(i) The different pathological and clinical pictures within the actual epidemic must be clarified
(ii) In Sweden a epidemiologic investigation speculated on a possible spread of PMWS from one single focus. Although this could not been confirmed (Wallgren et al. 2004), the data from Switzerland should be epidemiologically analyzed to attempt to identify the possible source of the PMWS epidemic
(iii) Serumsamples of sows from 1985 to 1989 are still available. Sows can be viremic but data of prevalence from viremic sows are not existent in the literature. These sera should be investigated to obtain the complete genome of Swiss PCV2 strains from that time and an estimation of the prevalence of viremia in the Swiss sow population from that time should be carried out.
PCV2 positive tissues or serum from current PMWS cases or from pigs from unaffected farms are momentarily easy to acquire
(iv) Time dependent molecular epidemiology of PCV2 strains should be carried out. We would amplify and sequence PCV2 strains in clusters of paraffin embedded tissues or from serum samples of sows from before 1995 and after 2003. The whole length of genomic DNA from viremic sow serum can be amplified and sequenced to characterize the complete gene of "old" Swiss Circovirus strains. Only shorter gene sequences can be amplified from paraffin material but a large part of the ORF2 gene of PCV2, which is used for phylogenetic analysis can be amplified from paraffin material (Grierson et al. 2004). With these results we can analyze the possible occurrence of different Swiss PCV2 strains or we can detect possible genetic changes. Subsequently, Swiss PCV2 strains can be compared in the GenBank with foreign strains
(v) If a genetic change of PCV2 had occurred before 1995 and after 2003 we could determine when this did occur. If the change is in the ORF2 we can do this retrospectively in paraffin embedded material, otherwise the serum bank from spring 2001 to spring 2002 is still available
