Abstract
Viral persistence in the central nervous system is the driving force behind the chronic progressive disease caused by natural canine distemper virus (CDV) infection in dogs. Persistence of CDV is associated with non-cytolytic spread and impaired viral budding. Since budding is to a large extend dependent on the nucleocapsid- (N) and matrixproteins (M) of the virus, we analyzed the nucleotide- and deduced amino acid sequences of the corresponding genes of a spectrum of CDV strains, that differ with respect to virulence and persistence in vivo and in vitro. The wild type CDV ( A75 17 ), which is capable of causing a persistent infection in vivo was compared to two tissue culture adapted CDV strains (passaged A75 17-CDV and Rockborn-CDV), which retain a residual virulence and the capacity to spontaneously persist in vitro. A modified distemper virus (Snyder Hill-CDV), which is neurovirulent but not capable of causing a persistent infection in vivo, and an avianized virus (Onderstepoort-CDV) which is completely apathogenic and spreads by budding in cell cultures were also examined. Differences were found in the C-terminal of the nucleocapsid protein, which — comparing the two extremes of the spectrum (wild A75 17-CDV and OP-CDV) — lead to changes of the predicted protein structure. Such changes could affect the budding process and thus play a role in persistence. Marked changes in the M-gene were found in its non-coding region: the nucleotide sequences of the SH-CDV and OP-CDV differed considerably from the other three strains. Moreover, an additional second open reading frame was detected in the ‘non-coding’ region of the M gene in the wild A75-CDV, the two tissue culture adapted CDV strains and SH-CDV, but not in OP-CDV. The presence of this additional open reading frame correlated with the ability to cause a spontaneous persistent infection in vitro. Our findings support the notion that both N- and M-genes of CDV harbor determinants of viral persistence.
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