Geology topics

Gael Kurath

Publications and source records attributed to Gael Kurath.

At least 73 records · Page 4Linked to original sources

USGS2013

Virulence of viral hemorrhagic septicemia virus (VHSV) genotypes Ia, IVa, IVb, and IVc in five fish species.

The susceptibility of yellow perch Perca flavescens , rainbow trout Oncorhynchus mykiss , Chinook salmon O. tshawytscha , koi Cyprinus carpio koi , and Pacific herring Clupea pallasii to 4 strains of viral hemorrhagic septicemia virus (VHSV) was assessed. Fish were challenged via intraperitoneal injection with high (1 × 10 6 plaque-forming units, PFU) and low (1 × 10 3 PFU) doses of a European strain (genotype Ia), and North American strains from the West coast (genotype IVa), Great Lakes (genotype IVb), and the East coast (genotype IVc). Pacific herring were exposed to the same VHSV strains, but at a single dose of 5 × 10 3 PFU ml -1 by immersion in static seawater. Overall, yellow perch were the most susceptible, with cumulative percent mortality (CPM) ranging from 84 to 100%, and 30 to 93% in fish injected with high or low doses of virus, respectively. Rainbow trout and Chinook salmon experienced higher mortalities (47 to 98% CPM) after exposure to strain Ia than to the other virus genotypes. Pacific herring were most susceptible to strain IVa with an average CPM of 80% and moderately susceptible (42 to 52% CPM) to the other genotypes. Koi had very low susceptibility (≤5.0% CPM) to all 4 VHSV strains. Fish tested at 7 d post challenge were positive for all virus strains, with yellow perch having the highest prevalence and concentrations of virus, and koi the lowest. While genotype Ia had higher virulence in salmonid species, there was little difference in virulence or host-specificity between isolates from subtypes IVa, IVb, and IVc.

Diseases of Aquatic Organisms↗

USGS2012

Viral fitness: definitions, measurement, and current insights

Viral fitness is an active area of research, with recent work involving an expanded number of human, non-human vertebrate, invertebrate, plant, and bacterial viruses. Many publications deal with RNA viruses associated with major disease emergence events, such as HIV-1, influenza virus, and Dengue virus. Study topics include drug resistance, immune escape, viral emergence, host jumps, mutation effects, quasispecies diversity, and mathematical models of viral fitness. Important recent trends include increasing use of in vivo systems to assess vertebrate virus fitness, and a broadening of research beyond replicative fitness to also investigate transmission fitness and epidemiologic fitness. This is essential for a more integrated understanding of overall viral fitness, with implications for disease management in the future.

Current Opinion in Virology↗

USGS2012

Analysis of host genetic diversity and viral entry as sources of between-host variation in viral load

Little is known about the factors that drive the high levels of between-host variation in pathogen burden that are frequently observed in viral infections. Here, two factors thought to impact viral load variability, host genetic diversity and stochastic processes linked with viral entry into the host, were examined. This work was conducted with the aquatic vertebrate virus, Infectious hematopoietic necrosis virus (IHNV), in its natural host, rainbow trout. It was found that in controlled in vivo infections of IHNV, a suggestive trend of reduced between-fish viral load variation was observed in a clonal population of isogenic trout compared to a genetically diverse population of out-bred trout. However, this trend was not statistically significant for any of the four viral genotypes examined, and high levels of fish-to-fish variation persisted even in the isogenic trout population. A decrease in fish-to-fish viral load variation was also observed in virus injection challenges that bypassed the host entry step, compared to fish exposed to the virus through the natural water-borne immersion route of infection. This trend was significant for three of the four virus genotypes examined and suggests host entry may play a role in viral load variability. However, high levels of viral load variation also remained in the injection challenges. Together, these results indicate that although host genetic diversity and viral entry may play some role in between-fish viral load variation, they are not major factors. Other biological and non-biological parameters that may influence viral load variation are discussed.

Virus Research↗

USGS2012

AquaPathogen X--A template database for tracking field isolates of aquatic pathogens

AquaPathogen X is a template database for recording information on individual isolates of aquatic pathogens and is available for download from the U.S. Geological Survey (USGS) Western Fisheries Research Center (WFRC) website (http://wfrc.usgs.gov). This template database can accommodate the nucleotide sequence data generated in molecular epidemiological studies along with the myriad of abiotic and biotic traits associated with isolates of various pathogens (for example, viruses, parasites, or bacteria) from multiple aquatic animal host species (for example, fish, shellfish, or shrimp). The simultaneous cataloging of isolates from different aquatic pathogens is a unique feature to the AquaPathogen X database, which can be used in surveillance of emerging aquatic animal diseases and clarification of main risk factors associated with pathogen incursions into new water systems. As a template database, the data fields are empty upon download and can be modified to user specifications. For example, an application of the template database that stores the epidemiological profiles of fish virus isolates, called Fish ViroTrak (fig. 1), was also developed (Emmenegger and others, 2011).

