Mucosal Immunity and Immune Evasion in Porcine Epidemic Diarrhea Virus Infection: Implications for Vaccine Development

Porcine epidemic diarrhea virus (PEDV) is an enteric coronavirus that causes severe diarrhea, dehydration, and high mortality in neonatal piglets, imposing enormous economic losses on the global swine industry. Because PEDV primarily infects intestinal epithelial cells, the intestinal mucosal immune system constitutes the first line of defense against viral invasion. Among the various protective mechanisms, secretory IgA (sIgA)—particularly milk-borne maternal sIgA—is regarded as the key determinant of protection against PEDV infection in nursing piglets. PEDV infection activates both innate and adaptive immune responses, including interferon production, antibody generation, and T cell activation. Concurrently, the virus has evolved multiple strategies to evade host immunity, including suppression of interferon signaling, interference with antigen presentation, manipulation of autophagy pathways, and weakening of intestinal barrier function. These immune evasion mechanisms facilitate viral replication and may partly account for the limited protective efficacy of current vaccines. In this review, we summarize recent advances in the understanding of mucosal immune responses elicited by PEDV infection, with a focus on innate immunity, adaptive immunity, immune evasion strategies, and the remodeling of the intestinal mucosal immune system. We further discuss recent progress in mucosal vaccine development and the challenges that remain in achieving robust protective immunity against PEDV.