Nucleotide and deduced amino acid sequences of the nucleocapsid protein of the virulent A75/17-CDV strain of canine distemper virus

• Published in: Veterinary microbiology 1995-05, Vol.44 (2), p.211-217
• Main Authors: Stettler, Marianne, Zurbriggen, Andreas
• Format: Article
• Language: English
• Subjects: ACIDE AMINE; Amino Acid Sequence; AMINO ACIDS; AMINOACIDOS; Base Sequence; Biological and medical sciences; Canine distemper virus; CHIEN; Distemper Virus, Canine - chemistry; Distemper Virus, Canine - genetics; Distemper Virus, Canine - pathogenicity; DOGS; Fundamental and applied biological sciences. Psychology; Microbiology; Molecular Sequence Data; MORBILLIVIRUS; Nucleocapsid protein; Nucleocapsid Proteins; Nucleoproteins; PATHOGENICITY; PERRO; PODER PATOGENO; POUVOIR PATHOGENE; Protein Structure, Secondary; PROTEINAS; PROTEINE; PROTEINS; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Viral Core Proteins - chemistry; Viral Core Proteins - genetics; Virology; Virulence; Virus persistence
• ISSN: 0378-1135; 1873-2542
• DOI: 10.1016/0378-1135(95)00014-2

Virus persistence is essential in the chronic inflammatory canine distemper virus (CDV)-induced demyelinating disease. In the case of CDV there is a close association between persistence and virulence. Virulent CDV isolated from dogs with distemper shows immediate persistence in primary dog brain cell cultures (DBCC) and in different cell lines. We have evidence that the nucleocapsid (NP) protein plays an important role in the development of persistence. The NP-protein, the most abundant structural virus protein, also influences virus assembly and has some regulatory functions in virus transcription and replication. In this study we compared the nucleotide and deduced amino acid sequence of a virulent CDV strain (A75/17-CDV) to a culture-attenuated non-virulent strain (OP-CDV). Viral RNA was extracted from DBCC infected with virulent CDV. Virulent CDV retains its in vivo properties, such as virulence and ability to cause demyelination, when propagated in these DBCC. The viral RNA was reverse transcribed and the resulting cDNA amplified by polymerase chain reaction for subsequent cloning. The nucleotide sequences of these clones were determined by the dideoxy chain termination method. The number of nucleotides and the putative NP-protein of the virulent strain matched the attenuated CDV strain. We observed a total of 105 nucleotide differences. Three were localised within the 3′ and five within the 5′ non-coding region of the NP-gene. The 97 nucleotide changes within the coding region resulted in 22 amino acid differences. 10 of these amino acid (AA) modifications were within the N-terminal region (AA 1 to 159) and 12 within the C-terminal area (AA 351 to 523). These regions flanked a highly conserved middle region (AA 160 to 350). No amino acid differences were found within the middle area of the CDV NP-protein. The secondary structure prediction of the A75/17-CDV NP-protein at the C-terminus resulted in obvious differences from OP-CDV. The present study provides a plausible molecular basis for the differences between a cytolytic and a persistent CDV-infection.