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spring viraemia of carp virus

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Datasheet

spring viraemia of carp virus

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Invasive Species
  • Preferred Scientific Name
  • spring viraemia of carp virus
  • Taxonomic Tree
  • Domain: Virus
  •   Unknown: "Positive sense ssRNA viruses"
  •     Unknown: "RNA viruses"
  •       Order: Mononegavirales
  •         Family: Rhabdoviridae

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Pictures

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PictureTitleCaptionCopyright
Spring viraemia of carp. (a) Lateral view of carp showing distended abdomen and haemorrhage in skin and in anal and caudal fin. (b) Ventral view of gross abdominal distension in experimentally infected carp (top) compared with control fish (bottom).
TitleSpring viraemia of carp
CaptionSpring viraemia of carp. (a) Lateral view of carp showing distended abdomen and haemorrhage in skin and in anal and caudal fin. (b) Ventral view of gross abdominal distension in experimentally infected carp (top) compared with control fish (bottom).
CopyrightN. Fijan
Spring viraemia of carp. (a) Lateral view of carp showing distended abdomen and haemorrhage in skin and in anal and caudal fin. (b) Ventral view of gross abdominal distension in experimentally infected carp (top) compared with control fish (bottom).
Spring viraemia of carpSpring viraemia of carp. (a) Lateral view of carp showing distended abdomen and haemorrhage in skin and in anal and caudal fin. (b) Ventral view of gross abdominal distension in experimentally infected carp (top) compared with control fish (bottom).N. Fijan
Spring viraemia of carp. Pale gills with haemorrhage in experimentally infected (a) carp compared with gills in control fish (b).
TitleSpring viraemia of carp
CaptionSpring viraemia of carp. Pale gills with haemorrhage in experimentally infected (a) carp compared with gills in control fish (b).
CopyrightN. Fijan
Spring viraemia of carp. Pale gills with haemorrhage in experimentally infected (a) carp compared with gills in control fish (b).
Spring viraemia of carpSpring viraemia of carp. Pale gills with haemorrhage in experimentally infected (a) carp compared with gills in control fish (b).N. Fijan
Histopathology of the moribund stage in experimentally induced SVC. Courtesy of M. Sulimanovi´c and T. Miyazaki. Haematoxylin and eosin (H & E). A. Intestine: necrosis and sloughing off of the epithelial layer; infiltration, oedema and necrosis in submucosa; oedema in the internal muscular layer; oedema and infiltration between internal and external muscular layer and in visceral peritoneum. x 80. B. Trunk kidney: diffuse necrosis of haematopoietic tissue. x 100. C. Detail from B: almost all cells of haematopoietic tissue are necrotic; a varying degree of cell degeneration and some necrosis in tubuli. x 250. D. Trunk kidney: focal infiltration in haematopoietic tissue; peritubular oedema, partial degeneration and necrosis in tubuli. x 120.
TitleHistopathology of the moribund stage in experimentally induced SVC
CaptionHistopathology of the moribund stage in experimentally induced SVC. Courtesy of M. Sulimanovi´c and T. Miyazaki. Haematoxylin and eosin (H & E). A. Intestine: necrosis and sloughing off of the epithelial layer; infiltration, oedema and necrosis in submucosa; oedema in the internal muscular layer; oedema and infiltration between internal and external muscular layer and in visceral peritoneum. x 80. B. Trunk kidney: diffuse necrosis of haematopoietic tissue. x 100. C. Detail from B: almost all cells of haematopoietic tissue are necrotic; a varying degree of cell degeneration and some necrosis in tubuli. x 250. D. Trunk kidney: focal infiltration in haematopoietic tissue; peritubular oedema, partial degeneration and necrosis in tubuli. x 120.
CopyrightN. Fijan
