Host p53 Expression During C. Parvum Infection…Does the Virus Play a Role?

C. parvum infection induces significant host cellular stress responses, particularly through the modulation of p53 expression underscoring its potential involvement in gastrointestinal malignancies. Understanding these mechanisms is crucial for developing targeted therapeutic interventions. This study investigated the effects of C. parvum infection on host p53 dynamics in HCT-8 cells and assessed the impact of antiviral agents Lamivudine and Amantadine on the virus CSpV1 present within the parasite C. parvum. Further, the study focuses on whether the p53 effect changes with the presence or absence of CSpV1. The p53 assay results showed a constant increase in p53 activity after infection of HCT-8 cells with C. parvum. Treatment with the antivirals Lamivudine and Amantadine, showed a significant increase in p53 activity (83% and 95%, respectively), likely due to a stress response. However, after 3 hours of infection, p53 activity decreased by nearly 2.5-fold, suggesting that the antiviral treatments contributed to the removal of CSpV1. The expression analysis was performed using specific primers to human and C. parvum (sestrin like protein). The 3-hour infection with C. parvum causes host p53 to increase slightly, however C. parvum sestrin like protein increased dramatically. Further treatment with antivirals lamivudine and amantadine reduced this effect at 1 hour and 3 hours, indicating role of antivirals in removal of virus, but no major change on host p53 was observed. Overall, the results indicate the removal of CSpV1 significantly affected C. parvum sestrin and potentially impacting parasite survival during the infection. Based on these observations, I would speculate that CSpV1 plays a role in C. parvum infection and host p53 expression.