Etiology: MNV is a nonenveloped RNA virus in the family Caliciviridae. There are 4 described strains designated MNV-1, MNV-2, MNV-3, and MNV-4, as well as multiple field strains.  The virus causes enteric infections and can also exit the gut to replicate in macrophages and dendritic cells in multiple organs, including mesenteric lymph nodes and liver.

Incidence:  Currently, MNV is the most prevalent viral infection in mice.

Transmission: Transmission occurs via the fecal-oral route.  Infected mice shed virus in feces for extended periods of time.

Clinical Signs:  MNV infection can result in clinical signs of weight loss, hunched posture, ruffled fur and even death in mice with deficiencies in aspects of the innate immune system; however, no clinical signs have been reported to occur in immunocompetent mice or immunocompromised mice with intact innate immunity.

Pathology: There is no pathology associated with natural infection.  Following experimental inoculation, STAT1-/- mice exhibit mortality with the lesions including encephalitis, cerebral vasculitis, pneumonia, meningitis and hepatitis [1].

Diagnosis: Serologic assays (MFI, IFA) detect all four strains of MNV as there is good serologic cross-reactivity. PCR of feces is a useful tool for screening due to the occurrence of prolonged fecal shedding [2].

1.            Karst, S.M., et al., STAT1-dependent innate immunity to a Norwalk-like virus. Science, 2003. 299(5612): p. 1575-8.

2.            Manuel, C.A., et al., Soiled-bedding sentinel detection of murine norovirus 4. J Am Assoc Lab Anim Sci, 2008. 47(3): p. 31-6.