Fact Sheet↗

USGS2012

An online database for IHN virus in Pacific Salmonid fish: MEAP-IHNV

The MEAP-IHNV database provides access to detailed data for anyone interested in IHNV molecular epidemiology, such as fish health professionals, fish culture facility managers, and academic researchers. The flexible search capabilities enable the user to generate various output formats, including tables and maps, which should assist users in developing and testing hypotheses about how IHNV moves across landscapes and changes over time. The MEAP-IHNV database is available online at http://gis.nacse.org/ihnv/ (fig. 1). The database contains records that provide background information and genetic sequencing data for more than 1,000 individual field isolates of the fish virus Infectious hematopoietic necrosis virus (IHNV), and is updated approximately annually. It focuses on IHNV isolates collected throughout western North America from 1966 to the present. The database also includes a small number of IHNV isolates from Eastern Russia. By engaging the expertise of the broader community of colleagues interested in IHNV, our goal is to enhance the overall understanding of IHNV epidemiology, including defining sources of disease outbreaks and viral emergence events, identifying virus traffic patterns and potential reservoirs, and understanding how human management of salmonid fish culture affects disease. Ultimately, this knowledge can be used to develop new strategies to reduce the effect of IHN disease in cultured and wild fish.

Fact Sheet↗

USGS2011

Detection of Viral Hemorrhagic Septicemia Virus by Quantitative Reverse Transcription Polymerase Chain Reaction from Two Fish Species at Two Sites in Lake Superior

Viral hemorrhagic septicemia virus (VHSV) was first detected in the Laurentian Great Lakes in 2005 during a mortality event in the Bay of Quinte, Lake Ontario. Subsequent analysis of archived samples determined that the first known isolation of VHSV in the Laurentian Great Lakes was from a muskellunge Esox masquinongy collected in Lake St. Clair in 2003. By the end of 2008, mortality events and viral isolations had occurred in all of the Laurentian Great Lakes except Lake Superior. In 2009, a focused disease surveillance program was designed to determine whether VHSV was also present in Lake Superior. In this survey, 874 fish from 7 sites along the U.S. shoreline of Lake Superior were collected during June 2009. Collections were focused on nearshore species known to be susceptible to VHSV. All fish were dissected individually by using aseptic techniques and were tested for the presence of VHSV genetic material by use of a quantitative reverse transcription (qRT) polymerase chain reaction (PCR) targeting the viral nucleoprotein gene. Seventeen fish from two host species at two different sites tested positive at low levels for VHSV. All attempts to isolate virus in cell culture were unsuccessful. However, the presence of viral RNA was confirmed independently in five fish by using a nested PCR that targeted the glycoprotein (G) gene. Partial G gene sequences obtained from three fish were identical to the corresponding sequence from the original 2003 VHSV isolate (MI03) from muskellunge. These detections represent the earliest evidence for the presence of VHSV in Lake Superior and illustrate the utility of the highly sensitive qRT-PCR assay for disease surveillance in aquatic animals.

Journal of Aquatic Animal Health↗

USGS2011

A nuclear localization of the infectious haematopoietic necrosis virus NV protein is necessary for optimal viral growth

The nonvirion (NV) protein of infectious hematopoietic necrosis virus (IHNV) has been previously reported to be essential for efficient growth and pathogenicity of IHNV. However, little is known about the mechanism by which the NV supports the viral growth. In this study, cellular localization of NV and its role in IHNV growth in host cells was investigated. Through transient transfection in RTG-2 cells of NV fused to green fluorescent protein (GFP), a nuclear localization of NV was demonstrated. Deletion analyses showed that the 32 EGDL 35 residues were essential for nuclear localization of NV protein, and fusion of these 4 amino acids to GFP directed its transport to the nucleus. We generated a recombinant IHNV, rIHNV-NV-ΔEGDL in which the 32 EGDL 35 was deleted from the NV. rIHNVs with wild-type NV (rIHNV-NV) or with the NV gene replaced with GFP (rIHNV-ΔNV-GFP) were used as controls. RTG-2 cells infected with rIHNV-ΔNV-GFP and rIHNV-NV-ΔEGDL yielded 12- and 5-fold less infectious virion, respectively, than wild type rIHNV-infected cells at 48 h post-infection (p.i.). While treatment with poly I:C at 24 h p.i. did not inhibit replication of wild-type rIHNVs, replication rates of rIHNV-ΔNV-GFP and rIHNV-NV-ΔEGDL were inhibited by poly I:C. In addition, both rIHNV-ΔNV and rIHNV-NV-ΔEGDL induced higher levels of expressions of both IFN1 and Mx1 than wild-type rIHNV. These data suggest that the IHNV NV may support the growth of IHNV through inhibition of the INF system and the amino acid residues of 32 EGDL 35 responsible for nuclear localization are important for the inhibitory activity of NV.

