TgMORN2, a MORN Family Protein Involved in the Regulation of Endoplasmic Reticulum Stress in Toxoplasma gondii.

MORN proteins play a key role in the cytoskeletal structure of eukaryotes and are essential for the close arrangement of the endoplasmic reticulum and plasma membrane. A gene with nine MORN motifs (TGGT1_292120, named TgMORN2) was identified in the Toxoplasma gondii genome; it was presumed to belong to the MORN protein family and to have the function of forming the cytoskeleton, which affects the survival of T. gondii. However, the genetic deletion of MORN2 did not noticeably affect parasite growth and virulence. Using adjacent protein labeling techniques, we identified a network of TgMORN2 interactions, which mainly included endoplasmic reticulum stress (ER stress)-related proteins. In exploring these data, we found that the pathogenicity of the KO-TgMORN2 strain was significantly reduced in the case of tunicamycin-induced ER stress. Reticulon TgRTN (TGGT1_226430) and tubulin ß-Tubulin were identified as interaction proteins of TgMORN2. Collectively, TgMORN2 plays a role in ER stress, which lays a foundation for further research on the function of the MORN protein in T. gondii.

Influenza A Virus Weakens the Immune Response of Mice to Toxoplasma gondii, Thereby Aggravating T. gondii Infection.

This study aimed to investigate the relationship between the T. gondii type II strain (Pru) and respiratory viral infections, specifically focusing on the co-infection with PR8 (influenza A/Puerto Rico/8/34). In this study, we found that the number of T. gondii (Pru) in the lungs of co-infected mice was significantly higher and lesions were more severe than those in the group infected with T. gondii (Pru) alone, whereas IAV (influenza A virus) copy numbers of co-infected and PR8 alone infected groups were negligible, suggesting that infection with IAV increased the pathogenicity of T. gondii (Pru) in mice. The invasion and proliferation assays demonstrated no significant effect of co-infection on T. gondii (Pru) infection or replication in vitro. To further explore the factors causing the altered pathogenicity of T. gondii (Pru) caused by co-infection, we found that decreased expression levels of IL-1ß, IL-6, and IL-12 in the co-infected group were associated with the early immune responses against T. gondii (Pru), which affected the division of T. gondii (Pru). Moreover, the significant decrease in the CD4+/CD8+ ratio indicated a weakened long-term immune killing ability of the host against T. gondii (Pru) following IAV infection. In conclusion, a T. gondii type II strain (Pru) could not be properly cleared by the host immune system after IAV infection, resulting in toxoplasmosis and even death in mice.