scholarly journals Specific nucleotides at the 3′-terminal promoter of viral hemorrhagic septicemia virus are important for virulence in vitro and in vivo

Virology ◽  
2015 ◽  
Vol 476 ◽  
pp. 226-232 ◽  
Author(s):  
Sung-Hyun Kim ◽  
Tz-Chun Guo ◽  
Vikram N. Vakharia ◽  
Øystein Evensen
Keyword(s):  
Viral Hemorrhagic Septicemia Virus ◽  
Viral Hemorrhagic Septicemia

scholarly journals Differences in Virulence of Marine and Freshwater Isolates of Viral Hemorrhagic Septicemia Virus In Vivo Correlate with In Vitro Ability To Infect Gill Epithelial Cells and Macrophages of Rainbow Trout (Oncorhynchus mykiss)

2008 ◽  
Vol 82 (21) ◽  
pp. 10359-10365 ◽  
Author(s):  
Bjørn E. Brudeseth ◽  
Helle F. Skall ◽  
Øystein Evensen
Keyword(s):  
Rainbow Trout ◽  
Epithelial Cells ◽  
Oncorhynchus Mykiss ◽  
Time Course ◽  
Primary Cultures ◽  
Head Kidney ◽  
Viral Hemorrhagic Septicemia Virus ◽  
Viral Hemorrhagic Septicemia

ABSTRACT Two strains of viral hemorrhagic septicemia virus (VHSV) with known different virulence characteristics in vivo were studied (by a time course approach) for their abilities to infect and translocate across a primary culture of gill epithelial cells (GEC) of rainbow trout (RBT; Oncorhynchus mykiss). The strains included one low-virulence marine VHSV (ma-VHSV) strain, ma-1p8, and a highly pathogenic freshwater VHSV (fw-VHSV) strain, fw-DK-3592B. Infectivities toward trout head kidney macrophages were also studied (by a time course method), and differences in in vivo virulence were reconfirmed, the aim being to determine any correlation between in vivo virulence and in vitro infectivity. The in vitro studies showed that the fw-VHSV isolate infected and caused a cytotoxic effect in monolayers of GEC (demonstrating virulence) at an early time point (2 h postinoculation) and that the same virus strain had translocated over a confluent, polarized GEC layer by 2 h postinoculation. The marine isolate did not infect monolayers of GEC, and delayed translocation across polarized GEC was seen by 48 h postinoculation. Primary cultures of head kidney macrophages were also infected with fw-VHSV, with a maximum of 9.5% virus-positive cells by 3 days postinfection, while for the ma-VHSV strain, only 0.5% of the macrophages were positive after 3 days of culture. In vivo studies showed that the fw-VHSV strain was highly virulent for RBT fry and caused high mortality, with classical features of viral hemorrhagic septicemia. The ma-VHSV showed a very low level of virulence (only one pool of samples from the dead fish was VHSV positive). This study has shown that the differences in virulence between marine and freshwater strains of VHSV following the in vivo infection of RBT correlate with in vitro abilities to infect primary cultures of GEC and head kidney macrophages of the same species.

scholarly journals Survey of Transcript Expression in Rainbow Trout Leukocytes Reveals a Major Contribution of Interferon-Responsive Genes in the Early Response to a Rhabdovirus Infection

2002 ◽  
Vol 76 (16) ◽  
pp. 8040-8049 ◽  
Author(s):  
Caroline O'Farrell ◽  
Nikta Vaghefi ◽  
Monique Cantonnet ◽  
Bénédicte Buteau ◽  
Pierre Boudinot ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Host Cell ◽  
Natural Infection ◽  
Viral Hemorrhagic Septicemia Virus ◽  
Nucleic Acid Binding ◽  
Global Knowledge ◽  
Viral Hemorrhagic Septicemia ◽  
Predominant Component ◽  
Induced Genes

