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Updated: Jul 11, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
STAT1-dependent innate immunity to a Norwalk-like virus
Stephanie M Karst1, Christiane E Wobus, Margarita Lay
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Researchers discovered a new murine norovirus. Innate immunity, specifically signal transducer and activator of transcription 1, is crucial for resisting norovirus infection, unlike adaptive immunity.
Area of Science:
- Virology
- Immunology
- Gastroenterology
Background:
- Noroviruses are a leading cause of epidemic gastroenteritis globally.
- Understanding norovirus pathogenesis is limited due to a lack of cell culture and animal models.
- Norwalk-like caliciviruses (Noroviruses) cause over 90% of nonbacterial epidemic gastroenteritis worldwide.
Purpose of the Study:
- To investigate the pathogenesis of norovirus infection.
- To identify host factors involved in norovirus resistance.
- To report the discovery of a novel murine norovirus.
Main Methods:
- Discovery and characterization of a new murine norovirus (Murine Norovirus 1).
- Analysis of Murine Norovirus 1 infection in a host context.
- Assessment of the roles of innate and adaptive immunity in norovirus resistance.
Main Results:
- A novel murine norovirus was identified.
- Signal transducer and activator of transcription 1 (STAT1)-dependent innate immunity is essential for norovirus resistance.
- T and B cell-dependent adaptive immunity is not essential for norovirus resistance.
Conclusions:
- Innate immunity plays a critical role in controlling norovirus infection.
- STAT1 is a key host molecule for norovirus resistance.
- Identifying host molecules for resistance may lead to new strategies against human norovirus diseases.
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