A comparison of mouse parvovirus 1 infection in BALB/c and C57BL/6 mice: susceptibility, replication, shedding, and

Kenneth S Henderson1, Kathleen R Pritchett-Corning2, Cheryl L Perkins3

  • 1Research Animal Diagnostic Services, Charles River, Wilmington, Massachusetts, USA ken.henderson@crl.com.

Comparative Medicine
|March 3, 2015
PubMed

Insights

BALB/c mice are more susceptible to mouse parvovirus 1 (MPV1e) infection than C57BL/6 mice. This difference is linked to higher viral replication, shedding, and delayed immune response in BALB/c mice.

Area of Science:

  • Veterinary Virology
  • Immunology
  • Infectious Disease

Background:

  • Mouse parvovirus 1 (MPV1e) is a significant pathogen in laboratory mouse colonies.
  • Understanding host strain susceptibility is crucial for managing MPV1e outbreaks and research integrity.

Purpose of the Study:

  • To characterize the differential susceptibility of C57BL/6NCrl (B6) and BALB/cAnNCrl (C) mice to MPV1e infection.
  • To investigate the impact of host genetic background on MPV1e pathogenesis, including viral replication, shedding, and host immune response.

Main Methods:

  • Mice (B6 and C strains) were challenged with a field isolate of MPV1e via oral gavage.
  • Quantitative PCR (qPCR) and RT-qPCR were used to measure viral load, infection, and replication in feces and tissues (mesenteric lymph nodes, ileum, spleen, blood).
  • Seroconversion was assessed using multiplexed fluorometric immunoassays.

Main Results:

  • BALB/c mice exhibited significantly higher susceptibility to MPV1e, with 50-100 times higher ID50 values compared to B6 mice.
  • Peak viral shedding, infection, and replication levels were substantially higher in BALB/c mice than in B6 mice.
  • While infection persisted in lymphoid tissues (MLN, spleen) and ileum in both strains, levels remained higher in BALB/c mice. Seroconversion was also delayed in BALB/c mice.

Conclusions:

  • C57BL/6 mice demonstrate lower susceptibility to MPV1e infection compared to BALB/c mice.
  • Genetic background significantly influences MPV1e pathogenesis, affecting viral load, replication kinetics, shedding patterns, and immune response timing.
  • These findings have implications for MPV1e surveillance, control strategies, and experimental design in research settings.

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