In vitro viral haemorrhagic septicaemia virus replication in excised fins of rainbow trout: correlation with resistance to waterborne challenge and genetic variation. (1/80)

In vitro viral haemorrhagic septicaemia virus replication in excised fin tissue (VREFT) was investigated as a possible criterion to predict the resistance of groups or individuals to viral haemorrhagic septicaemia virus (VHSV) in rainbow trout. Adipose and rayed fins were compared for VREFT response, and a statistically significant correlation was found. Correlation between VREFT and survival after waterborne viral challenge was estimated on a set of 27 groups of trout, and was highly significant (R = 0.72). A further experiment with fish individually tagged and challenged some time after fin clipping for determination of VREFT confirmed that the mean value of resistant (surviving) fish was significantly lower than the mean value of susceptible (dead) ones, but there was a wide variation within each of these groups. In particular, a large proportion of fish expected to be resistant based on VREFT values died all the same. Using clones, we showed that the correlation between VREFT and survival was dramatically high (R = 0.96). Genetic analyses of the data from the different groups available in the experiment consistently indicated a large amount of genetic determination of VREFT, an encouraging result for selection purposes. Though these results were obtained in experimentally controlled conditions not identical to those in the field, they shed new light on the analysis of defence mechanisms against the virus and on the possibility of performing indirect selection for resistance, using VREFT as the secondary character.  (+info)

Rhabdovirus infection induces public and private T cell responses in teleost fish. (2/80)

Many viruses induce a strong T cell response that contributes to the elimination of infected cells presenting viral peptides by MHC molecules. The structure and expression of genes encoding molecules homologous to mammalian alphabeta TCRs have been recently characterized in rainbow trout and in several teleost species, but the alphabeta T cell response against pathogens has not been directly demonstrated. To study the modifications of the T cell repertoire during an acute viral infection in rainbow trout, we adapted the immunoscope methodology, which consists of spectratyping the complementarity-determining region 3 length of the TCRbeta chain. We showed that the naive T cell repertoire is polyclonal and highly diverse in the naive rainbow trout. Using viral hemorrhagic septicemia virus (VHSV), which provokes an acute infection in rainbow trout, we identified skewed complementarity-determining region 3 size profiles for several VbetaJbeta combinations, corresponding to T cell clonal expansions during primary and secondary response to VHSV. Both public and private T cell expansions were shown by immunoscope analysis of spleen cells from several infected individuals of a rainbow trout clone sharing the same genetic background. The public response to VHSV consisted of expansion of Vbeta4Jbeta1 T cell, which appeared early during the primary response and was strongly boosted during the secondary response.  (+info)

Viral hemorrhagic septicemia virus alters turbot Scophthalmus maximus macrophage nitric oxide production. (3/80)

The effect of viral hemorrhagic septicemia virus (VHSV) in vitro infection on the nitric oxide (NO) production by turbot Scophthalmus maximus kidney macrophages has been addressed in the past. Previously, we had determined that only a small fraction of turbot possess head kidney macrophages that respond to a single exposure of lipopolysaccharide (LPS) with NO production (LPS-responsive macrophages), whereas macrophage cultures from other individuals were not activated by LPS alone and needed a combination of stimuli to respond (LPS-non-responsive macrophages). In the current work, we examined the effect of VHSV on NO production by macrophages characterized as LPS-responsive macrophages or LPS-non-responsive macrophages. Combinations of LPS and tumor necrosis factor alpha (TNF-alpha) and macrophage-activating factor (MAF) were also used to stimulate the cells for NO production. The effect of VHSV on NO production depends on the response to LPS alone. When a low multiplicity of infection was used (1.78 x 10(-3)), the NO production in response to LPS in LPS-responsive macrophages was significantly decreased. However, LPS-non-responsive macrophage cultures produced NO when a combination of LPS and VHSV was used. In the case of a higher VHSV multiplicity of infection (1.78), no significant change was observed in LPS-non-responsive animals. Combinations of LPS with TNF-alpha, LPS with MAF, and TNF-alpha with MAF were used to induce NO production in LPS-non-responsive macrophages. In all these cases, VHSV suppressed NO production, although at a significant level only when a combination of TNF-alpha and MAF was used for the induction of NO.  (+info)

Distribution of viral haemorrhagic septicaemia virus in wild fish species of the North Sea, north east Atlantic Ocean and Irish Sea. (4/80)

A surveillance programme was initiated on the occurrence and distribution of viral haemorrhagic septicaemia virus (VHSV) in wild marine fish. Six research cruises were undertaken in an 18 mo period during 1997 and 1998, covering the North Sea, the Atlantic waters off the north and west coasts of Scotland and the Irish Sea. A total of 19,293 fish were sampled from 23 different species including cod, haddock, Norway pout, herring and sprat. Individual fish lengths were recorded and the fish were checked for lesions, haemorrhaging and other signs of disease. Pools of organ samples were taken for virus assay. The majority of fish sampled did not display clinical signs indicative of viral haemorrhagic septicaemia. A small number of cod were found with skin lesions and haddock with skin haemorrhaging. Of the 2081 organ and skin sample pools collected, 21 tested positive for VHSV by tissue culture and enzyme-linked immunosorbent assay. Seventeen of the isolates originated from Norway pout Trisopterus esmarkii, one from cod Gadus morhua (skin lesion), one from herring Clupea harengus, one from whiting Merlangius merlangus, and one from a previously unreported host species, poor cod Trisopterus minutus.  (+info)

