Abstract
The factors responsible for the emergence of post-weaning multisystemic wasting syndrome (PMWS) as an epidemic disease with significant impact upon the pig industry are not all known. Porcine circovirus type 2 (PCV-2) has been shown to be necessary but not sufficient for the expression of PMWS. Retrospective serological and molecular surveys have shown that PCV-2 was widespread and was maintained with only occasional reports of sporadic PMWS in the 30 year period prior to the recent emergence of the epidemic form of the syndrome. However, the recent spread of the disease in Europe and elsewhere has pointed to the transmission of a novel pathogen. One explanation to reconcile this paradox is that PWMS is caused by a unique PCV-2 variant that is being spread through pig populations. To test this hypothesis, complete genomes (1767 bp) of 10 Dutch PCV-2 isolates from 4 PMWS affected premises and 6 farms without PMWS were sequenced. Phylogenetic analysis showed that these sequences were grouped together although they differed on 77 nucleotide positions relative to each other (95.6–100% identity between the 10 isolates). None of these nucleotide changes identified impacted upon transcriptional elements or other important recognised features of the genome of the PCV-2. Amino acid changes were recorded on 4 positions in ORF1 and on 16 positions in ORF2 but, importantly, no consistent pattern was evident between PCV-2 isolates from affected and control pigs. These data provide further evidence to suggest that factor(s) in addition to PCV-2 are necessary in the development of PMWS.
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