Spring viremia of carp (SVC)

Abstract

Spring viremia of carp (SVC) is an important disease affecting cyprinids, mainly common carp Cyprinus carpio. The disease is widespread in European carp culture, where it causes significant morbidity and mortality. Designated a notifiable disease by the Office International des Epizooties, SVC is caused by a rhabdovirus, spring viremia of carp virus (SVCV). Affected fish show destruction of tissues in the kidney, spleen and liver, leading to hemorrhage, loss of water-salt balance and impairment of immune response. High mortality occurs at water temperatures of 10 to 17 degrees C, typically in spring. At higher temperatures, infected carp develop humoral antibodies that can neutralize the spread of virus and such carp are protected against re-infection by solid immunity. The virus is shed mostly with the feces and urine of clinically infected fish and by carriers. Waterborne transmission is believed to be the primary route of infection, but bloodsucking parasites like leeches and the carp louse may serve as mechanical vectors of SVCV. The genome of SVCV is composed of a single molecule of linear, negative-sense, single-stranded RNA containing 5 genes in the order 3'-NPMGL-5' coding for the viral nucleoprotein, phosphoprotein, matrix protein, glycoprotein, and polymerase, respectively. Polyacrylamide gel electrophoresis of the viral proteins, and sequence homologies between the genes and gene junctions of SVCV and vesicular stomatitis viruses, have led to the placement of the virus as a tentative member of the genus Vesiculovirus in the family Rhabdoviridae. These methods also revealed that SVCV is not related to fish rhabdoviruses of the genus Novirhabdovirus. In vitro replication of SVCV takes place in the cytoplasm of cultured cells of fish, bird and mammalian origin at temperatures of 4 to 31 degrees C, with an optimum of about 20 degrees C. Spring viremia of carp can be diagnosed by clinical signs, isolation of virus in cell culture and molecular methods. Antibodies directed against SVCV react with the homologous virus in serum neutralization, immunofluorescence, immunoperoxidase, or enzyme-linked immunosorbent assays, but they cross-react to various degrees with the pike fry rhabdovirus (PFR), suggesting the 2 viruses are closely related. However, SVCV and PFR can be distinguished by certain serological tests and molecular methods such as the ribonuclease protection assay.

Characterization of two thymosins as immune-related genes in common carp (Cyprinus carpio L.)

“…Nine-month-old carp at an average weight of 100-150 g were raised in clean tanks at 15°C. This temperature is optimal for SVCV infectivity (Ahne et al, 2002). Sixty carps were randomly divided into two groups, control and SVCV-infection.…”

Cloning of common carp SOCS-3 gene and its expression during embryogenesis, GH-transgene and viral infection

“…The virus titers, given as tissue culture infective dose (TCID 50/0.1 ml), were calculated by the method of Reed and Muench [21]. Nine-month-old carp at an average weight of 100e150 g were raised in clean tanks at 15 C. This temperature is optimal for SVCV infectivity [22]. Sixty carps were randomly divided into two groups, control and SVCV infection.…”

Structure, organization and expression of common carp (Cyprinus carpio L.) NKEF-B gene

“…The virus titers, given as tissue culture infective dose (TCID 50/0.1 ml), were calculated by the method of Reed and Muench [26]. Nine-month-old carp at an average weight of 100-150 g were raised in clean tanks at 15 C. This temperature is optimal for SVCV infectivity [27]. Forty carp were randomly divided into two groups, control and SVCV-infection.…”