Abstract

The murine norovirus (MNV) is a recently discovered mouse pathogen, representing the most common contaminant in laboratory mouse colonies. Nevertheless, the effects of MNV infection on biomedical research are still unclear. We tested the hypothesis that MNV infection could alter immune response in mice with acute lung infection. Here we report that co-infection with MNV increases survival of mice with Pseudomonas aeruginosa acute lung injury and decreases in vivo production of pro-inflammatory cytokines. Our results suggest that MNV infection can deeply modify the parameters studied in conventional models of infection and lead to false conclusions in experimental models.

Highlights

  • The first murine norovirus, MNV1, was isolated in 2003 from the brain of an immunocompromised mouse lacking recombination-activating gene two and signal transducer and activator of transcription one (RAG2/STAT1-/-) [1]

  • Murine norovirus infection increases survival of mice with P. aeruginosa induced lung injury To determine whether an established infection with MNV affected P. aeruginosa infection, survival was analysed for 96 h

  • Murine norovirus infection decreases P. aeruginosa induced lung injury and dissemination A dose of 2.106 CFU of P. aeruginosa was inoculated and all the analyses were performed at 24 h after the bacterial challenge

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Summary

Introduction

The first murine norovirus, MNV1, was isolated in 2003 from the brain of an immunocompromised mouse lacking recombination-activating gene two and signal transducer and activator of transcription one (RAG2/STAT1-/-) [1]. Murine noroviruses are non-enveloped, positive-strand RNA viruses that belong to the Norovirus genus in the Caliciviridae family. This virus is related to the human norovirus which is estimated to be responsible for up to 90% of nonbacterial epidemic gastroenteritis worldwide [2]. Similar prevalence rates were observed in Japan and South Korea after serological or RT-PCR analysis of murine samples [11,12,13]. This worldwide high prevalence provides a tremendous potential for this virus to interfere with mouse models of

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