Related Experiment Video
Updated: Apr 20, 2026
Quantifying Human Norovirus Virus-like Particles Binding to Commensal Bacteria Using Flow Cytometry
Published on: April 29, 2020
Commensal microbes and interferon-λ determine persistence of enteric murine norovirus infection
Megan T Baldridge1, Timothy J Nice1, Broc T McCune1
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Abstract:
The capacity of human norovirus (NoV), which causes >90% of global epidemic nonbacterial gastroenteritis, to infect a subset of people persistently may contribute to its spread. How such enteric viruses establish persistent infections is not well understood. We found that antibiotics prevented persistent murine norovirus (MNoV) infection, an effect that was reversed by replenishment of the bacterial microbiota. Antibiotics did not prevent tissue infection or affect systemic viral replication but acted specifically in the intestine. The receptor for the antiviral cytokine interferon-λ, Ifnlr1, as well as the transcription factors Stat1 and Irf3, were required for antibiotics to prevent viral persistence. Thus, the bacterial microbiome fosters enteric viral persistence in a manner counteracted by specific components of the innate immune system.
Insights
The gut microbiome promotes persistent norovirus infections, but the innate immune system can counteract this. Antibiotics disrupted this process by altering the gut bacteria, highlighting a link between the microbiome and viral persistence.
Area of Science:
- Virology
- Immunology
- Microbiology
Background:
- Human norovirus (NoV) causes significant global epidemic nonbacterial gastroenteritis.
- The mechanisms underlying persistent enteric viral infections are not fully understood.
- Persistent infections may contribute to the spread of noroviruses.
Purpose of the Study:
- To investigate the role of the bacterial microbiome in persistent murine norovirus (MNoV) infection.
- To elucidate the innate immune mechanisms involved in controlling enteric viral persistence.
Main Methods:
- Treatment of mice with antibiotics to disrupt the gut microbiota.
- Assessment of MNoV infection and viral replication.
- Analysis of the role of interferon-λ receptor (Ifnlr1) and transcription factors (Stat1, Irf3) in antiviral defense.
Main Results:
- Antibiotics prevented persistent MNoV infection, an effect reversible by restoring the microbiota.
- Antibiotics acted specifically in the intestine, without affecting systemic viral replication.
- Ifnlr1, Stat1, and Irf3 were essential for the antibiotic-mediated prevention of viral persistence.
Conclusions:
- The bacterial microbiome plays a crucial role in fostering enteric viral persistence.
- Innate immune components, including the interferon-λ pathway, counteract microbiome-mediated viral persistence.
- Targeting the gut microbiome or enhancing innate immunity could be strategies to control norovirus infections.
