Little is known of the factors contributing to viral disease severity or the anti-viral immune responses. Scientists in Korea recently published research that helps fill this knowledge gap and widens understanding of the immune responses triggered upon infection with the economically devastating porcine reproductive and respiratory syndrome (PRRS) virus. Not only does PRRS lead to reproductive disorder in sows, but it also causes respiratory problems in infected newborn and growing pigs.
Unfortunately, researchers say the high genetic variability of the virus and differing virulence hinders vaccine development and complicates disease management.
Scientists believe understanding this knowledge gap can help facilitate vaccine development and disease management, protecting the swine industry and associated economy. The research showed changes in immune cell composition in lungs during infection with PRRS virus of varying severity. They identified regulators of cell death in severe infections, and protective immune cells in infection with virus of intermediate strength, paving the way for targeted disease management.
Jun-Mo Kim, associate professor in the Department of Animal Science and Technology at Chung-Ang University, Korea, has focused his research efforts in this area.
“Using a PRRSV infection model, our goal is to advance the comprehensive understanding of the infection and response mechanism in order to minimize industrial damage,” Kim said in a release.
Recently, his group analyzed protein-coding RNA transcripts isolated from single cells and fluid collected from lungs of PRRS-infected pigs. They also monitored immune cell alterations triggered by PRRS virus strains of varying virulence.
The study pointed out that high virulence PRRS virus strain triggered early, severe lung damage and overall immune imbalance marked by significant reduction in macrophages. In contrast, PRRS virus strain of intermediate strength led to delayed lung damage with fewer immune alterations. Importantly, higher numbers of protective anti-inflammatory M2-like macrophages were observed in less virulent infections, suggesting a potential role in promoting lung healing, the release said.
Although fewer than 5% of macrophages were directly infected by virus, cell death and immune responses were “widespread indicating that extracellular vesicles or exosomes containing microRNAs released from the PRRSV-infected cells likely contributed to pathogenesis and cell death in non-infected bystander cells.”
“Our study findings will aid the development of innovative therapeutic strategies with the potential to mitigate severe lung damage and promote efficient recovery in PRRSV-infected animals, paving the way for effective viral disease management,” Kim says.
In addition to the obvious impact on livestock health, global food security, and in securing the economy of the swine industry, Kim says the findings from this study may find a parallel in other human respiratory viruses and therapeutic strategies are likely to be applicable and effective broadly.
This study was published in Volume 16 Issue 1 of Nature Communications.
