|Kehrli Jr, Marcus|
Submitted to: Canadian Journal of Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 25, 2005
Publication Date: July 1, 2006
Citation: Wesley, R.D., Lager, K.M., Kehrli, Jr., M.E. 2006. Infection with porcine reproductive and respiratory syndrome virus stimulates an early gamma interferon response in the serum of pigs. Canadian Journal of Veterinary Research. 70(3):176-182. Interpretive Summary: Porcine Reproductive and Respiratory Syndrome (PRRS) is a viral-induced disease that costs the U.S. swine industry approximately $600 million per year and occurs worldwide. The pig's immune defense against PRRS is unconventional and standard host responses to infection are weak and slow to develop. We have investigated a key element for effective host immunity against PRRS, namely gamma interferon. We found that gamma interferon was induced in vivo much earlier than previously recognized and that the immune pathways used against PRRS infections more closely resembled immune responses to infections by intracellular bacteria and protozoa. The information is useful to develop new therapeutic strategies against PRRS.
Technical Abstract: The early release of cytokines by cells involved in innate immunity, i.e., macrophages and natural killers (NK) cells, is an important host response to intracellular pathogens. Gamma interferon (IFN-gamma) is the most important of the cytokines produced during the early stages of an infection and is also a central cytokine mediator for the induction of cellular or Th1 immunity. To better understand innate and adaptive immune responses to porcine reproductive and respiratory syndrome virus (PRRSV), serum IFN-gamma concentrations and the duration of viremia were investigated. For 2 strains of atypical PRRSV, IFN-gamma was detectable in swine serum soon after infection and lasted for approximately 3 weeks. Serum levels of IFN-gamma peaked at about 10 days post inoculation and returned to approximate baseline levels by day 22 post-infection. However, individual pigs manifested short sporadic increases of IFN-gamma from 18 to 50 days post-infection. Prior vaccination blocked the serum IFN-gamma response with homologous virus challenge and altered the kinetics of the response following heterologous challenge. Other respiratory viruses of pigs do not appear to induce serum IFN-gamma. The early production of IFN-gamma in PRRSV infected pigs might result from activation of NK cells which is more characteristic of immune pathways stimulated by intracellular bacterial and protozoan infections.