If you thought morning sickness was an ordeal, try dealing with PRRS infection during pregnancy. Porcine reproductive and respiratory syndrome (PRRS) is one of the most important diseases of pig production. Infection in pregnancy results in abortion and reduced litter size and viability, which has a major impact on production, welfare and the pork industry’s environmental footprint.
In light of those implications, understanding reproductive PRRS and creating data to validate genomic results from previous studies is essential to developing new tools for combatting the virus. To achieve these goals, researchers initiated the Genome Alberta-led project “Is PRRSV-induced fetal death predicted by variation in a region of SC7”. The project is led by Dr. Graham Plastow from the University of Alberta and Dr. John Harding from the University of Saskatchewan.
The virus specifically targets antigen presenting cells and leads to a disruption in normal immune function, thereby increasing an animal’s susceptibility to secondary infection.
Finding answers in acronyms
“Our previous reproductive PRRS research identified a single genetic marker (SNP) on chromosome 7 that was associated with a substantial improvement in fetal viability following PRRS infection of pregnant dams,” said Haesu Ko, PhD student, Faculty of Agricultural, Life and Environmental Science at the University of Alberta.
“This region contains genes involved in thyroid hormone metabolism, including a gene involved in the metabolism of thyroxin,” said Ko. “We have since learned that fetal and maternal thyroxin levels in serum decrease following PRRSV infection, which undoubtedly has a negative impact on fetal growth and development. Such levels during late gestation may also induce a critical endocrine state responsible for a significant portion of virus-induced fetal deaths. We believe that in critical fetal tissues, the activity of this gene may compensate for the low thyroid hormone levels observed in PRRSV-infected fetuses. It seems that a failure to compensate for this drop has adverse consequences for the fetus, including death.”
Thus the goal of this project is to determine if this mechanism is associated with fetal viability in the face of PRRSV infection. This is significant, as confirmation of that association will enable selection for more PRRS resilient fetuses. In doing so, science could provide an alternative means to control reproductive PRRS that is not reliant on genetic modification or editing.
“Ultimately, our aim is to find fetal genetic factors associated with resilience as it relates to PRRS,” said Ko. “If we find that a particular fetus has certain markers causing it to develop a less severe case of PRRS or have a lower viral load, that is our ideal outcome. We can then use those markers to select replacement gilts and sires that are more likely to produce resilient fetuses.”
A strain on the system
Given the economic impact of PRRS, a better means of controlling it cannot come soon enough. PRRS remains one of the most economically significant diseases affecting the North American pork industry, resulting in losses of $664 million in the United States alone. Around 45% of this cost is attributable to the reproductive form of PRRS. Since the virus first emerged in the early 1990s, Alberta producers have largely contended with low-virulent PRRS strains, but that may be changing as a number of moderately virulent strains have recently emerged in Alberta and Manitoba.
Though studies detailing the impact of PRRS have not been undertaken in Alberta, a recent single outbreak in Ontario grower finisher operations caused a loss of $4 million due to reduced pig performance in the subsequent year.
Perhaps there is no perfect solution to PRRS, but if science can at least limit the damage to a cash-strapped pork industry, that’s the next best thing.