ABSTRACT Virus infections induce changes in the expression of host cell genes. A global knowledge of these modifications should help to better understand the virus/host cell interactions. To obtain a more comprehensive view of the rainbow trout response to a viral infection, we used the subtractive suppressive hybridization methodology in the viral hemorrhagic septicemia model of infection. We infected rainbow trout leukocytes with viral hemorrhagic septicemia virus (VHSV), and total RNA from infected and mock-infected cells was compared at 40 h postinfection. Twenty-four virus-induced genes were ultimately retrieved from the subtracted cDNA library, and their differential expression was further confirmed by semiquantitative reverse transcription-PCR and Northern blot analysis. Among these sequences, three were already described as VHSV-induced genes. Eight sequences with known homologs were extended to full-length cDNA using 5′ and 3′ rapid amplification of cDNA ends, and they were subsequently divided into three functional subsets. Four genes were homologous to mammalian interferon responsive genes, three were similar to chemo-attractant molecules (CXC chemokine, galectin), and two had nucleic acid binding domains. All of the virus-induced genes were also induced by rainbow trout interferon, indicating that the interferon pathway is the predominant component of the anti-VHSV response. They were also expressed in vivo in experimentally infected fish, indicating their biological relevance in natural infection.

scholarly journals Genomic and immunogenic changes over the history of the Viral Hemorrhagic Septicemia (VHS-IVb) fish virus (=Piscine novirhabdovirus) in the Laurentian Great Lakes

2020 ◽  
Author(s):  
Megan D. Niner ◽  
Carol A. Stepien ◽  
Bartolomeo Gorgoglione ◽  
Douglas W. Leaman
Keyword(s):  
Great Lakes ◽  
Fish Host ◽  
Laurentian Great Lakes ◽  
Viral Hemorrhagic Septicemia Virus ◽  
Coding Region ◽  
Nucleotide Substitutions ◽  
Whole Genome Analysis ◽  
Viral Hemorrhagic Septicemia ◽  
History Of

AbstractViral Hemorrhagic Septicemia Virus (VHSV) (=Piscine novirhabdovirus) appeared in the Laurentian Great Lakes in 2005, constituting a unique and highly virulent genogroup (IVb), which killed >32 fish species in large 2005 and 2006. Periods of apparent dormancy punctuated smaller outbreaks in 2007, 2008, and 2017. We conducted the first whole genome analysis of IVb, evaluating its evolutionary changes using 46 isolates, in reference to immunogenicity in cell culture, and the genomes of other VHS genogroups (I–IVa) and other Novirhabdoviruses. IVb isolates had 253 genomic nucleotide substitutions (2.3% of the total 11,158 nucleotides), with 85 (16.6%) being non-synonymous. The greatest number of substitutions occurred in the non-coding region (NCDS; 4.3%) followed by the Nv- (3.8%), and M- (2.8%) genes. The M-gene possessed the greatest proportions of amino acid changes (52.9%), followed by the Nv- (50.0%), G- (48.6%), N- (35.7%) and L- (23.1%) genes. Among VHS genogroups, IVa from the northeastern Pacific exhibited the fastest substitution rate (2.01×10-3), followed by Ivb (6.64×10−5), and I/III from Europe (4.09×10−5). A 2016 gizzard shad isolate from Lake Erie was the most divergent IVb isolate (38 NT, 15.0%, 15 AA), yet exhibited reduced virulence with in vitro immunogenicity analyses, as did other 2016 isolates, in comparison to the first IVb isolate (2003). The 2016 isolates exhibited lower impact on innate antiviral responses, suggesting phenotypic effects. Results suggest continued sequence change and lower virulence over the history of IVb, which may facilitate its long-term persistence in fish host populations.

scholarly journals Genomic and immunogenic changes of Piscine novirhabdovirus (Viral Hemorrhagic Septicemia Virus) over its evolutionary history in the Laurentian Great Lakes

PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0232923
Author(s):  
Megan D. Niner ◽  
Carol A. Stepien ◽  
Bartolomeo Gorgoglione ◽  
Douglas W. Leaman
Keyword(s):  
Great Lakes ◽  
Evolutionary History ◽  
Fish Host ◽  
Laurentian Great Lakes ◽  
Viral Hemorrhagic Septicemia Virus ◽  
Sequencing Analysis ◽  
Dorosoma Cepedianum ◽  
Coding Region ◽  
Viral Hemorrhagic Septicemia