PLoS ONE↗

USGS2011

Development of an aquatic pathogen database (AquaPathogen X) and its utilization in tracking emerging fish virus pathogens in North America

The AquaPathogen X database is a template for recording information on individual isolates of aquatic pathogens and is freely available for download (http://wfrc.usgs.gov). This database can accommodate the nucleotide sequence data generated in molecular epidemiological studies along with the myriad of abiotic and biotic traits associated with isolates of various pathogens (e.g. viruses, parasites and bacteria) from multiple aquatic animal host species (e.g. fish, shellfish and shrimp). The cataloguing of isolates from different aquatic pathogens simultaneously is a unique feature to the AquaPathogen X database, which can be used in surveillance of emerging aquatic animal diseases and elucidation of key risk factors associated with pathogen incursions into new water systems. An application of the template database that stores the epidemiological profiles of fish virus isolates, called Fish ViroTrak, was also developed. Exported records for two aquatic rhabdovirus species emerging in North America were used in the implementation of two separate web-accessible databases: the Molecular Epidemiology of Aquatic Pathogens infectious haematopoietic necrosis virus (MEAP-IHNV) database (http://gis.nacse.org/ihnv/) released in 2006 and the MEAP- viral haemorrhagic septicaemia virus (http://gis.nacse.org/vhsv/) database released in 2010.

Journal of Fish Diseases↗

USGS2011

Restricted growth of U-type infectious haematopoietic necrosis virus (IHNV) in rainbow trout cells may be linked to casein kinase II activity

Previously, we demonstrated that a representative M genogroup type strain of infectious haematopoietic necrosis virus (IHNV) from rainbow trout grows well in rainbow trout‐derived RTG‐2 cells, but a U genogroup type strain from sockeye salmon has restricted growth, associated with reduced genome replication and mRNA transcription. Here, we analysed further the mechanisms for this growth restriction of U‐type IHNV in RTG‐2 cells, using strategies that assessed differences in viral genes, host immune regulation and phosphorylation. To determine whether the viral glycoprotein (G) or non‐virion (NV) protein was responsible for the growth restriction, four recombinant IHNV viruses were generated in which the G gene of an infectious IHNV clone was replaced by the G gene of U‐ or M‐type IHNV and the NV gene was replaced by NV of U‐ or M‐type IHNV. There was no significant difference in the growth of these recombinants in RTG‐2 cells, indicating that G and NV proteins are not major factors responsible for the differential growth of the U‐ and M‐type strains. Poly I:C pretreatment of RTG‐2 cells suppressed the growth of both U‐ and M‐type IHNV, although the M virus continued to replicate at a reduced level. Both viruses induced type 1 interferon (IFN1) and the IFN1 stimulated gene Mx1, but the expression levels in M‐infected cells were significantly higher than in U‐infected cells and an inhibitor of the IFN1‐inducible protein kinase PKR, 2‐aminopurine (2‐AP), did not affect the growth of U‐ or M‐type IHNV in RTG‐2 cells. These data did not indicate a role for the IFN1 system in the restricted growth of U‐type IHNV in RTG‐2 cells. Prediction of kinase‐specific phosphorylation sites in the viral phosphoprotein (P) using the NetPhosK program revealed differences between U‐ and M‐type P genes at five phosphorylation sites. Pretreatment of RTG‐2 cells with a PKC inhibitor or a p38MAPK inhibitor did not affect the growth of the U‐ and M‐type viruses. However, 100 μ m of the casein kinase II (CKII) inhibitor, 5,6‐dichloro‐1‐β‐ d ‐ribofuranosylbenzimidazole (DRB), reduced the titre of the U type 8.3‐fold at 24 h post‐infection. In contrast, 100 μ m of the CKII inhibitor reduced the titre of the M type only 1.3‐fold at 48 h post‐infection. Our data suggest that the different growth of U‐ and M‐type IHNV in RTG‐2 cells may be linked to a differential requirement for cellular protein kinases such as CKII for their growth.

