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BVDV isolates from either genotype can be of a cytopathic or non-cytopathic biotype. Noncytopathic (ncp) viruses produce no visible effects in cell culture, whereas infection with cytopathic (cp) viruses gives cell vacuolation and death. Although non-cytopathic isolates are responsible for the majority of BVDV infections worldwide, cytopathogenicity gives no indication of disease-causing potential. Cytopathic biotypes of bovine viral diarrhoea virus are always isolated alongside non-cytopathic strains, and are found in cases of mucosal disease, a fatal BVD-associated condition.  
 
BVDV isolates from either genotype can be of a cytopathic or non-cytopathic biotype. Noncytopathic (ncp) viruses produce no visible effects in cell culture, whereas infection with cytopathic (cp) viruses gives cell vacuolation and death. Although non-cytopathic isolates are responsible for the majority of BVDV infections worldwide, cytopathogenicity gives no indication of disease-causing potential. Cytopathic biotypes of bovine viral diarrhoea virus are always isolated alongside non-cytopathic strains, and are found in cases of mucosal disease, a fatal BVD-associated condition.  
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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).
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Cytopathic viruses originate from non-cytopathic strains by mutation, including viral gene rearrangements, duplications and deletions<sup>17</sup>, and insertions of cellular origin, such as ubiquitin sequences. Point mutations in the NS2 region and various RNA recombination events are also important<sup>?<sup>. 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 non-cytopathic virus<sup>18, 19, 20</sup>. This marker molecule arises from when NS2-3, expressed in non-cytopathic isolates, is cleaved at a site created by the mutations above<sup>21</sup>.
 
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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).
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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==
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