Abstract
Norwalk-like caliciviruses (Noroviruses) cause over 90% of nonbacterial epidemic gastroenteritis worldwide, but the pathogenesis of norovirus infection is poorly understood because these viruses do not grow in cultured cells and there is no small animal model. Here, we report a previously unknown murine norovirus. Analysis of Murine Norovirus 1 infection revealed that signal transducer and activator of transcription 1-dependent innate immunity, but not T and B cell-dependent adaptive immunity, is essential for norovirus resistance. The identification of host molecules essential for murine norovirus resistance may provide targets for prevention or control of an important human disease.
Publication types
- Research Support, U.S. Gov't, P.H.S.
MeSH terms
- Animals
- B-Lymphocytes / immunology
- Brain / virology
- Caliciviridae Infections / immunology*
- DNA-Binding Proteins / genetics
- DNA-Binding Proteins / physiology*
- Genes, RAG-1
- Genome, Viral
- Homeodomain Proteins / physiology
- Immunity, Innate*
- Immunocompromised Host
- Interferon gamma Receptor
- Intestines / virology
- Liver / virology
- Membrane Proteins
- Mice
- Mutation
- Norovirus / classification
- Norovirus / immunology*
- Norovirus / isolation & purification*
- Norovirus / pathogenicity
- Phylogeny
- RNA, Viral / analysis
- Receptor, Interferon alpha-beta
- Receptors, Interferon / genetics
- Receptors, Interferon / physiology
- STAT1 Transcription Factor
- Spleen / virology
- T-Lymphocytes / immunology
- Trans-Activators / genetics
- Trans-Activators / physiology*
- Virulence
Substances
- DNA-Binding Proteins
- Homeodomain Proteins
- Membrane Proteins
- RNA, Viral
- Rag2 protein, mouse
- Receptors, Interferon
- STAT1 Transcription Factor
- Stat1 protein, mouse
- Trans-Activators
- V(D)J recombination activating protein 2
- RAG-1 protein
- Receptor, Interferon alpha-beta