Deletion of Toxoplasma Rhoptry Protein 38 (PruΔrop38) as a Vaccine Candidate for Toxoplasmosis in a Murine Model

Toxoplasmosis is a serious zoonotic disease that threatens human and animal health. Here, we evaluated the vaccine potential of the deletion of Toxoplasma rhoptry protein 38 (Pru Delta rop38) through its pathogenicity and immunoprotective efficacy in mice. Mice inoculated intraperitoneally with 1 x 10(3), 2 x 10(3), or 4 x 10(3) Pru Delta rop38 showed no visible signs, whereas mice inoculated with 1 x 10(3) parental Pru strain showed obvious wasting and bow-back, suggesting a significantly lower pathogenicity of Pru Delta rop38 in mice. Vaccination with 1 x 10(2) Pru Delta rop38 triggered a mixed Th1/Th2 response (Th1 response predominant), with higher IgG, IgG2a, and IgG1 levels in serum from week 3 to week 12, and a significant increase in IFN-gamma, IL-12, and IL-10 in suspensions of splenocytes at 30 or 60 days post-immunization. All vaccinated mice survived when infected intraperitoneally with tachyzoites (RH, Pru, VEG, or TgcatBJ1) or when infected orally with cysts (Pru or ME49). The brain parasite burden during Pru tachyzoite, Pru cyst and ME49 cyst challenges were significantly reduced in vaccinated mice. The duration of immunization showed that vaccination with Pru Delta rop38 could protect mice from challenge with different varied genotypes of Toxoplasma strains against different routes of infection. Collectively, these findings indicate that Pru Delta rop38 is an attenuated strain that provides long-term protective efficacy against acute or chronic toxoplasmosis in mice.

Automated summary

This study evaluated the potential of Toxoplasma rhoptry protein 38 (Pru Delta rop38) as a vaccine. The results showed that Pru Delta rop38 had lower pathogenicity in mice and triggered a mixed Th1/Th2 immune response, leading to increased antibody levels and immune factors. Vaccination with Pru Delta rop38 provided long-term protection against different Toxoplasma strains and routes of infection in mice.