Histopathology of the moribund stage in experimentally induced SVC. Courtesy of M. Sulimanovi´c and T. Miyazaki. Haematoxylin and eosin (H & E). A. Intestine: necrosis and sloughing off of the epithelial layer; infiltration, oedema and necrosis in submucosa; oedema in the internal muscular layer; oedema and infiltration between internal and external muscular layer and in visceral peritoneum. x 80. B. Trunk kidney: diffuse necrosis of haematopoietic tissue. x 100. C. Detail from B: almost all cells of haematopoietic tissue are necrotic; a varying degree of cell degeneration and some necrosis in tubuli. x 250. D. Trunk kidney: focal infiltration in haematopoietic tissue; peritubular oedema, partial degeneration and necrosis in tubuli. x 120.
Histopathology of the moribund stage in experimentally induced SVCHistopathology of the moribund stage in experimentally induced SVC. Courtesy of M. Sulimanovi´c and T. Miyazaki. Haematoxylin and eosin (H & E). A. Intestine: necrosis and sloughing off of the epithelial layer; infiltration, oedema and necrosis in submucosa; oedema in the internal muscular layer; oedema and infiltration between internal and external muscular layer and in visceral peritoneum. x 80. B. Trunk kidney: diffuse necrosis of haematopoietic tissue. x 100. C. Detail from B: almost all cells of haematopoietic tissue are necrotic; a varying degree of cell degeneration and some necrosis in tubuli. x 250. D. Trunk kidney: focal infiltration in haematopoietic tissue; peritubular oedema, partial degeneration and necrosis in tubuli. x 120.N. Fijan
Histological sections of gills and heart of carp with signs of SVC 7 days after experimental infection. A. Degeneration of a small blood-vessel (a) near the gill arch, surrounded by inflammation in oedematous loose connective tissue; b = cartilage. B. Ventricle of the heart. Endocarditis (c), focal degeneration and necrosis in myocardium (d). H & E. x 180.
TitleHistology of carp
CaptionHistological sections of gills and heart of carp with signs of SVC 7 days after experimental infection. A. Degeneration of a small blood-vessel (a) near the gill arch, surrounded by inflammation in oedematous loose connective tissue; b = cartilage. B. Ventricle of the heart. Endocarditis (c), focal degeneration and necrosis in myocardium (d). H & E. x 180.
CopyrightN. Fijan
Histological sections of gills and heart of carp with signs of SVC 7 days after experimental infection. A. Degeneration of a small blood-vessel (a) near the gill arch, surrounded by inflammation in oedematous loose connective tissue; b = cartilage. B. Ventricle of the heart. Endocarditis (c), focal degeneration and necrosis in myocardium (d). H & E. x 180.
Histology of carpHistological sections of gills and heart of carp with signs of SVC 7 days after experimental infection. A. Degeneration of a small blood-vessel (a) near the gill arch, surrounded by inflammation in oedematous loose connective tissue; b = cartilage. B. Ventricle of the heart. Endocarditis (c), focal degeneration and necrosis in myocardium (d). H & E. x 180.N. Fijan
Bullet-shaped virion of spring viraemia of carp virus showing an array of surface spicules. Courtesy of P. de Kinkelin.|Bullet-shaped virion of SVCV showing an array of surface spicules. Courtesy of P. de Kinkelin.
TitleBullet-shaped virion of SVCV
CaptionBullet-shaped virion of spring viraemia of carp virus showing an array of surface spicules. Courtesy of P. de Kinkelin.|Bullet-shaped virion of SVCV showing an array of surface spicules. Courtesy of P. de Kinkelin.
CopyrightN. Fijan
Bullet-shaped virion of spring viraemia of carp virus showing an array of surface spicules. Courtesy of P. de Kinkelin.|Bullet-shaped virion of SVCV showing an array of surface spicules. Courtesy of P. de Kinkelin.
Bullet-shaped virion of SVCVBullet-shaped virion of spring viraemia of carp virus showing an array of surface spicules. Courtesy of P. de Kinkelin.|Bullet-shaped virion of SVCV showing an array of surface spicules. Courtesy of P. de Kinkelin.N. Fijan
Cytopathic effect of SVCV in EPC cells. Rounding up and detachment of cells in a focal area. x 230.
TitleCytopathic effect of SVCV in EPC cells
CaptionCytopathic effect of SVCV in EPC cells. Rounding up and detachment of cells in a focal area. x 230.
CopyrightN. Fijan
Cytopathic effect of SVCV in EPC cells. Rounding up and detachment of cells in a focal area. x 230.
Cytopathic effect of SVCV in EPC cellsCytopathic effect of SVCV in EPC cells. Rounding up and detachment of cells in a focal area. x 230.N. Fijan

