Work

Immunogenicity and protective efficacy of the novel candidate antigen Eg174 against Echinococcus granulosus infection in a murine model

Year: 2026

Type: article

Abstract: Echinococcosis is a zoonotic parasitic disease caused by the larval stages of cestodes of the genus Echinococcus . The two major species, Echinococcus granulosus (Eg) and Echinococcus multilocularis (Em), are the causative agents of cystic echinococcosis (CE) and alveolar echinococcosis (AE), respectively, posing public health threats. Although vaccine development for canids has been reported, work is still required to identify effective candidate antigens. Based on preliminary 3-day larval cDNA library screening, Eg174 was identified as a candidate antigen. To assess its immunoprotective potential in an experimental system, two recombinantly expressed splice variants—the full-length (FL) protein and the C-terminal (CT) protein—were evaluated in a mouse model, which is widely used for preliminary antigen screening. Following bioinformatics analysis, the recombinant proteins rEg174-CT and rEg174-FL were obtained through prokaryotic expression. ICR mice were immunized with these proteins, and protection was evaluated by liver cyst counts after protoscolex challenge and in vitro killing assays. Humoral and cellular immune responses were assessed by ELISA and flow cytometry, respectively. The rEg174-CT-immunized group exhibited a significantly higher cyst reduction rate than the rEg174-FL group, accompanied by a stronger Th1-biased antibody response, as indicated by higher IgG titers and predominance of IgG2a over IgG1. Cellular immune analysis further demonstrated that rEg174-CT induced stronger and more sustained Th1/Th17-biased responses, including IFN-γ, IL-17A, and TNF-α production. Overall, these results identify rEg174-CT as a promising candidate antigen, and its superior immunoprotective effect in the mouse model provides a foundation for further evaluation in the target host.

Source: Parasites & Vectors

DOI: 10.1186/s13071-026-07614-8