Journal of Fish Diseases↗

USGS2011

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↗

USGS2011

In vivo fitness correlates with host-specific virulence of Infectious hematopoietic necrosis virus (IHNV) in sockeye salmon and rainbow trout

The relationship between virulence and overall within-host fitness of the fish rhabdovirus Infectious hematopoietic necrosis virus (IHNV) was empirically investigated in vivo for two virus isolates belonging to different IHNV genogroups that exhibit opposing host-specific virulence. U group isolates are more virulent in sockeye salmon and M group isolates are more virulent in rainbow trout. In both single and mixed infections in the two fish hosts, the more virulent IHNV type exhibited higher prevalence and higher viral load than the less virulent type. Thus, a positive correlation was observed between higher in vivo fitness and higher host-specific virulence in sockeye salmon and rainbow trout. Comparisons of mean viral loads in single and mixed infections revealed no evidence for limitation due to competition effects between U and M viruses in either rainbow trout or sockeye salmon co-infections.

Virology↗

USGS2011

In Vivo fitness associated with high virulence in a vertebrate virus is a complex trait regulated by host entry, replication, and shedding

The relationship between pathogen fitness and virulence is typically examined by quantifying only one or two pathogen fitness traits. More specifically, it is regularly assumed that within-host replication, as a precursor to transmission, is the driving force behind virulence. In reality, many traits contribute to pathogen fitness, and each trait could drive the evolution of virulence in different ways. Here, we independently quantified four viral infection cycle traits, namely, host entry, within-host replication, within-host coinfection fitness, and shedding, in vivo , in the vertebrate virus Infectious hematopoietic necrosis virus (IHNV). We examined how each of these stages of the viral infection cycle contributes to the fitness of IHNV genotypes that differ in virulence in rainbow trout. This enabled us to determine how infection cycle fitness traits are independently associated with virulence. We found that viral fitness was independently regulated by each of the traits examined, with the largest impact on fitness being provided by within-host replication. Furthermore, the more virulent of the two genotypes of IHNV we used had advantages in all of the traits quantified. Our results are thus congruent with the assumption that virulence and within-host replication are correlated but suggest that infection cycle fitness is complex and that replication is not the only trait associated with virulence.

Journal of Virology↗

USGS2011

Emergence of viral hemorrhagic septicemia virus in the North American Great Lakes region is associated with low viral genetic diversity

Viral hemorrhagic septicemia virus (VHSV) is a fish rhabdovirus that causes disease in a broad range of marine and freshwater hosts. The known geographic range includes the Northern Atlantic and Pacific Oceans, and recently it has invaded the Great Lakes region of North America. The goal of this work was to characterize genetic diversity of Great Lakes VHSV isolates at the early stage of this viral emergence by comparing a partial glycoprotein (G) gene sequence (669 nt) of 108 isolates collected from 2003 to 2009 from 31 species and at 37 sites. Phylogenetic analysis showed that all isolates fell into sub-lineage IVb within the major VHSV genetic group IV. Among these 108 isolates, genetic diversity was low, with a maximum of 1.05% within the 669 nt region. There were 11 unique sequences, designated vcG001 to vcG011. Two dominant sequence types, vcG001 and vcG002, accounted for 90% (97 of 108) of the isolates. The vcG001 isolates were most widespread. We saw no apparent association of sequence type with host or year of isolation, but we did note a spatial pattern, in which vcG002 isolates were more prevalent in the easternmost sub-regions, including inland New York state and the St. Lawrence Seaway. Different sequence types were found among isolates from single disease outbreaks, and mixtures of types were evident within 2 isolates from individual fish. Overall, the genetic diversity of VHSV in the Great Lakes region was found to be extremely low, consistent with an introduction of a new virus into a geographic region with previously naïve host populations.

Diseases of Aquatic Organisms↗

USGS2011

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↗

USGS2011

Exxon Valdez oil spill restoration project final report: Prince William Sound Herring disease program (HDP), restoration project 070819

Surveys of pathogens in Pacific herring from 2007 – 2010 indicated that Ichthyophonus , viral hemorrhagic septicemia virus, and erythrocytic necrosis virus are endemic in Prince William Sound and throughout the NE Pacific. Laboratory studies with VHSV indicated that multiple herring stocks are equally susceptible to the resulting disease, Pacific herring shed copious levels of VHSV (as high at 5x10 8 plaque-forming units/day) shortly after exposure, chronic and persistent infections can occur in Pacific herring, susceptibility of Pacific herring to VHS extends to the larval life stages but not the embryonic stages, and the prior exposure history of Pacific herring to VHSV can be determined post hoc. Laboratory studies involving Ichthyophonus indicated that schizonts can be inactivated with chlorine and iodine solutions, the parasite can survive for extended periods in saltwater but not freshwater, a low potential exists for cross contamination between in vitro explant cultures, infectious schizonts are released from the skin surface of infected herring, schizonts are not uniformly distributed throughout the skeletal muscle of infected Pacific herring, multiple types of Ichthyophonus exist with different genotypes and phenotypic traits, and temperature is an important factor influencing the infectivity of Ichthyophonus . Additional field and laboratory studies indicated that Ichthyophonus negatively influences the swimming performance of infected hosts and the negative impacts effects are exacerbated by increasing temperatures, American shad are an important reservoir of Ichthyophonus in the NE Pacific, Pacific herring are not susceptible to infectious hematopoietic necrosis (IHN), and Pacific herring will accept surgically implanted acoustic tags with negligible impacts on survival.