Identity

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Preferred Scientific Name

  • spring viraemia of carp virus

International Common Names

  • English: rhabdovirus carpio; spring viremia of carp virus

English acronym

  • RVC
  • SVCV

Taxonomic Tree

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  • Domain: Virus
  •     Unknown: "Positive sense ssRNA viruses"
  •         Unknown: "RNA viruses"
  •             Order: Mononegavirales
  •                 Family: Rhabdoviridae
  •                     Genus: Vesiculovirus
  •                         Species: spring viraemia of carp virus

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AzerbaijanNo information availableOIE Handistatus, 2005
BahrainDisease never reportedOIE Handistatus, 2005
BhutanNo information availableOIE Handistatus, 2005
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
China
-Hong KongDisease never reportedOIE Handistatus, 2005
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndonesiaDisease not reportedOIE Handistatus, 2005
IranDisease never reportedOIE Handistatus, 2005
Iraq2002OIE Handistatus, 2005
IsraelNo information availableOIE Handistatus, 2005
JapanDisease never reportedOIE Handistatus, 2005
JordanNo information availableOIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofDisease not reportedOIE Handistatus, 2005
Kuwait1997OIE Handistatus, 2005
LebanonDisease not reportedOIE Handistatus, 2005
Malaysia
-Peninsular MalaysiaDisease never reportedOIE Handistatus, 2005
-SabahNo information availableOIE Handistatus, 2005
-SarawakNo information availableOIE Handistatus, 2005
MongoliaDisease never reportedOIE Handistatus, 2005
MyanmarNo information availableOIE Handistatus, 2005
NepalNo information availableOIE Handistatus, 2005
OmanNo information availableOIE Handistatus, 2005
PhilippinesNo information availableOIE Handistatus, 2005
QatarNo information availableOIE Handistatus, 2005
SingaporeDisease never reportedOIE Handistatus, 2005
Sri LankaDisease never reportedOIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanDisease never reportedOIE Handistatus, 2005
TajikistanNo information availableOIE Handistatus, 2005
ThailandDisease not reportedOIE Handistatus, 2005
TurkeyNo information availableOIE Handistatus, 2005
TurkmenistanDisease not reportedOIE Handistatus, 2005
United Arab EmiratesNo information availableOIE Handistatus, 2005
UzbekistanDisease never reportedOIE Handistatus, 2005
VietnamNo information availableOIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005

Africa

AlgeriaNo information availableOIE Handistatus, 2005
AngolaNo information availableOIE Handistatus, 2005
BeninNo information availableOIE Handistatus, 2005
BotswanaDisease never reportedOIE Handistatus, 2005
Burkina FasoNo information availableOIE Handistatus, 2005
BurundiDisease never reportedOIE Handistatus, 2005
CameroonDisease never reportedOIE Handistatus, 2005
Cape VerdeDisease not reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE Handistatus, 2005
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireNo information availableOIE Handistatus, 2005
DjiboutiDisease not reportedOIE Handistatus, 2005
EgyptDisease never reportedOIE Handistatus, 2005
EritreaDisease never reportedOIE Handistatus, 2005
EthiopiaDisease never reportedOIE Handistatus, 2005
GhanaDisease not reportedOIE Handistatus, 2005
Guinea-BissauNo information availableOIE Handistatus, 2005
KenyaDisease never reportedOIE Handistatus, 2005
LibyaNo information availableOIE Handistatus, 2005
MadagascarDisease never reportedOIE Handistatus, 2005
MalawiNo information availableOIE Handistatus, 2005
MaliNo information availableOIE Handistatus, 2005
MauritiusDisease not reportedOIE Handistatus, 2005
MoroccoNo information availableOIE Handistatus, 2005
MozambiqueNo information availableOIE Handistatus, 2005
NigeriaNo information availableOIE Handistatus, 2005
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE Handistatus, 2005
Sao Tome and PrincipeNo information availableOIE Handistatus, 2005
SenegalNo information availableOIE Handistatus, 2005
SeychellesNo information availableOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaDisease never reportedOIE Handistatus, 2005
SudanDisease never reportedOIE Handistatus, 2005
SwazilandDisease never reportedOIE Handistatus, 2005
TanzaniaNo information availableOIE Handistatus, 2005
TogoDisease never reportedOIE Handistatus, 2005
TunisiaDisease not reportedOIE Handistatus, 2005
UgandaDisease not reportedOIE Handistatus, 2005
ZambiaNo information availableOIE Handistatus, 2005
ZimbabweDisease never reportedOIE Handistatus, 2005

