Can the transformation of TGEV to PRCV repeat itself for PEDV?

Monday, October 6, 2014

For the last 20 years, we have lived under the sheltering umbrella of porcine respiratory coronavirus providing protection against transmissible gastroenteritis. Now some are wondering if the same phenomenon could be repeated with porcine epidemic diarrhea virus

by ERNEST SANFORD

Inquisitive minds have been asking if we could not do to porcine epidemic diarrhea (PED) what we did to transmissible gastroenteritis (TGE) that made TGE become the much less significant disease that it is today. A fair question, but to answer it properly requires a trip back down memory lane to relate what we did to transform TGE.

Actually, the truth is, we didn't do anything. Nature did it all for us. TGE was a major disease with repeated outbreaks in the 1960s through to the 1990s, but has since become a minor, almost insignificant, disease in the new millennium. There is an intriguing story behind the miniaturization of TGE from its former position as the feared disease monster.

The story begins in Belgium in 1984. In May, Dr. Maurice Pensaert, virology professor at Ghent University, identified 68 per cent of blood samples from 265 slaughterhouse sows originating from different geographical locations in Belgium testing TGE-positive on his routine serological tests. This was cause for considerable alarm, as Dr. Pensaert had been doing these tests on slaughterhouse sows at regular intervals since 1968. Over that time, his tests always identified 12-24 per cent of sows positive for TGE, which usually correlated with the number of clinical TGE outbreaks reported and diagnosed in Belgium during the winter preceding the surveys.

There was no such correlation with the 68 per cent TGE-positive sows in the May 1984 sampling. The number of outbreaks in the previous winter had not been higher than normal. Furthermore, since vaccination against TGE was not permitted in Belgium, the sows would not have become TGE-positive via vaccination. Something had changed!

An intense series of field and laboratory studies followed, which resulted in the identification of a new TGE virus (TGEV)-related, nonpathogenic coronavirus which infected the respiratory tract of pigs, but not the intestinal tract. The studies revealed deletions in two areas of the TGEV genome giving rise to this different coronavirus. This new coronavirus cross-reacted with TGEV but not with other known coronaviruses. The new virus spread rapidly across Europe and had become endemic in swine populations throughout Europe by the end of the 1980s.

Soon thereafter, the same or a very similar virus showed up in Indiana in 1989 and it also spread rapidly, becoming endemic across North America by the mid-1990s. The new virus was named porcine respiratory coronavirus (PRCV) by Dr. Pensaert.

It didn't take long for veterinarians, producers and diagnosticians in Europe and North America to realize that outbreaks of TGE that had plagued the swine industry in previous years had subsided considerably as we moved through the 1990s. Not only were TGE outbreaks less common, but when they did occur, they were less devastating than before. The link between seroconversion to PRCV and the near disappearance of clinical cases of TGE was only too obvious. So, for the last 20 years, we have lived under the sheltering umbrella, thankfully, of PRCV providing partial or complete protection against TGE.

It's not much of a stretch to ask if this same phenomenon, or something similar, could not be repeated with the porcine epidemic diarrhea virus (PEDV) so that, via a deletion (field or laboratory), it gets transformed into a relatively harmless, nonpathogenic coronavirus that makes PED become a nonentity.

It might be wishful thinking on my part, but that would seem to be a distinct possibility. Perhaps not by spontaneous transformation of PEDV in the field, but what about manipulation in the laboratory by molecular virologists to knock out or perform a deletion similar to the TGE deletion that creates such a transformed virus? The possibility is certainly there.

I suspect such a hope would have to come from intentional intervention by the gene jockeys. It took at least 40 years for the spontaneous mutation to occur to TGEV in the field and create PRCV. We probably would not want to wait for 40 years for a similar mutation to occur to PEDV, if it ever would occur spontaneously at all.

Having said that, I must remind myself that we have already exceeded the 40-year mark for when PEDV first appeared. Its first appearance was in the United Kingdom in 1971. Maybe we're closer than I think, although I doubt we should expect such a favourable chance occurrence to repeat itself. BP

S. Ernest Sanford, DVM, Dip. Path., Diplomate ACVP, is a swine specialist with Boehringer Ingelheim Vetmedica (Canada) in Burlington. ernest.sanford@boehringer-ingelheim.com