Live virus Immunization (LVI) with a recent 1-7-4 PRRSV isolate elicits broad protection against PRRSV challenge in finishing age swine

Authors: VAN GEELEN, ALBERT - Orise Fellow; BUCKLEY, ALEXANDRA - Orise Fellow; KULSHRESHTHA, VIKAS - Iowa State University; Brockmeier, Susan; Miller, Laura; FLEMING, DAMARIUS - Orise Fellow; Loving, Crystal; Faaberg, Kay; Lager, Kelly

Submitted to: American Association of Swine Veterinarians Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 3/3/2018
Publication Date: 3/3/2018
Citation: Van Geelen, A.G., Buckley, A., Kulshreshtha, V., Brockmeier, S., Miller, L.C., Fleming, D., Loving, C.L., Faaberg, K.S., Lager, K.M. 2018. Live virus Immunization (LVI) with a recent 1-7-4 PRRSV isolate elicits broad protection against PRRSV challenge in finishing age swine. American Association of Swine Veterinarians 49th Annual Meeting, March 3-6, 2018, San Diego, California. Paper No. 69.

Interpretive Summary:

Technical Abstract: PRRSV infection is the most economically important disease affecting domestic swine herds in the United States and in many countries. Commercially available vaccines are often based on older viral strains and offer limited efficacy against heterologous challenge. Live virus immunization (LVI), a form of autologous vaccine, is based on immunizing healthy swine with serum from a diseased pig infected with a recent local isolate affecting that farm or area. Since the emergence of PRRS, this practice has been frequently utilized with reported success in immunizing replacement gilts, suggesting it does confer better protection than commercial vaccines. However, recently there have been field reports that LVI is not as efficacious as it once was, implying there may have been a change in how PRRSV interacts with the pig. Materials and Methods: To evaluate the efficacy of LVI with contemporary 1-7-4 strains, 60 finishing age swine were used in this study and divided into 7 groups. Three groups were challenged with 2ml serum I.M. from an NADC34 infected pig, a current 1-7-4 strain. Each of these LVI groups were again challenged after six weeks intranasally with 5 x 10E4 TCID50 of either NADC34 (homologous challenge), NADC36, a close relative (98.4% homologous whole genome), or SDSU73, a known moderately pathogenic 1-4-4 strain that is 83.2% homologous with NADC34. Each of these groups were compared with an equivalent but naïve group and evaluated for pyrexia, ADG, viral load, lung lesions and virus neutralization titer. Results: LVI with NADC34 protected all three LVI groups against homologous or heterologous challenge by lowering viral load by almost three logs, by eliminating negative effects on ADG of all three viruses and by eliciting broadly neutralizing calculated antibody titers of greater than 100 at 50% inhibition in 5 out of 8 pigs in the homologous challenge group, 5 out 8 in the NADC36 group, and 7 out of 9 in the SDSU73 group. Conclusions: LVI with NADC34 induces equivalent neutralization and protection per group from challenge with the NADC34, NADC36 or heterologous virus SDSU73. When sera of individual pigs were examined by western blotting, individually distinct reactivity patterns against viral proteins were observed between pigs in a group, suggesting individually distinct anti-PRRSV antibody responses. Future work aims to elucidate if a predictive value can be gleaned from these patterns for efficacy of protection against future challenge.