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Updated: Jun 16, 2026
Reverse Genetics Mediated Recovery of Infectious Murine Norovirus
Published on: June 24, 2012
Effect of murine norovirus infection on mouse parvovirus infection
Susan R Compton1, Frank X Paturzo, James D Macy
1Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut, USA. susan.compton@yale.edu
Abstract:
Enzootic infection with mouse parvovirus (MPV) remains a common problem in laboratory colonies, and diagnosis of MPV infection is complicated by viral and host factors. The effect of an underlying viral infection on MPV infection has not previously been investigated. We assessed the effect of murine norovirus (MNV) infection, the most prevalent infectious agent in laboratory mice, on MPV shedding, tissue distribution and transmission. Fecal MPV shedding persisted longer in BALB/c mice infected with MNV 1 wk prior to MPV infection than in mice infected with MPV only, but transmission of MPV to soiled-bedding sentinels was not prolonged in coinfected mice. MPV DNA levels in coinfected BALB/c mice were higher in mesenteric lymph nodes and spleens at 1 and 2 wk after inoculation and in small intestines at 1 wk after inoculation compared with levels in mice infected with MPV only. In C57BL/6 mice, fecal shedding was prolonged, but no difference in soiled bedding transmission or MPV DNA levels in tissues was detected between singly and coinfected mice. MPV DNA levels in singly and coinfected SW mice were similar. MPV DNA levels were highest in SW, intermediate in BALB/c and lowest in C57BL/6 mice. MPV DNA levels in mesenteric lymph nodes of BALB/c and SW mice exceeded those in small intestines and feces, whereas the inverse occurred in C57BL/6 mice. In conclusion, MNV infection increased the duration of MPV shedding and increased MPV DNA levels in tissues of BALB/c mice.
Insights
Murine norovirus (MNV) coinfection prolongs mouse parvovirus (MPV) shedding and increases MPV DNA in tissues, particularly in BALB/c mice. This interaction impacts MPV diagnosis and control in research settings.
Area of Science:
- Veterinary Virology
- Immunology
- Laboratory Animal Science
Background:
- Enzootic mouse parvovirus (MPV) infection is a persistent challenge in laboratory animal facilities.
- Diagnosis of MPV is complicated by viral and host factors, with limited understanding of how concurrent infections influence outcomes.
- The impact of murine norovirus (MNV), a prevalent infectious agent, on MPV infection dynamics has not been previously studied.
Purpose of the Study:
- To investigate the effect of concurrent murine norovirus (MNV) infection on mouse parvovirus (MPV) shedding, tissue distribution, and transmission.
- To compare MPV infection parameters in mice singly infected with MPV versus those coinfected with both MNV and MPV.
- To assess strain-specific differences in MPV response to MNV coinfection.
Main Methods:
- BALB/c, C57BL/6, and SW mice were infected with MNV prior to MPV inoculation or with MPV only.
- Fecal shedding of MPV was monitored over time.
- MPV DNA levels were quantified in various tissues (mesenteric lymph nodes, spleen, small intestine) and feces.
- Transmission to soiled-bedding sentinels was assessed.
Main Results:
- In BALB/c mice, MNV coinfection prolonged fecal MPV shedding and increased MPV DNA levels in mesenteric lymph nodes, spleen, and small intestine compared to MPV-only infected mice.
- In C57BL/6 mice, MNV coinfection prolonged fecal shedding but did not significantly alter MPV DNA levels in tissues or transmission.
- MPV DNA levels varied significantly by mouse strain, being highest in SW, intermediate in BALB/c, and lowest in C57BL/6 mice.
Conclusions:
- MNV infection exacerbates MPV shedding duration and increases MPV viral load in specific tissues, notably in BALB/c mice.
- The interaction between MNV and MPV is strain-dependent, affecting shedding, tissue distribution, and potentially diagnostic sensitivity.
- Understanding these viral interactions is crucial for effective MPV control and accurate diagnosis in research animal populations.