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaDisease never reportedOIE Handistatus, 2005
MexicoDisease never reportedOIE Handistatus, 2005
USAOIE Handistatus, 2005

Central America and Caribbean

BarbadosDisease never reportedOIE Handistatus, 2005
BelizeDisease never reportedOIE Handistatus, 2005
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease never reportedOIE Handistatus, 2005
Costa RicaDisease never reportedOIE Handistatus, 2005
CubaDisease never reportedOIE Handistatus, 2005
CuraçaoNo information availableOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicDisease never reportedOIE Handistatus, 2005
El SalvadorNo information availableOIE Handistatus, 2005
GuadeloupeNo information availableOIE Handistatus, 2005
GuatemalaDisease never reportedOIE Handistatus, 2005
HaitiDisease never reportedOIE Handistatus, 2005
HondurasDisease never reportedOIE Handistatus, 2005
JamaicaDisease never reportedOIE Handistatus, 2005
MartiniqueDisease not reportedOIE Handistatus, 2005
NicaraguaDisease never reportedOIE Handistatus, 2005
PanamaDisease never reportedOIE Handistatus, 2005
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease not reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaDisease never reportedOIE Handistatus, 2005
BoliviaDisease not reportedOIE Handistatus, 2005
BrazilDisease not reportedOIE Handistatus, 2005
ChileDisease never reportedOIE Handistatus, 2005
ColombiaDisease never reportedOIE Handistatus, 2005
EcuadorNo information availableOIE Handistatus, 2005
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaNo information availableOIE Handistatus, 2005
GuyanaDisease never reportedOIE Handistatus, 2005
ParaguayDisease never reportedOIE Handistatus, 2005
PeruDisease never reportedOIE Handistatus, 2005
UruguayDisease never reportedOIE Handistatus, 2005
VenezuelaDisease never reportedOIE Handistatus, 2005

Europe

AndorraDisease never reportedOIE Handistatus, 2005
AustriaNo information availableOIE Handistatus, 2005
Belarus1996OIE Handistatus, 2005
BelgiumNo information availableOIE Handistatus, 2005
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaDisease never reportedOIE Handistatus, 2005
Croatia1980OIE Handistatus, 2005
CyprusDisease never reportedOIE Handistatus, 2005
Czech Republic2003OIE Handistatus, 2005
Denmark2003OIE Handistatus, 2005
EstoniaDisease not reportedOIE Handistatus, 2005
FinlandDisease never reportedOIE Handistatus, 2005
FrancePresentOIE Handistatus, 2005
GermanyPresentOIE Handistatus, 2005
GreeceDisease not reportedOIE Handistatus, 2005
HungaryOIE Handistatus, 2005
IcelandDisease never reportedOIE Handistatus, 2005
IrelandDisease never reportedOIE Handistatus, 2005
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyPresentOIE Handistatus, 2005
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE Handistatus, 2005
LiechtensteinDisease not reportedOIE Handistatus, 2005
Lithuania1990OIE Handistatus, 2005
LuxembourgDisease not reportedOIE Handistatus, 2005
MacedoniaPresentOIE Handistatus, 2005
MaltaDisease not reportedOIE Handistatus, 2005
Moldova1990OIE Handistatus, 2005
NetherlandsPresentOIE Handistatus, 2005
NorwayDisease never reportedOIE Handistatus, 2005
PolandPresentOIE Handistatus, 2005
PortugalDisease not reportedOIE Handistatus, 2005
RomaniaDisease not reportedOIE Handistatus, 2005
Russian FederationOIE Handistatus, 2005
Slovakia1999OIE Handistatus, 2005
Slovenia1996OIE Handistatus, 2005
SpainNo information availableOIE Handistatus, 2005
SwedenDisease never reportedOIE Handistatus, 2005
Switzerland2003OIE Handistatus, 2005
UKOIE Handistatus, 2005
-Northern IrelandDisease never reportedOIE Handistatus, 2005
UkraineDisease not reportedOIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)No information availableOIE Handistatus, 2005

