Date of Award
Spring 5-16-2015
Author's School
College of Arts & Sciences
Author's Department/Program
Biology
Degree Name
Bachelor of Arts
Abstract
Human norovirus (HNV) is the leading cause of acute non-bacterial epidemic gastroenteritis worldwide and affects millions of people every year. HNV does not grow in tissue culture so murine norovirus (MNV), which does have a culture system, is a useful model to study the lifecycle and virus-host interactions of noroviruses. Previous research in the Virgin lab has shown that the MNV protein NS1/2 interacts with the host protein vesicle associated membrane protein (VAMP)-associated-protein A (Vapa) which is an integral endoplasmic reticulum (ER) membrane protein that is involved in cholesterol homoeostasis. In addition, we observed that fluorescently tagged NS1/2 and Vapa co-localized when overexpressed in 293T cells. Because of this, we hypothesize that cholesterol is important for MNV infection, and Vapa mediates this relationship. Through multiple measures, MNV infection does not lead to a change in cholesterol levels in RAW 264.7 cells. Surprisingly, depleting cholesterol by growing cells in lipoprotein depleted serum (LPDS) media showed no effect on cell viability or viral titers. However, Vapa-knockout cells showed increased cell viability during infection, further suggesting that Vapa is important during MNV infection.
Language
English (en)
Advisor/Committee Chair
Herbert W. Virgin IV
Advisor/Committee Chair's Department
Pathology and Immunology
Recommended Citation
Condiff, Emily, "Investigating the Role of Cholesterol During Murine Norovirus Infection" (2015). Undergraduate Theses—Restricted. 43.
https://openscholarship.wustl.edu/undergrad_honors/43