Abstract
INTRODUCTION: Drosophila melanogaster is a quintessential model organism that has been used in many scientific studies. The intestinal immune response of flies is a critical component of their innate immune system. Given that flies primarily consume decaying organic matter, harmful microorganisms present in their food can enter the intestine, leading to frequent infections by exogenous pathogens. When these pathogens are introduced into the intestinal environment, a cascade of immune responses is triggered within the intestinal tissue, aimed at preserving the integrity of the intestinal barrier and ensuring the proper physiological functions of the gut. Porcine rotavirus (PoRV) is a key pathogen that causes diarrhea in pigs, and PoRV infection can significantly reduce piglet survival rates. METHODS: In this study, wild-type flies were orally administered PoRV to establish an effective intestinal damage animal model, and a detailed investigation of the antiviral immune defense mechanism in the fly intestine was performed. RESULTS AND DISCUSSION: Our study revealed that PoRV infection caused a reduction in the survival rate of flies and an increase in intestinal epithelial cell death. Concurrently, PoRV infection significantly promoted the proliferation and differentiation of intestinal cells, contributing to the maintenance of intestinal homeostasis. After the activation of JAK/STAT signaling in the intestines of infected Drosophila, there was an increase in the levels of reactive oxygen species (ROS). This elevation was concomitant with the release of antimicrobial peptides (AMPs), which play a crucial role in pathogen clearance. Additionally, we identified substantial aggregation of hemocytes in the midgut. The composition of the intestinal microbiota also underwent changes, potentially playing a role in intestinal immune defense. Moreover, PoRV can evade clearance via the RNA interference (RNAi) pathway. In summary, PoRV infection in the fly intestine activates multiple immune defense mechanisms to eliminate the pathogen, offering a theoretical basis for PoRV prevention and control.