Oceania

AustraliaDisease never reportedOIE Handistatus, 2005
French PolynesiaDisease never reportedOIE Handistatus, 2005
New CaledoniaNo information availableOIE Handistatus, 2005
New ZealandDisease never reportedOIE Handistatus, 2005
SamoaNo information availableOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathogen Characteristics

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The aetiological role of a virus in SVC was confirmed by Baudouy (1975), Rudikov et al. (1975), Ahne (1977), Hill (1977), Tesarcík et al. (1977), Bèkèsi and Szabó (1979), Bucke and Finlay (1979), and Osadcaja and Rudenko (1981). Ahne (1973) and Bachmann and Ahne (1973, 1974) reported a rhabdovirus from carp with clinical signs of swim bladder inflammation (SBI), established its pathogenicity and named it SBI virus. They noted its serological similarity with Rhabdovirus carpio (Bachmann and Ahne, 1974). The virus induced haemorrhage and inflammation of the swim-bladder, a typical clinical sign in the initial stages of SBI. However, serological comparison by de Kinkelin and Le Berre (1974) and Hill (1975) showed the SBI virus to be indistinguishable from Rhabdovirus carpio. Furthermore, Krizanac et al. (1981) could not isolate virus from typical (Arshaniza and Bauer, 1973) cases of SBI.

Spring viraemia of carp virus is 60-90 nm wide and 90-180 nm long. It has the typical bullet form of the family Rhabdoviridae. Virions bear a regular array of spicules on the surface. They pass through filters of 450 and 200 nm porosity, but are retained by 100 nm membranes. The inner nucleocapsid has helical symmetry, consists of a ribonucleic acid (RNA)-protein (polymerase [L], nucleocapsid [N] and non-structural [NS]) complex and measures about 50 nm in diameter. The nucleocapsid is surrounded by a lipid-containing envelope (matrix [M] protein) with spikes (glycoprotein [G protein]).

Defective interfering particles of SVCV (de Kinkelin and Le Berre, 1974) usually appear in cell cultures infected with a high virus input. Production of normal virions in cell culture can be secured by dilution of inocula to ensure a low multiplicity of infection. These particles measure about two-thirds of the length of infective virions (Bishop and Smith, 1977).

The purified SVCV has a buoyant density of 1.195-1.200 g ml-1 in caesium chloride (Ahne, 1973; Bachmann and Ahne, 1973) and 1.16 g ml-1 in a linear 15-60% sucrose gradient (Lenoir, 1973). The single-stranded (ss) linear RNA molecule sediments at 38-40 S in a 5-25% sucrose gradient (Hill, 1975). Structural proteins of SVCV are similar to those of vesicular stomatitis virus (VSV) (Lenoir, 1973; Sokol et al., 1974; Roy and Clewley, 1978a; Deuter et al., 1982). In these studies the molecular mass for L protein varied from 90 to 190 kDa, for the G protein from 70 to 88 kDa, for the N protein from 40 to 52 kDa, for the NS protein from 43 to 53 kDa and for the M protein from 19 to 27 kDa. The RNA polymerase of the virus is RNA-dependent, with optimum in vitro enzymatic activity at 22°C; its 5' nucleotide is pppAP (Roy and Clewley, 1978b). The glycoprotein on the virion's surface is responsible for its infectivity and immunogenicity (Bishop and Smith, 1977). The NS protein contains two related phosphoproteins, NS1 and NS2 (Roy, 1981). Studies on the 5'-terminal structure of RNA (Gupta et al., 1979), the mechanisms of messenger RNA (mRNA) capping (Gupta and Roy, 1980, 1981), the base sequence at the 3¢ end of the RNA (Roy et al., 1984) and the sequence analysis of mRNA coding for the M protein (Kiuchi and Roy, 1984) have elucidated properties and mechanism of synthesis of SVCV RNA and its similarities with VSV. They indicate a common ancestor of SVCV and VSV (Kiuchi and Roy, 1984). A close relationship between SVCV and VSV was confirmed by comparison of the nucleotide sequences of their L- and G-genes, their gene junctions and their transcription initiation sequences and transcription/polyadenylation sequences (Björklund et al., 1995, 1996). The M protein of SVCV, like that of VSV, completely blocks the transport of snRNAs, spliced mRNAs and snRNPs, as well as slowing the transport of other molecules through nuclear pore complexes; the effect of this is uncertain, but may reduce the host cell's ability to produce interferons following virus infection (Petersen et al., 2002). The virus lacks the non-virion (NV) gene which exists in three lyssa-type fish rhabdoviruses (Kurath et al., 1994, 1997) assigned to the recently created genus Novirhabdovirus (van Regenmortel et al., 2000). The complete genomic sequence of SVCV has been determined by Hoffmann et al. (2002). The genome comprises 111,019 nucleotides, which is consistent with the predicted size of rhabdovirus genomes, and contains 5 open reading frames coding for the N, P, M, G, and L genes. The deduced aminio acid sequences of SVCV were compared with deduced sequences of other rhabdoviruses, and the highest homologies were with VSV, confirming the placement of SVCV in the Vesiculovirus genus.

