Establishment of inflammatory model induced by Pseudorabies virus infection in mice

Background: Pseudorabies virus (PRV) infection leads to high mortality in swine. Despite extensive efforts, effective treatments against PRV infection are limited. Furthermore, the inflammatory response induced by PRV strain GXLB-2013 is unclear. Objectives: Our study aimed to investigate the inflammatory response induced by PRV strain GXLB-2013, establish an inflammation model to elucidate the pathogenesis of PRV infection further, and develop effective drugs against PRV infection. Methods: Kunming mice were infected intramuscularly with medium, LPS, and different doses of PRV-GXLB-2013. Viral spread and histopathological damage to brain, spleen, and lung were determined at 7 days post-infection (dpi). Immune organ indices, levels of reactive oxygen species (ROS), nitric oxide (NO), and inflammatory cytokines, as well as levels of activity of COX-2 and iNOS were determined at 4, 7, and 14 dpi. Results: At 10(5)-10(6) TCID50 PRV produced obviously neurological symptoms and 100% mortality in mice. Viral antigens were detectable in kidney, heart, lung, liver, spleen, and brain. In addition, inflammatory injuries were apparent in brain, spleen, and lung of PRV-infected mice. Moreover, PRV induced increases in immune organ indices, ROS and NO levels, activity of COX-2 and iNOS, and the content of key pro-inflammatory cytokines, including interleukin (IL)-1 beta, IL-6, tumor necrosis factor-alpha, interferon-gamma and MCP-1. Among the tested doses, 10(2) TCID50 of PRV produced a significant inflammatory mediator increase. Conclusions: An inflammatory model induced by PRV infection was established in mice, and 10(2) TCID50 PRV was considered as the best concentration for the establishment of the model.

Automated summary

The study established an inflammatory model induced by PRV infection in mice, with 10(2) TCID50 PRV considered as the optimal concentration for model establishment. PRV infection caused increased immune organ indices, ROS and NO levels, inflammatory mediators, and oxidative stress.