Objective—To determine whether a group of 3 genetic
differences in the nonstructural protein (NS1) or 1
genetic difference in the structural protein (VP2) of
Aleutian disease parvovirus (ADV) is responsible for an
increase in the in vivo replication and pathogenicity of
G/U-8, a chimera of ADV-G (nonpathogenic) and ADVUtah
(pathogenic), compared with G/U-10.
Procedure—Chimeric viruses were constructed,
propagated in vitro, and used to inoculate mink.
Antiviral antibody responses, presence of serum viral
nucleic acid, and serum gamma globulin concentrations
were monitored for 120 days following inoculation.
Histologic examination of the liver, kidneys,
spleen, and mesenteric lymph nodes was performed
Results—A chimera containing only the 3 amino acid
substitutions in NS1 did not elicit measurable
responses indicative of replication or pathogenicity in
inoculated mink. Serum antiviral antibody responses,
frequency of detection of viral nucleic acid in serum,
gamma globulin response, and histologic changes in
mink inoculated with chimeras containing a valine
residue at codon 352 (352V) of VP2 capsid were
increased, compared with values from mink inoculated
with chimeric viruses that did not contain 352V.
Conclusion and Clinical Relevance—A valine
residue at codon 352 in the VP2 capsid protein of ADV
affects in vivo viral replication and pathogenicity. This
amino acid may be part of an incompletely defined
pathogenic determinant of ADV. Further characterization
of the pathogenic determinant may allow future
development of focused preventive and therapeutic
interventions for Aleutian disease of mink. (Am J Vet