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Pigs were introduced into Australia and New Zealand in the 18th and 19th centuries, with some establishing feral populations. With few records of pig introductions into these two countries, molecular phylogenetic analysis was used to assess their origins. Mitochondrial (mt) control region sequence and nuclear glucosephosphate isomerase pseudogene (GPIP) restriction fragments were used, as distinct European and Asian domestic pig and Wild Boar control region clades and GPIP genotypes can be recognised. Feral pig control region sequences clustered with either European or Asian domestic pig sequences and both Asian and European GPIP alleles were segregating. It was not possible to distinguish direct importation of Asian domestic animals into Australia and New Zealand from indirect introgression of Asian domestic sequences via Europe. However, the clustering of three feral control region sequences of pigs from northern Australia with Asian Wild Boar implies unrecorded introduction of Wild Boar or crossbred animals into Australia. However, two of these feral pigs had European GPIP alleles. In combination, analyses of control region and GPIP markers suggest that both European and Asian pigs have contributed in similar frequencies to the origins of Australian feral pigs.

Since porcine endogenous retroviruses (PERVs) can infect cultured human cells, they are a potential hazard to xenotransplantation. For this reason, endogenous retroviruses from the Westran (Westmead Hospital transplantation) inbred line of pigs were analyzed by using consensus primers for the type A and type B viruses to amplify 1.8-kb envelope gene fragments. After preliminary analysis with restriction enzymes KpnI and MboI, 31 clones were sequenced. Between types A and B, five recombinant clones were identified. Fifty-five percent of clones (17 of 31) had premature stop codons within the envelope protein-encoding region. Endogenous retroviruses in Westran pigs were physically mapped by fluorescence in situ hybridization (FISH) using PERV-A and PERV-B envelope clones as probes to identify at least 32 integration sites (19 PERV-A sites and 13 PERV-B sites). The chromosomal sites of integration in the Westran strain are quite different from those in the European Large White pig. The recombinant clones suggest that defective PERVs could become infective through recombination and further that PERVs might recombine with human endogenous retroviruses in xenotransplants.