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. 2013 Aug 12:185–349. doi: 10.1007/978-3-642-20718-1_14

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© Springer-Verlag Berlin Heidelberg 2013

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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Fig. 14.16 — Recombination events in the genome of BVDV. In the non-cytopathogenic strains (BVDV SD-1), no cleavage occurs between proteins NS2 and NS3, and both remain fused and act as a protease to cleave the non-structural part of the precursor protein. In cytopathogenic strains, various recombinations with cellular DNA are found. In such cases, ubiquitin sequences (U) are integrated into the viral RNA genomes upstream of the NS3 region (strains CP1 and Osloss). Cleavage and release of NS3 proteins is performed by the cellular ubiquitin hydrolase. Alternatively, recombination events may occur in the cytopathogenic strains, which rearrange the N^pro sequences amino-terminally to the NS3 region. The proteolytic activity of N^pro leads subsequently to autocatalytic cleavage and the formation of an NS3 protein in addition to the NS2–NS3 fusion product (strain Pe515CP). Furthermore, there are defective viral genomes lacking the regions for the structural and NS2–NS3 proteins but which have rearranged the N^pro region upstream of the sequences of NS3 (strain CP9) similarly to strain Pe515CP. These defective viruses become pathogenic when they are present in animals in combination with non-cytopathogenic, infectious strains (SD-1)