Abstract Title
Dissecting the Mechanism of Glycocholic Acid–Mediated Enhancement of Human Sapovirus Infection in Caco-2 MC Cells
Presenter
Miyabi Arai, Kitasato University
Co-Author(s)
Miyabi Arai1, Yuya Fukuda2, Reiko Todaka1, Ryoka Ishiyama1, Kei Haga1 and Kazuhiko Katayama1 1 Kitasato University 2 Sapporo Medical University School of Medicine
Abstract Category
Entry and Replication
Abstract
In vitro culture of sapovirus requires the supplementation of bile acids in the culture medium. Our recently developed human sapovirus (HuSaV) culture system using Caco-2 MC cells also depends on the presence of the bile acid glycocholic acid (GCA). However, the mechanism by which GCA promotes HuSaV replication remains poorly understood.
In this study, we first examined whether GCA acts on virus particles to promote infection or on host cells to facilitate viral replication. We also investigated the involvement of GCA in HuSaV infection via a host factor that we previously identified as being essential for HuSaV infection to Caco-2 MC cells.
To further explore the cellular pathways influenced by GCA, we performed transcriptome analysis of Caco-2 MC cells following bile acid treatment to identify bile acid–responsive genes. Among these, several bile acid–related genes were individually knocked out using the CRISPR/Cas9 system, and their roles in HuSaV replication were evaluated.
These approaches allowed us to identify candidate cellular pathways and factors involved in bile acid–mediated enhancement of HuSaV replication, providing new insights into the virus–host interaction mechanisms of enteric caliciviruses.
In this study, we first examined whether GCA acts on virus particles to promote infection or on host cells to facilitate viral replication. We also investigated the involvement of GCA in HuSaV infection via a host factor that we previously identified as being essential for HuSaV infection to Caco-2 MC cells.
To further explore the cellular pathways influenced by GCA, we performed transcriptome analysis of Caco-2 MC cells following bile acid treatment to identify bile acid–responsive genes. Among these, several bile acid–related genes were individually knocked out using the CRISPR/Cas9 system, and their roles in HuSaV replication were evaluated.
These approaches allowed us to identify candidate cellular pathways and factors involved in bile acid–mediated enhancement of HuSaV replication, providing new insights into the virus–host interaction mechanisms of enteric caliciviruses.