Name
Polymicrobial Interactions in the Gut: The Effect of Candida albicans on Rotavirus Replication and PGE₂ Production
Presenter
Nikita Barron, University of the Free State
Co-Author(s)
Nikita Barron, Carolina H Pohl, Jacobus Albertyn, Hester G O’Neill
Department of Microbiology and Biochemistry, University of the Free State, Bloemfontein, South Africa
Abstract Category
Pathogenesis and Immunity
Abstract
The human gastrointestinal tract hosts a diverse array of microbial communities that influence susceptibility to infection. While most research on gut polymicrobial interactions focuses on bacteria and enteric viruses, the role of fungal species such as Candida albicans remains largely unexplored. C. albicans, a common gut commensal, produces prostaglandin E₂ (PGE₂), a lipid mediator known to enhance rotavirus (RV) attachment and internalization. However, the potential interaction between C. albicans and RV remains unclear. This study investigates the effect of C. albicans on RV replication and PGE₂ secretion using an in vitro co-infection model in MA104 cells.
RT-qPCR quantification of VP6-gene copies revealed that C. albicans co-infection reduced intracellular RV replication at 4 hours post-infection regardless of which organism was introduced first. However, VP6-gene copies in culture supernatants remained unchanged, suggesting that C. albicans does not inhibit viral entry. PGE₂ levels were significantly higher in RV-infected cells compared to C. albicans alone. When C. albicans was added first, PGE₂ levels in co-infected cells were comparable to RV infection alone, with normalisation confirming a fungal contribution. In contrast, when RV was added first, PGE₂ levels were lower in co-infected cells compared to RV alone, a decrease attributable to reduced VP6 copy numbers rather than a direct effect of C. albicans. These findings suggest that C. albicans modulates RV replication independently of viral entry while contributing to PGE₂ production. This study provides the first evidence of indirect C. albicans-RV interactions and highlights the need for further research into the underlying molecular mechanisms.
RT-qPCR quantification of VP6-gene copies revealed that C. albicans co-infection reduced intracellular RV replication at 4 hours post-infection regardless of which organism was introduced first. However, VP6-gene copies in culture supernatants remained unchanged, suggesting that C. albicans does not inhibit viral entry. PGE₂ levels were significantly higher in RV-infected cells compared to C. albicans alone. When C. albicans was added first, PGE₂ levels in co-infected cells were comparable to RV infection alone, with normalisation confirming a fungal contribution. In contrast, when RV was added first, PGE₂ levels were lower in co-infected cells compared to RV alone, a decrease attributable to reduced VP6 copy numbers rather than a direct effect of C. albicans. These findings suggest that C. albicans modulates RV replication independently of viral entry while contributing to PGE₂ production. This study provides the first evidence of indirect C. albicans-RV interactions and highlights the need for further research into the underlying molecular mechanisms.