An outbreak of VHSV (viral hemorrhagic septicemia virus) infection in farmed Japanese flounder Paralichthys olivaceus in Japan. (5/80)

A rhabdoviral disease occurred in farmed populations of market sized Japanese flounder (hirame) Paralichthys olivaceus in the Seto Inland Sea of Japan in 1996. The causative agent was identified as viral hemorrhagic septicemia virus (VHSV) based on morphological, immunological, and genetic analyses. Diseased fish that were artificially injected with a representative virus isolate showed the same pathological signs and high mortality as observed in the natural outbreak. This is the first report of an outbreak of VHSV infection in cultured fish in Japan. Clinical signs of diseased fish included dark body coloration, an expanded abdomen due to ascites, congested liver, splenomegaly, and a swollen kidney. Myocardial necrosis was most prominent and accompanied by inflammatory reactions. Necrotic lesions also occurred in the liver, spleen and hematopoietic tissue, and were accompanied by circulatory disturbances due to cardiac failure. Hemorrhagic lesions did not always appear in the lateral musculature. Transmission electron microscopy revealed many rhabdovirus particles and associated inclusion bodies containing nucleocapsids in the necrotized myocardium. The histopathological findings indicated that the necrotizing myocarditis could be considered a pathognomonic sign of VHSV infection in Japanese flounder.  (+info)

Experimental susceptibility of Atlantic salmon Salmo salar and turbot Scophthalmus maxim us to European freshwater and marine isolates of viral haemorrhagic septicaemia virus. (6/80)

A number of viral haemorrhagic septicaemia (VHS) virus isolates of European marine origin were shown to be of low pathogenicity or non-pathogenic to Atlantic salmon parr by water-borne infection. A reference freshwater VHS virus isolate known to be highly pathogenic to rainbow trout was also of low pathogenicity to Atlantic salmon. Virus was detected in some mortalities, however, demonstrating viral entry and replication. European marine VHS virus isolates do not appear to pose an imminent threat to the Atlantic salmon culture industry. Turbot were found to be refractive or of low susceptibility to marine VHS virus isolates of sprat origin and to a reference freshwater isolate, with mortalities of 0 to 13.5%. Conversely, turbot were susceptible by varying degrees to a number of VHS virus isolates taken from herring, with mortalities ranging from 16 to 68%. These results emphasise the vulnerability of turbot culture to the VHS virus isolates that are enzootic to the European marine environment.  (+info)

Inactivation of infectious salmon anaemia virus, viral haemorrhagic septicaemia virus and infectious pancreatic necrosis virus in water using UVC irradiation. (7/80)

The UVC irradiation doses necessary for a 99.9% (3-log) inactivation of 3 different fish pathogenic viruses diluted in freshwater/seawater and wastewater from a fish processing plant were determined. The results showed that both infectious salmon anaemia virus (ISAV) and viral haemorrhagic septicaemia virus (VHSV) were very sensitive to UVC irradiation, showing a 3-log reduction of infectivity in freshwater of 33 +/- 3.5 and 7.9 +/- 1.5 J m(-2), respectively, while that of infectious pancreatic necrosis virus (IPNV) was substantially higher, 1188 +/- 57 J m(-2). Using ISAV as a model, a comparison of the effect of UVC irradiation on virus isolation versus reverse transcription polymerase chain reaction (RT-PCR) showed that considerably higher UVC doses, depending on the length of the amplified product, were necessary to abolish RT-PCR detection of viral RNA.  (+info)

Heterologous exchanges of the glycoprotein and the matrix protein in a Novirhabdovirus. (8/80)

Infectious hematopoietic necrosis virus (IHNV) and viral hemorrhagic septicemia virus (VHSV) are two salmonid rhabdoviruses replicating at low temperatures (14 to 20 degrees C). Both viruses belong to the Novirhabdovirus genus, but they are only distantly related and do not cross antigenically. By using a recently developed reverse-genetic system based on IHNV (S. Biacchesi et al., J. Virol. 74:11247-11253, 2000), we investigated the ability to exchange IHNV glycoprotein G with that of VHSV. Thus, the IHNV genome was modified so that the VHSV G gene replaced the complete IHNV G gene. A recombinant virus expressing VHSV G instead of IHNV G, rIHNV-Gvhsv, was generated and was shown to replicate as well as the wild-type rIHNV in cell culture. This study was extended by exchanging IHNV G with that of a fish vesiculovirus able to replicate at high temperatures (up to 28 degrees C), the spring viremia of carp virus (SVCV). rIHNV-Gsvcv was successfully recovered; however, its growth was restricted to 14 to 20 degrees C. These results show the nonspecific sequence requirement for the insertion of heterologous glycoproteins into IHNV virions and also demonstrate that an IHNV protein other than the G protein is responsible for the low-temperature restriction on growth. To determine to what extent the matrix (M) protein interacts with G, a series of chimeric pIHNV constructs in which all or part of the M gene was replaced with the VHSV counterpart was engineered and used to recover the respective recombinant viruses. Despite the very low percentage (38%) of amino acid identity between the IHNV and VHSV matrix proteins, viable chimeric IHNVs, harboring either the matrix protein or both the glycoprotein and the matrix protein from VHSV, were recovered and propagated. Altogether, these data show the extreme flexibility of IHNV to accommodate heterologous structural proteins.  (+info)

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