A unique and highly virulent subgenogroup (-IVb) of Piscine novirhabdovirus, also known as Viral Hemorrhagic Septicemia Virus (VHSV), suddenly appeared in the Laurentian Great Lakes, causing large mortality outbreaks in 2005 and 2006, and affecting >32 freshwater fish species. Periods of apparent dormancy have punctuated smaller and more geographically-restricted outbreaks in 2007, 2008, and 2017. In this study, we conduct the largest whole genome sequencing analysis of VHSV-IVb to date, evaluating its evolutionary changes from 48 isolates in relation to immunogenicity in cell culture. Our investigation compares genomic and genetic variation, selection, and rates of sequence changes in VHSV-IVb, in relation to other VHSV genogroups (VHSV-I, VHSV-II, VHSV-III, and VHSV-IVa) and with other Novirhabdoviruses. Results show that the VHSV-IVb isolates we sequenced contain 253 SNPs (2.3% of the total 11,158 nucleotides) across their entire genomes, with 85 (33.6%) of them being non-synonymous. The most substitutions occurred in the non-coding region (NCDS; 4.3%), followed by the Nv- (3.8%), and M- (2.8%) genes. Proportionally more M-gene substitutions encoded amino acid changes (52.9%), followed by the Nv- (50.0%), G- (48.6%), N- (35.7%) and L- (23.1%) genes. Among VHSV genogroups and subgenogroups, VHSV-IVa from the northeastern Pacific Ocean has shown the fastest substitution rate (2.01x10-3), followed by VHSV-IVb (6.64x10-5) and by the VHSV-I, -II and-III genogroups from Europe (4.09x10-5). A 2016 gizzard shad (Dorosoma cepedianum) from Lake Erie possessed the most divergent VHSV-IVb sequence. The in vitro immunogenicity analysis of that sample displayed reduced virulence (as did the other samples from 2016), in comparison to the original VHSV-IVb isolate (which had been traced back to 2003, as an origin date). The 2016 isolates that we tested induced milder impacts on fish host cell innate antiviral responses, suggesting altered phenotypic effects. In conclusion, our overall findings indicate that VHSV-IVb has undergone continued sequence change and a trend to lower virulence over its evolutionary history (2003 through present-day), which may facilitate its long-term persistence in fish host populations.

scholarly journals Limited Interference at the Early Stage of Infection between Two Recombinant Novirhabdoviruses: Viral Hemorrhagic Septicemia Virus and Infectious Hematopoietic Necrosis Virus

2010 ◽  
Vol 84 (19) ◽  
pp. 10038-10050 ◽  
Author(s):  
Stéphane Biacchesi ◽  
Annie Lamoureux ◽  
Emilie Mérour ◽  
Julie Bernard ◽  
Michel Brémont
Keyword(s):  
Early Stage ◽  
Cell Monolayer ◽  
Infectious Hematopoietic Necrosis Virus ◽  
Viral Hemorrhagic Septicemia Virus ◽  
Antiviral Protein ◽  
Necrosis Virus ◽  
Interference Phenomenon ◽  
Viral Hemorrhagic Septicemia ◽  
Infectious Hematopoietic Necrosis

ABSTRACT The genome sequence of a hypervirulent novirhabdovirus, viral hemorrhagic septicemia virus (VHSV) French strain 23-75, was determined. Compared to the genome of the prototype Fil3 strain, a number of substitutions, deletions, and insertions were observed. Following the establishment of a plasmid-based minigenome replication assay, recombinant VHSV (rVHSV) was successfully recovered. rVHSV exhibits wild-type-like growth properties in vitro as well as in vivo in rainbow trout. The dispensable role of NV for the novirhabdovirus replication was confirmed by generating rVHSV-ΔNV, in which the NV gene was deleted. This deletion mutant was shown to be as debilitated as that previously described for infectious hematopoietic necrosis virus (IHNV), a distantly related novirhabdovirus (S. Biacchesi, M. I. Thoulouze, M. Bearzotti, Y. X. Yu, and M. Bremont, J. Virol. 74:11247-11253, 2000). Recombinant VHSV and IHNV expressing tdTomato and GFPmax reporter genes, respectively, were generated, demonstrating the potential of these rhabdoviruses to serve as viral vectors. Interestingly, rIHNV-GFPmax could be recovered using the replicative complex proteins of either virus, whereas rVHSV-Tomato could be recovered only by using its own replicative complex, reflecting that the genome signal sequences of VHSV are relatively distant from those of IHNV and do not allow their cross-recognition. Moreover, the use of heterologous protein combinations underlined the importance of strong protein-protein interactions for the formation of a functional ribonucleoprotein complex. The rIHNV-GFPmax and rVHSV-Tomato viruses were used to simultaneously coinfect cell monolayers. It was observed that up to 74% of the cell monolayer was coinfected by both viruses, demonstrating that a limited interference phenomenon exists during the early stage of primary infection, and it was not mediated by a cellular antiviral protein or by some of the viral proteins.

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