They say “you can’t stop progress”, but Genome Alberta researchers hope that understanding the mechanisms of PRRSV infection will help halt the disease’s progression in its tracks. That was the focus of a project to classify fetal resilience to porcine reproductive and respiratory syndrome virus (PRRSV) based on the amount of virus detected in maternal tissues and fetuses in late gestation.
“PRRSV is a huge deal for the pork industry in North America as it is one of the most costly diseases,” said Carolina Malgarin, a PhD student in the Department of Large Animals Clinical Sciences at the Western College of Veterinary Medicine, University of Saskatchewan.
“Although PRRSV readily crosses the maternal fetal interface (MFI) in third trimester, fetal resilience varies within litters. The aim of this study was to characterize PRRSV-2 concentration in MFI and fetuses at five time points after experimental inoculation of late gestation gilts. Using this information, we could then classify potentially resistant, resilient and susceptible fetuses.”
The study involved inoculating fifteen pregnant gilts with PRRSV and sham-inoculating three control gilts. Data was then collected from three infected gilts and one control gilt at 2, 5, 8, 12 and 14 days post infection. By observing the progression of the disease, researchers could examine the mechanisms of infection from the mother to the fetus and how the fetus reacts to that infection.
Two weeks, one technique
“Over those two weeks, we collected many fetal tissue samples. My main role at that point was quantifying the virus in fetal and maternal tissues, using a special technique that detects the RNA of the virus to determine how much was present each day.”
Based on tissue analysis, one important finding related to the endometrium (the tissue lining the inner cavity of the uterus) and the placenta.
“While we knew that gilts have a high level of virus in their blood by two days after infection, we found that the placenta is also highly infected by that point. No one knows exactly how this infection of the placenta occurs, but we can now confirm that the virus crossed the barrier between endometrium and placenta by day 2. The implication is that the mechanism of viral transmission through that barrier is very efficient and happens quickly.”
By day 5, researchers had their first infected fetus, and the first fetal death occurred on day 8. At that point, all fetal tissues were positive for the virus, indicating that it takes about a week to completely infect fetuses and start to compromise them.
Negative fetuses a big positive
Apart from infection rates, which are of great interest to scientists, another intriguing result was the lack of infection in one dam.
“On the last day we had a gilt whose entire litter was negative for the virus. We believe she may have a genetic factor that causes litter resistance, and we also found that within litters there were both PRRSV positive and negative fetuses. Clearly, you can have resistance factors in both the gilt and the fetus, so this will be our next area of study.”
Interestingly, it was the smaller fetuses lacking in nutrients that showed greater resistance to PRRSV.
“That was a very surprising result from a previous experiment that we confirmed with this new data. Intuitively, you would think the weakest fetuses would be the most susceptible. There was something in these fetuses preventing the virus from crossing the barrier and replicating, and that’s exciting. The more we can understand these natural mechanisms of resistance, the better equipped we will be to select for animals with this trait.”
This was truly a historic project. Examining PRRSV step-by-step to see what is happening and how it is growing, and identifying a timeline of disease progression, has never been done before. If it’s true that “knowledge is power”, our ability to fight this deadly and costly disease just got a whole lot stronger.