Phocine distemper virus: characterization of the morbillivirus causing the seal epizootic in northwestern Europe in 2002

Abstract

In 2002, 14 years after the first devastating die-off in the northwestern European seal population in 1988, a second epizootic was caused by the re-emergence of phocine distemper virus (PDV) in this area. The nucleotide sequence of the surface hemagglutinin (H) gene from the PDV of 2002 and the deduced amino acid sequence were determined and aligned with those of PDV isolates from 1988. There was a 98–99% nucleotide and a 98% amino acid identity of the H protein between the PDV isolates. From the close relationship shown in this study, it was concluded that PDV seems to be a strictly seal-adapted virus with only minor genetic variability over a longer period. In 1988, a fatal phocine distemper epizootic in seals from northwestern European waters led to the death of nearly 23,000 animals [13]. After the recovery of the seal population in the following years, a second mass die-off caused by phocine distemper virus (PDV) occurred in 2002 with the loss of approximately 30,000 seals [13]. Both epizootics showed similarities regarding the clinical and pathological findings, but some distinct features regarding the time of disease outbreak and epidemiologic progress were noticed [13, 22]. Until today, the origin and geographic distribution of PDV in northwestern Europe remain unclear in many aspects. It has been hypothesized that migrating seal species from other regions may act as carriers for PDV in the European seal populations [7]. PDV is a member of the genus Morbillivirus, closely related to canine distemper virus (CDV). In contrast, two other morbilliviruses from marine mammals, i.e. the porpoise and the dolphin morbilliviruses, are more closely related to the rinderpest (RPV) and the peste des petits ruminants viruses, respectively [2]. The surface and core proteins of PDV causing the first epizootic in Europe have been characterized in detail [2, 6, 18]. Both surface proteins, the hemagglutinin (H) and fusion (F) proteins, play an important role in viral attachment to and fusion with the host cell and formation of syncytia [2]. Variation in these proteins may cause changes in virulence and host-cell tropism. Earlier studies revealed a high identity between the F proteins from different CDV and PDV isolates, whereas the H protein was more variable [18, 24]. In order to analyse whether modifications of virulence and host range had occurred between the PDV isolates from both epizootics, the nucleotide and deduced amino acid sequences of the H gene of a PDV isolate from 2002 (PDV/ 02) were determined and compared to sequences from previous isolates. O.C.T-embedded lung tissue samples from three seals that died during the seal distemper epidemic in 2002 at the German North Sea, were obtained for evaluation. The samples were shock-frozen in liquid nitrogen and stored at -80 C until use. For verification of the PDV infection, a set of universal morbillivirus primers based on a conserved sequence of the phosphoprotein P gene was used as G. Muller U. Kaim P. Wohlsein W. Baumgartner Department of Pathology, University of Veterinary Medicine Hannover, Bunteweg 17, 30559 Hannover, Germany