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Scroll up the page to read the Gardiner Hypothesis. The writer did not think that that some years ago, long after retirement, he would produce an hypothesis that is well on the way to being proved.
Porcine Circovirus did indeed prove to be one very nasty disease complex, capable of many manifestations and changes.
Herein lie the clues to the constant animal and human epidemics plaguing Britain and hospitals and pig farming worldwide.
The end of an exhausting and dangerous eleven year struggle is now in sight.
We should have controlled the activities of a greedy and reckless veterinary industry and they should have abandoned vicious cover-ups run by devious British government veterinarians.
But they thought it easier to harass, libel and persecute a retired man trying to live a quiet rural idyll.
And spend other peoples' money on a PR barrage to cover up pig disease dangerous to humans.
Britain's hopelessly corrupt vetocracy badly misjudged that line of organised crime too.
Alas, Porcine Circovirus is a genie that is going to resist being put back into the bottle.
Full abstract here
JVI Accepts, published online ahead of print on 24 August 2011
J. Virol. doi:10.1128/JVI.05156-11
J. Virol. doi:10.1128/JVI.05156-11
Porcine circovirus 2 major genotype group members' co-replication as a prerequisite to co-evolution that may explain the variable disease manifestations
ABSTRACT
A member of the Circoviridae family, porcine circovirus type 2 (PCV2) is associated with postweaning multisystemic wasting syndrome (PMWS), a recent emerging disease worldwide. PCV2 is also found in clinical asymptomatic animals. This paradoxical finding makes the syndrome etiology challenging.We developed new assays to study PCV2...
... Unexpectedly, all PCV2 infectedanimals carried both PCV2a and PCV2b genotype group members. Using confocal microscopy, genotype single cell infections and cell superinfections were visible. Additionally, we discriminated replicative DNA from total PCV2 DNA isoforms with FISH...
... In infected cells with replicating virus, both genotype groups were equally present. These findings suggest PCV2 genotype group members relaxed replication regulation requirements and, may even point to PCV2 replication cooperativity in vivo. These observations explain the readily seen PCV2 DNA recombinations and the high overall PCV2 genome plasticity. Hence, we suggest a novel mechanism to syndrome etiology that consists of a continuously changing PCV2 genome pool in hosts and pig herds posing a constant challenge to individual maturing immune system.
