ABSTRACT
Porcine epidemic diarrhea virus (PEDV) targets the intestinal mucosa in pigs. To protect against PEDV invasion, a mucosal vaccine is utilized effectively. In this study, we generated a recombinant adenovirus vaccine encoding the heat-labile enterotoxin B (LTB) and the core neutralizing epitope (COE) of PEDV (rAd-LTB-COE). The fusion protein LTB-COE was successfully expressed by the recombinant adenovirus in HEK293 cells, and the immunogenicity of the vaccine candidate was assessed in BALB/c mice and piglets. Three intramuscular or oral vaccinations with rAd-LTB-COE at two-week intervals induced robust humoral and mucosal immune responses. Moreover, a cell-mediated immune response was promoted in immunized mice, and the neutralizing antibody inhibited both the vaccine strain and the emerging PEDV isolate. Immunization experiments in piglets revealed that rAd-LTB-COE was immunogenic and induced good immune responses in piglets. Further studies are required to evaluate the efficacy of rAd-LTB-COE against a highly virulent PEDV challenge.
Subject(s)
Coronavirus Infections/prevention & control , Coronavirus Infections/veterinary , Porcine epidemic diarrhea virus/immunology , Swine Diseases/prevention & control , Viral Vaccines/immunology , Adenoviridae/genetics , Adenoviridae/immunology , Animals , Cell Line , Coronavirus Infections/immunology , Enterotoxins/genetics , Enterotoxins/immunology , Epitopes/genetics , Epitopes/immunology , Escherichia coli/immunology , Escherichia coli/pathogenicity , Female , HEK293 Cells , Humans , Mice , Mice, Inbred BALB C , Porcine epidemic diarrhea virus/genetics , Recombinant Fusion Proteins/immunology , Swine , Swine Diseases/immunology , Swine Diseases/virology , Viral Vaccines/administration & dosage , Viral Vaccines/therapeutic useABSTRACT
Kawasaki syndrome (KS) is an acute vasculitis in children complicated by the development of heart disease. Despite its description over 50 years ago, the etiology of coronary artery disease in KS is unknown. High dose intravenous immunoglobulin is the most effective approach to reduce cardiovascular complications. It remains unclear why patients with KS develop coronary artery aneurysms. A subset of patients is resistant to immunoglobulin therapy. Given the heterogeneity of clinical features, variability of history, and therapeutic response, KS may be a cluster of phenotypes triggered by multiple infectious agents and influenced by various environmental, genetic, and immunologic responses. The cause of KS is unknown, and a diagnostic test remains lacking. A better understanding of mechanisms leading to acute KS would contribute to a more precision medicine approach for this complex disease. In the current viewpoint, we make the case for microbial superantigens as important causes of KS.