The evolution of bovine viral diarrhea: a review

Abstract

The economic importance of bovine viral diarrhea is increasing with the emergence of seemingly more virulent viruses, as evidenced by outbreaks of hemorrhagic syndrome and severe acute bovine viral diarrhea beginning in the 1980s and 1990s. It appears that evolutionary changes in bovine viral diarrhea virus were responsible for these outbreaks. The genetic properties of the classical bovine viral diarrhea virus that contribute to the basis of current diagnostic tests, vaccines, and our understanding of pathogenic mechanisms are now being reevaluated because of these "new" virus strains. This shift in virulence has confounded both nomenclature and the significance of current bovine viral diarrhea virus categorization. The purpose of this review is to summarize our current understanding of bovine viral diarrhea virus with a chronological review of prevailing scientific tenets and practices as described in clinical and scientific North American veterinary journals and textbooks. The first part of this review describes how we have arrived at our current understanding of the viruses, the diseases, and their nomenclature. The second part of the review deals with current concepts in virology and how these concepts may both explain and predict bovine viral diarrhea virus pathogenesis. By reviewing how knowledge of bovine viral diarrhea has evolved and the theories of how the virus itself is able to evolve, the interpretation of diagnostic tests are more effectively utilized in the control and treatment of bovine viral diarrhea virus associated disease.

Figure 1. Examples of multiple natural recombination and rearrangements in bovine viral diarrhea virus (BVDV) genomes and deletions of a defective interfering particle thought to be responsible for expression of p80/NS3 and the cytopathic biotype. A) protein genes of a noncytopathic (ncp) BVDV open reading frame (ORF), B) insertion of bovine (ubiquitin) sequence into the NS2/3 gene, C) duplication of BVDV sequence, D) “DI” genomes with large deletions can be packaged into a BVDV vrion using normal virus proteins. Arrows indicate additional internal protease cleavage site resulting in the cleavage of NS2/3 protein into NS2 and NS3 (p80). Adapted from (29).