Spring viraemia of carp virus is inactivated by lipid solvents, heating (60°C for 15 min), glycerol, ozone and diethylpyrocarbonate, as well as by pH below 4 and above 10. Formalin (3%), sodium hydroxide (NaOH) (2%), chlorine (500 mg L-1), actomar (0.01% I2), gamma irradiation (103 krads) and ultraviolet (UV) irradiation (254 nm) inactivate the virus within 10 min (Ahne, 1982a,b). Normal handling in the laboratory does not cause undue loss of infectivity. Serum concentrations of 2 or 5% have a pronounced protective effect on the infectivity during storage at 4°C and at room and freezing temperatures, freeze-thaw cycles and lyophilization (Ahne, 1973; de Kinkelin and Le Berre, 1974). The infectivity is retained in tap water at 10°C, in mud (pH 7.4) at 4°C for 42 days, in stream water at 10°C for 14 days and after drying at 4-21°C for 21 days (Ahne, 1982a,b). The SVCV adsorbs to the plasma membrane and enters the host cell by receptor-mediated endocytosis. The first sign of viral replication is the formation of inclusion bodies in the cytoplasm. A budding process at the plasma membrane and, later in infection, at membranes of dilated Golgi vesicles secure maturation and release of virus (Granzow et al., 1997).

The virus replicates in a variety of fish and other vertebrate primary cell cultures and cell lines, causing a clear cytopathic effect. The best systems for viral replication are cell lines from cyprinid fishes, such as Epithelioma papulosum cyprini (EPC) (Fijan et al., 1983), fathead minnow (FHM) (Gravell and Malsberger, 1965) and carp leucocyte culture (CLC) (Faisal and Ahne, 1990) cells. Each produces high virus yields (108-109 tissue culture infective dose at 50% end-point (TCID50 ml-1). Channel catfish ovary (CCO) cells (Bowser and Plumb, 1980a,b) are also quite susceptible to SVCV (N. Fijan, unpublished data). A number of other widely used fish cell lines, such as bluegill fry (BF-2), brown bullhead (BB) and rainbow trout gonad (RTG-2), also support replication of SVCV, but the yields are somewhat or much lower. Chicken embryo cells and the mammalian cell lines fetal calf kidney, pig kidney, baby hamster kidney (BHK/21), Vero, MDCK, SK (Ahne, 1973; Bachmann and Ahne, 1974), human diploid lung (WI-38) and several reptilian cell lines (Clark and Soriano, 1974), are also susceptible if incubated at 20-22°C. SVCV caused apoptosis in EPC cells, as demonstrated by changes in cell morphology and DNA fragmentation (Björklund et al., 1997). Apoptosis was inhibited by human endogenous acid cysteine proteinase inhibitor. Zebrafish liver (ZFL) cells were used in molecular and functional studies on a zebrafish interferon gene (Altmann et al., 2003), using SVCV as challenge virus. ZFL cells transfected with zebrafish interferon were partially protected against infection with SVCV. The effect of pesticides (atrazine and lindane) on the growth of SVCV in EPC cell cultures was investigated, as they could possibly contaminate fish by run-off from land into water courses. However, they were found not to influence virus titres (Cossarini-Dunier and Hattenberger, 1988).