Alaska, Washington↗

USGS2011

About viral hemorrhagic septicemia (VHS) virus. Potential threat of Great Lakes VHS virus in Western United States

Viral hemorrhagic septicemia (VHS) is a disease caused by a virus (VHSV). There are different strains of the virus that can infect marine and freshwater fish species, and the different strains may affect species differently. VHSV has recently invaded the Great Lakes, resulting in many large-scale fish die-offs and new regulatory restrictions for aquaculture throughout the region.

Report↗

USGS2010

A reverse genetics system for the Great Lakes strain of viral hemorrhagic septicemia virus: the NV gene is required for pathogenicity

Viral hemorrhagic septicemia virus (VHSV), belonging to the genus Novirhabdovirus in the family of Rhabdoviridae , causes a highly contagious disease of fresh and saltwater fish worldwide. Recently, a novel genotype of VHSV, designated IVb, has invaded the Great Lakes in North America, causing large-scale epidemics in wild fish. An efficient reverse genetics system was developed to generate a recombinant VHSV of genotype IVb from cloned cDNA. The recombinant VHSV (rVHSV) was comparable to the parental wild-type strain both in vitro and in vivo, causing high mortality in yellow perch ( Perca flavescens ). A modified recombinant VHSV was generated in which the NV gene was substituted with an enhanced green fluorescent protein gene (rVHSV-ΔNV-EGFP), and another recombinant was made by inserting the EGFP gene into the full-length viral clone between the P and M genes (rVHSV-EGFP). The in vitro replication kinetics of rVHSV-EGFP was similar to rVHSV; however, the rVHSV-ΔNV-EGFP grew 2 logs lower. In yellow perch challenges, wtVHSV and rVHSV induced 82-100% cumulative per cent mortality (CPM), respectively, whereas rVHSV-EGFP produced 62% CPM and rVHSV-ΔNV-EGFP caused only 15% CPM. No reversion of mutation was detected in the recovered viruses and the recombinant viruses stably maintained the foreign gene after several passages. These results indicate that the NV gene of VHSV is not essential for viral replication in vitro and in vivo, but it plays an important role in viral replication efficiency and pathogenicity. This system will facilitate studies of VHSV replication, virulence, and production of viral vectored vaccines.

Marine Biotechnology↗

USGS2010

Differential growth of U and M type infectious haematopoietic necrosis virus in a rainbow trout–derived cell line, RTG-2

Infectious haematopoietic necrosis virus (IHNV) is one of the most important viral pathogens of salmonids. In rainbow trout, IHNV isolates in the M genogroup are highly pathogenic, while U genogroup isolates are significantly less pathogenic. We show here that, at a multiplicity of infection (MOI) of 1, a representative U type strain yielded 42‐fold less infectious virus than an M type strain in the rainbow trout–derived RTG‐2 cell line at 24 h post‐infection (p.i.). However, at an MOI of 10, there was only fivefold difference in the yield of infectious virus between the U and M strains. Quantification of extracellular viral genomic RNA suggested that the number of virus particles released from cells infected with the U strain at a MOI of 1 was 47‐fold lower than from M‐infected cells, but U and M virions were equally infectious by particle to infectivity ratios. At an MOI of 1, U strain intracellular viral genome accumulation and transcription were 37‐ and 12‐fold lower, respectively, than those of the M strain at 24 h p.i. Viral nucleocapsid (N) protein accumulation in U strain infections was fivefold lower than in M strain infections. These results suggest that the block in U type strain growth in RTG‐2 cells was because of the effects of reduced genome replication and transcription. The reduced growth of the U strain does not seem to be caused by defective genes, because the U and M strains grew equally well in the permissive epithelioma papulosum cyprini cell line at an MOI of 1. This suggests that host‐specific factors in RTG‐2 cells control the growth of the IHNV U and M strains differently, leading to growth restriction of the U type virus during the RNA synthesis step.

Journal of Fish Diseases↗