Norovirus Regulation by Host and Microbe. Issue 12 (December 2016)

• Record Type: Journal Article
• Authors: Baldridge, Megan T.; Turula, Holly; Wobus, Christiane E.
• Is Part Of: Trends in molecular medicine. Volume 22:Issue 12(2016)
• Page Start: 1047
• Page End: 1059
• Publication Date: 2016-12
• Subjects: immunity -- microbiome -- microbiota -- norovirus; Molecular biology -- Periodicals; Pathology, Molecular -- Periodicals; Physiology, Pathological -- Periodicals; 572.8
• DOI: 10.1016/j.molmed.2016.10.003
• Languages: English
• ISSNs: 1471-4914

Abstract

Abstract : Norovirus (NoV) infection is the leading cause of epidemic gastroenteritis globally, and can lead to detrimental chronic infection in immunocompromised hosts. Despite its prevalence as a cause of diarrheal illness, the study of human NoVs (HNoVs) has historically been limited by a paucity of models. The use of murine NoV (MNoV) to interrogate mechanisms of host control of viral infection has facilitated the exploration of different genetic mouse models, revealing roles for both innate and adaptive immunity in viral regulation. MNoV studies have also recently identified important interactions between the commensal microbiota and NoV with clear extensions to HNoVs. In this review, we discuss the most current understanding of how the host, the microbiome, and their interactions regulate NoV infections. Trends: Murine norovirus provides a practical model to study norovirus infections and pathogenesis. Murine and human noroviruses share a tropism for immune cells and intestinal epithelial cells. Norovirus infection is regulated by multiple host genes, including viral entry factors, innate immune mediators, and components of the adaptive immune system. The commensal bacteria of the gastrointestinal microbiome can modulate norovirus infection. Recent findings indicate that norovirus and commensal bacteria stimulate overlapping host immune pathways, and furthermore, that certain bacteria are required to mediate some of the pathologic effects of norovirus infection. Host and microbial effects on norovirus may function in complex combinations to regulate viral infection and pathogenesis.