Replication in cell cultures takes place between 4 and 32°C, with the optimum at 20-22°C. The cytopathic effect is characterized by rounding, detachment and lysis of cells. Margination of nuclear chromatin and cytoplasmic vacuolation precede rounding of cells and can be seen in fixed and stained cell sheets. Fathead minnow cells incubated at 20°C synthesize first progeny virus 4-6 h after infection and peak titres of both cell-associated and cell-free virus are reached between 10 and 22 h. One growth cycle lasts 8-10 h (Bachmann and Ahne, 1974; de Kinkelin and Le Berre, 1974). Well-defined plaques are formed after 3 days at 20°C.

Antigenic studies with rabbit polyclonal neutralizing antibodies indicate that all isolates examined belong to a single serotype, although Bachmannn and Ahne (1974) suggested that one isolate from carp may represent a serological sub-type of SVCV. Dikkeboom et al. (2004) reported that an SVCV isolate from the USA did not react in an immunocytochemical test with an antiserum prepared against a European isolate, and was not neutralized to the same degree as a European isolate, but it did cross-react strongly in an enzyme-linked immunosorbent assay (ELISA). Spring viraemia of carp virus is serologically unrelated to salmonid rhabdoviruses which cause viral haemorrhagic septicaemia (VHS virus) and infectious haematopoietic necrosis (IHN virus) and to other fish rhabdoviruses, except pike fry rhabdovirus (PFR). The possibility of a serological relationship between these two rhabdoviruses of the Vesiculovirus genus was confirmed by Jørgensen et al. (1989). Immunochemical and biological examinations of 22 rhabdovirus isolates from Cyprinidae, Esocidae and Siluridae show that SVCV and PFR share common antigenic determinants on the G, N and M proteins which prevent the two viruses being distinguished by an indirect fluorescent antibody test (IFAT). Spring viraemia of carp virus and PFR can be differentiated by an ELISA and by a virus neutralization test, if the rabbit antiserum is heat-inactivated and no complement is added. Jørgensen et al. (1989) suggested that SVCV and PFR are two serotypes of a single virus species. Heat-inactivated hyperimmune carp anti-SVCV serum can also distinguish SVCV from PFR (Petrinec, 1984).

The virulence of individual isolates may vary with the species or age of fish from which the virus was isolated (Ahne, 1986; Shchelkunov and Shchelkunova, 1989). It can be reduced by passage in mammalian and fish cell lines (Fijan et al., 1977b; Kölbl, 1980).

Vectors and Intermediate Hosts

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VectorSourceReferenceGroupDistribution
Argulus foliaceusCrustacean
Piscicola geometraAnnelid

References

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Ahne W, 1973. Zellkulturen aus verschiedenen Süsswasserteleosteergeweben und Untersuchung über die Ätiologie der Schwimmblasenentzündung der Karpfen. PhD dissertation. Munich: Ludwig-Maximilians Universität.

Ahne W, 1977. Evidence for the systemic character of Rhabdovirus carpio infection. (Summary). Bulletin de l'Office International des Epizooties, 87(5/6):435-436.

Ahne W, 1982. Comparative studies on the stability of four fish-pathogenic viruses (VHSV, PFR, SVCV, IPNV). Zentralblatt fur Veterinarmedizin, B, 29(6):457-476.

Ahne W, 1982. Survival of fish viruses. Fortschritte der Veterinarmedizin, No.35:305-309.

Ahne W, 1986. Different biological properties of four rhabdoviruses isolated from cyprinid fish. Journal of Veterinary Medicine, B (Infectious Diseases, Immunology, Food Hygiene, Veterinary Public Health), 33(4):253-259.

Altmann SM; Mellon MT; Distel DL; Kim CH, 2003. Molecular and functional analysis of an interferon gene from the zebrafish, Danio rerio. Journal of Virology, 77(3):1992-2002.

Arshaniza NM; Bauer ON, 1973. The epizootiology, diagnosis and prophylaxis of swim-bladder inflammation of cyprinids (SBI). In: Dill WA, ed. Symposium on the Major Communicable Fish Diseases in Europe and Their Control. European Inland Fisheries Advisory Commission. Technical Paper 17, Supplement 2, Rome, 140-144.

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