortality in Pekin ducks. Serotype 1 isolates varied in virulence, but the most consistent pattern was higher mortality in male ducks than in females. We found no evidence that isolates found in sediment vs. water, between Pacific and Central flyways, or during El Nino years had consistently different virulence. We also found a number of non-serotype 1 isolates that were avirulent in Pekin ducks. Isolates had DNA fingerprint profiles similar to those found in birds that died during avian cholera outbreaks.

Journal of Wildlife Diseases↗

Specificity of DNA vaccines against the U and M genogroups of infectious hematopoietic necrosis virus (IHNV) in rainbow trout (Oncorhynchus mykiss)

Infectious hematopoietic necrosis virus (IHNV) is a fish rhabdovirus that causes significant mortality in salmonid species. In North America IHNV has three major genogroups designated U, M, and L. Host-specificity of the M and U genogroups of IHNV has been established both in the field and in experimental challenges, with M isolates being more prevalent and more virulent in rainbow trout (Oncorhynchus mykiss), and U isolates being more prevalent and highly virulent in sockeye salmon (Oncorhynchus nerka). In this study, efficacy of DNA vaccines containing either M (pM) or U (pU) virus glycoprotein genes was investigated during intra- and cross-genogroup challenges in rainbow trout. In virus challenges at 7 days post-vaccination (early antiviral response), both pM and pU were highly protective against either M or U IHNV. In challenges at 28 days post-vaccination (specific antiviral response), both pM and pU were protective against M IHNV but the homologous pM vaccine was significantly more protective than pU in one of two experiments. At this stage both pM and pU induced comparably high protection against U IHNV challenge. Correlates of protection were also investigated by assessing the expression of the interferon-stimulated gene Mx-1 and the production of neutralizing antibodies (NAbs) following pM or pU DNA vaccination. Mx-1 gene expression, measured at 4 and 7 days post-vaccination as an indicator of the host innate immune response, was found to be significantly higher after pM than pU vaccination in some cases. Neutralizing antibody was produced in response to the two vaccines, but antibody titers did not show consistent correlation with protection. The results show that the rainbow trout innate and adaptive immune responses have some ability to distinguish between the U and M genogroup IHNV, but overall the pM and pU vaccines were protective against both homologous and cross-genogroup challenges.

Fish and Shellfish Immunology↗