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Bovine Viral Diarrhoea Virus (view source)
Revision as of 18:33, 23 August 2010
, 18:33, 23 August 2010→Virus Genotypes
===Virus Genotypes===
===Virus Genotypes===
There are two recognised genotypes of BVDV; type 1 and type 2. These differ antigenically (Paton et al., 1995), although classification based on sequence variation is more precise. Analysis of the 5’UTR has divided BVDV1 into 11 subtypes and BVDV2 into 3 subtypes (Vilcek et al., 2001). Despite large intra-genotype antigenic differences, type 1 vaccines give some degree of cross-protection against disease caused by type 2 viruses (Carman et al., 1998; Cortese et al., 1998; van Oirschot et al., 1999).
A split in virulence between genotypes is evident. BVDV1 species, including classical strains and common vaccine strains, tend to cause milder disease (Deregt, 2004) and are found worldwide. Alternatively, BVDV2 isolates typically cause more severe disease, characterised by fever, diarrhoea, thrombocytopaenia, haemorrhage, respiratory signs, and high abortion and mortality rates (Corapi et al., 1989; Carman et al, 1998). These viruses were first reported in Canada and the USA, although their distribution is widening. The first British case of type 2 BVDV was identified in 2002 (Drew et al., 2002).
However, genotype is not always an accurate indicator of virulence. Some type 2 strains cause only subclinical or mild disease (Ahn et. al, 2005), and the spectrum of type 1 disease is also broad.
===Virus Biotypes===
Within both BVDV genotypes, isolates can be classified as one of two biotypes. Noncytopathic (ncp) viruses produce no visible cytopathic effect in cell cultures, and infected cells appear normal (Figure 1.2a). Conversely, cytopathic (cp) viruses cause cell vacuolation and death (Figure 1.2b) within 24-48 hours post-infection. Cytopathogenicity gives no indication of disease-causing potential.Noncytopathic BVDV is responsible for the majority of acute and persistent BVDV infections worldwide. Cytopathic biotypes are usually found in cases of the fatal BVD-associated condition, mucosal disease, and are always isolated alongside noncytopathic strains.
Cytopathic viruses have been shown to originate from noncytopathic strains by several mechanisms of mutation. These include insertions of cellular origin, such as ubiquitin sequences, and viral gene rearrangements, duplications and deletions (Deregt and Loewen, 1995). Accumulation of point mutations in the NS2 region and various RNA recombination events are also important (Tautz et al., 1994).
Serologically, the two BVDV biotypes are indistinguishable, but on a molecular level cytopathic viruses produce an additional protein, NS3, not found in cells infected with noncytopathic virus (Donis and Dubovi 1987; Pocock et al., 1987; Magar et al. 1998). This marker of cytopathic viruses is a smaller version of the larger structural protein, NS2-3, expressed in noncytopathic isolates. The mutational generation of cytopathic strains gives a cleavage site in NS2-3, resulting in the independent expression of NS3 as well as the larger protein in these strains (Meyers and Thiel, 1996).
Figure 2 summarises the classification of BVDV down to the biotype level. For each biotype, there are many virus strains all with varying virulence and distribution.
==Transmission and Epidemiology==
==Transmission and Epidemiology==