Construction of Pathogenic Molecular Clones of Aleutian Mink Disease Parvovirus that Replicate Both in Vivoand in Vitro

• Published in: Virology (New York, N.Y.) N.Y.), 1998, Vol.251 (2), p.288-296
• Main Authors: Bloom, Marshall E., Fox, James M., Berry, Bradley D., Oie, Katrina L., Wolfinbarger, James B.
• Format: Article
• Language: English
• ISSN: 0042-6822; 1096-0341
• DOI: 10.1006/viro.1998.9426

The ADV-G isolate of Aleutian mink disease parvovirus (ADV) replicates permissively in Crandell feline kidney (CRFK) cells but is nonpathogenic for mink, whereas the highly pathogenic ADV-Utah isolate is nonviable in CRFK cells. To assign control of host range in CRFK cells and pathogenicity to specific regions of the ADV genome, we constructed a full-length molecular clone chimeric between ADV-G and ADV-Utah. If either the map unit (MU) 54–65 (clone G/U-5) or MU 65–88 (clone G/U-7) sections were ADV-Utah, viability in CRFK cells was abolished, thus indicating that in vitrohost range was controlled by two independent determinants: A in the MU 54–65 segment and B in the MU 65–88 segment. Determinant B could be divided into two subregions, B1 (MU 65–69) and B2 (MU 73–88), neither of which alone could inhibit replication in CRFK cells, an observation suggesting that expression of the B determinant required interaction between noncontiguous sequences. Adult mink of Aleutian genotype inoculated with G/U-8 or G/U-10 developed viremia, antiviral antibody, and histopathological changes characteristic of progressive Aleutian disease. The capsid sequences of G/U-8 and G/U-10 differed from ADV-G at five and four amino acid residues, respectively. Our results suggested that the host range and pathogenicity of ADV are regulated by sequences in the capsid protein gene.