classical swine fever virus

Identity

Preferred Scientific Name

• classical swine fever virus

Other Scientific Names

• hog cholera virus

English acronym

• CSFV
• HCV

Taxonomic Tree

• Domain: Virus
•     Unknown: "Positive sense ssRNA viruses"
•         Unknown: "RNA viruses"
•             Order: Nidovirales
•                 Family: Flaviviridae
•                     Genus: Pestivirus
•                         Species: classical swine fever virus

Distribution Table

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.

Pathogen Characteristics

Classical swine fever virus (CSFV) has an RNA genome contained in a capsid of about 28 nm, surrounded by an envelope. The virion has a size of between 40 and 50 nm. The single-stranded linear RNA genome is infective and encompasses about 12.3 kilobases. The open-reading frame encodes one large polyprotein of 3898 amino acids that is cleaved by proteases to yield mature viral proteins. The open-reading frame is flanked by a 5’-noncoding region of almost 400 nucleotides and a 3’-noncoding region of about 200 nucleotides. The order of the gene products is as follows:

NH₂ -(N^pro-C-E^rns-E1-E2-p7-NS2.3-NS4A-NS4B-NS5A-NS5B)-COOH.

The left part of the genome is coding for the capsid (C) protein, and the three envelope (E) proteins. The E^rns protein has RNase activity, which is unique among virus proteins (Schneider et al., 1993; Hulst et al., 1994). The E2 is the most immunodominant and is composed of two independently formed antigenic domains (Rijn et al., 1994). The rest of the genome codes solely for nonstructural proteins, of which NS2.3 is the most conserved.

The differentiation of CSFV from bovine viral diarrhoea virus (BVDV) and border disease virus (BDV), which can both infect pigs, can easily be done on the basis of sequence differences in the 5’-noncoding region, the E2 and NS5B genes. The genome of CSFV is relatively stable (Vanderhallen et al., 1999; Widjojoatmodjo et al., 1999); however, CSFV strains have been classified into two major groups, and subgroups have also been distinguished (Lowings et al., 1996; Greiser-Wilke et al., 1998).

Antigenically, CSFV is closely related to BVDV and BDV, but by the use of monoclonal antibodies a clear distinction can be made (Wensvoort et al., 1989; Edwards et al., 1991).

The resistance to physical or chemical treatment is partly dependent on the virus strain and the material that contains the virus. For instance, in cell culture fluid virus was inactivated in 10 minutes at 60°C, whereas it was not inactivated in defibrinated blood at 68°C for 30 minutes (Torrey and Prather, 1963). The viral infectivity is quickly destroyed below pH 4 and above pH 11. Because the virus envelope contains lipids, solvents such as ether or detergents easily inactivate the virus. It can remain infectious in pork for months (Mebus et al., 1997), and can survive for weeks in liquid pig manure (Haas et al., 1995). For disinfection of tools, footwear, etc., 1-2% sodium hydroxide is still considered most suitable.

Normally, CSFV induces no or minimal cytopathology in cell culture. However, CSFV showed a cytopathic effect in bone marrow stroma cell cultures (Shimizu et al., 1995), and strains that contained defective interfering particles also gave rise to a cytopathic effect in cell culture (Meyers and Thiel, 1995; Kosmidou et al., 1998). Inactivation of the RNA activity of the E^rns protein also resulted in cytopathogenicity (Hulst et al., 1994) and in attenuation of the virus in the pig (Meyers et al., 1999).

There is a wide range in virulence among CSFV strains. Highly virulent strains cause acute severe disease often resulting in mortality, whereas strains with low virulence give rise to mild disease or subclinical infection.

The disease associated with this pathogen is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). Please see the AHPC library for further information from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.

Vectors and Intermediate Hosts

References

Edwards S; Moennig V; Wensvoort G, 1991. The development of an international reference panel of monoclonal antibodies for the differentiation of hog cholera virus from other pestiviruses. Veterinary Microbiology, 29(2):101-108; 10 ref.

Greiser-Wilke I; Depner K; Fritzemeier J; Haas L; Moennig V, 1998. Application of a computer program for genetic typing of classical swine fever virus isolates from Germany. Journal of Virological Methods, 75(2):141-150; 12 ref.

Haas R; Ahl R; Böhm R; Strauch D, 1995. Inactivation of viruses in liquid manure. Revue Science and Technique Office Internationales des Epizooties, 14:435-445.

Hulst MM; Himes G; Newbigin E; Moormann RJM, 1994. Glycoprotein E2 of classical swine fever virus: expression in insect cells and identification as a ribonuclease. Virology (New York), 200(2):558-565; 37 ref.

Kosmidou A; Büttner M; Meyers G, 1998. Isolation and characterization of cytopathogenic classical swine fever virus (CSFV). Archives of Virology, 143(7):1295-1309; 34 ref.

Lowings P; Ibata G; Needham J; Paton D, 1996. Classical swine fever virus diversity and evolution. Journal of General Virology, 77(6):1311-1321; 28 ref.

Mebus C; Arias M; Pineda JM; Taiador J; House C; Sánchez-Vizcaíno JM, 1997. Survival of several porcine viruses in different Spanish dry-cured meat products. Food Chemistry, 59(4):555-559; 10 ref.

Meyers G; Saalmüller A; Büttner M, 1999. Mutations abrogating the RNase activity in glycoprotein E of the pestivirus classical swine fever virus lead to virus attenuation. Journal of Virology, 73(12):10224-10235; 41 ref.

Meyers G; Thiel HJ, 1995. Cytopathogenicity of classical swine fever virus caused by defective interfering particles. Journal of Virology, 69(6):3683-3689; 41 ref.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

Rijn PAvan; Miedema GKW; Wensvoort G; Gennip HGPvan; Moormann RJM, 1994. Antigenic structure of envelope glycoprotein E1 of hog cholera virus. Journal of Virology, 68(6):3934-3942; 37 ref.

Schneider R; Unger G; Stark R; Schneider-Scherzer E; Thiel H-J, 1993. Identification of a structural glycoprotein of an RNA virus as a ribonuclease. Science, 261:1169-1171.

Shimizu M; Yamada S; Nishimori T, 1995. Cytocidal infection of hog cholera virus in porcine bone marrow stroma cell cultures. Veterinary Microbiology, 47(3/4):395-400; 17 ref.

Torrey JP; Prather JK, 1963. Heat inactivation of hog cholera virus. I. Studies with difibrinated blood and serum. Proceedings Annual Meeting U.S. Livestock Sanitary Association, 67:414-418.

Vanderhallen H; Mittelhozer C; Hofmann MA; Koenen F, 1999. Classical swine fever virus is genetically stable in vitro and in vivo. Archives of Virology, 144(9):1669-1677; 29 ref.

Wensvoort G; Terpstra C; Kluijver EPde; Kragten C; Warnaar JC, 1989. Antigenic differentiation of pestivirus strains with monoclonal antibodies against hog cholera virus. Veterinary Microbiology, 21(1):9-20; 27 ref.

Widjojoatmodjo MN; Gennip HGPvan; Smit AJde; Moormann RJM, 1999. Comparative sequence analysis of classical swine fever virus isolates from the epizootic in the Netherlands in 1997-1998. Veterinary Microbiology, 66(4):291-299; 18 ref.

Distribution Maps