Abstract
The porcine respiratory disease complex (PRDC) is responsible for significant economic losses in the pig industry worldwide. Porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza virus are major viral contributors to PRDC. Vaccines are cost-effective measures for controlling PRRS, however, their efficacy in the context of co-infections has been poorly investigated. In this study, we aimed to determine the effect of PRRSV-2 and swine influenza H3N2 virus co-infection on the efficacy of PRRSV modified live virus (MLV) vaccination, which is widely used in the field. Following simultaneous challenge with contemporary PRRSV-2 and H3N2 field isolates, we found that the protective effect of PRRS MLV vaccination on clinical disease and pathology was abrogated, although viral load was unaffected and antibody responses were enhanced. In contrast, co-infection in non-immunized animals reduced PRRSV-2 viremia and H3N2 virus load in the upper respiratory tract and potentiated T cell responses against both PRRSV-2 and H3N2 in the lung. Further analysis suggested that an upregulation of inhibitory cytokines gene expression in the lungs of vaccinated pigs may have influenced responses to H3N2 and PRRSV-2. These findings provide important insights into the effect of viral co-infections on PRRS vaccine efficacy that may help identify more effective vaccination strategies against PRDC in the field.
Highlights
Porcine reproductive and respiratory syndrome (PRRS) is a viral disease responsible for major economic losses in the global pig industry [1]
To investigate whether concurrent infection with H3N2 and Porcine reproductive and respiratory syndrome virus (PRRSV)-2 can interfere with the efficacy of PRRS modified live virus (MLV) vaccination, groups of 6 pigs were immunized with a commercial PRRS MLV (Vac) or mock vaccinated with PBS (Ctrl) by intramuscular injection (Figure 1A)
None of the vaccinated pigs infected with PRRSV-2 (Vac + PRRSV-2) showed hyperthermia but 4/6 of the pigs vaccinated and co-infected with PRRSV-2/H3N2 (Vac + PRRSV-2/H3N2) developed fever (≥40°C) which lasted for 3 consecutive days in one pig (Supplementary Table 3)
Summary
Porcine reproductive and respiratory syndrome (PRRS) is a viral disease responsible for major economic losses in the global pig industry [1]. The first clinical description of PRRS dates to the late 1980’s, with genetically distinct PRRSV isolates described in Europe and North America, which are recognized as two separate species PRRSV-1 (Betaarterivirus suid 1) and -2 (Betaarterivirus suid 2), respectively [7]. Both species have since spread globally, but PRRSV-1 remains predominant in Europe, while PRRSV-2 predominates in the Americas and Asia. The rapid evolution of PRRSV due to a high mutation rate when replicating its genome, and recombination between strains have resulted in substantial genetic diversity, which poses challenges for the control of PRRS by vaccination [8]
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