Since its discovery, Porcine reproductive and respiratory syndrome (PRRS) has had a huge impact on the farming industry. The virus that causes PRRS is Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), and because of its genetic diversity and the complexity of the immune response, the eradication of PRRS has been a challenge. To provide scientific references for PRRSV control and vaccine development, this study describes the processes of PRRSV-induced infection and escape, as well as the host adaptive immune response to PRRSV. It also discusses the relationship between PRRSV and the adaptive immune response.

Canine parainfluenza virus (CPIV) is a zoonotic virus that is widely distributed and is the main pathogen causing canine infectious respiratory disease (CIRD), also known as “kennel cough,” in dogs. The CPIV-V protein is the only nonstructural protein of the virus and plays an important role in multiple stages of the virus life cycle by inhibiting apoptosis, altering the host cell cycle and interfering with the interferon response. In addition, studies have shown that the V protein has potential applications in the field of immunotherapy in oncolytic virus therapy or self-amplifying RNA vaccines. In this review, the biosynthesis, structural characteristics and functions of the CPIV-V protein are reviewed with an emphasis on how it facilitates viral immune escape and its potential applications in the field of immunotherapy. Therefore, this review provides a scientific basis for research into the CPIV-V protein and its potential applications.

Background/Objectives: IncI2 and IncX4 plasmids are important vehicles for dissemination of the mobile colistin resistance gene mcr-1. We evaluated whether sanguinarine (SA) reduces conjugative transfer of these two mcr-1-carrying plasmid types and examined biological changes accompanying the transfer phenotype. Methods: Conjugation was measured in Escherichia coli carrying pIncI2-mcr-1 or pIncX4-mcr-1 after exposure to 2–8 µg/mL SA. Growth-related measurements, intracellular ATP signal, glycogen content, enzyme activities, targeted energy metabolomics, RNA sequencing, reactive oxygen species (ROS), and membrane permeability were assessed, with biological profiling focused on the IncI2 system. pIncI2-mcr-1 transfer was also examined in a mouse-gut model. Results: SA caused no detectable reduction in the reported OD₆₀₀-based growth curves or viable donor/recipient counts under the tested conditions. At 8 µg/mL, SA reduced IncI2-mcr-1 and IncX4-mcr-1 conjugation frequency by approximately 176-fold and 117-fold, respectively. In the IncI2 system, lower luciferase-based ATP signals, glycogen accumulation, altered GAPDH and G6PDH activities, and decreased abundance of transfer-related transcripts accompanied the reduction in transfer. Targeted LC–MS/MS independently confirmed a dose-associated decrease in ATP and identified lower pools of several glycolysis-associated metabolites. In mice, the mean IncI2 transfer-frequency estimate was 8.41 × 10⁻³ in controls and 2.49 × 10⁻³ with SA (n = 10 per group; p < 0.0001). Conclusions: SA reduced transfer of the two tested mcr-1-carrying plasmids under the experimental conditions. The metabolic and transcriptional observations support an energy-associated explanatory model for the IncI2 system and highlight SA’s potential as a conjugation inhibitor to curb the spread of colistin resistance.