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Pathogenicity of fibroblast- and lymphocyte-specific variants of minute virus of mice
Abstract:
We tested two strains of the minute virus of mice (MVM) for pathogenic effects and patterns of infection in laboratory mice. The two strains differ in their ability to infect differentiated cultured cells: the prototype virus, MVMp, infects only fibroblasts, while its variant, MVMi, is restricted to lymphocytes. We find that neither strain has any demonstrable effects on the T-cell function of mice infected as adults. In contrast, MVMi, but not MVMp, is able to induce a runting syndrome accompanied by mild immune deficiencies upon the infection of newborn mice. After neonatal infection, MVMi spreads to many organs, and the presence of viral replicative form DNA is evident in nucleic acid hybridization experiments. In contrast, replication of MVMp can be detected only by the seroconversion of infected animals. Newborn mice that grow abnormally as a result of MVMi infection also have low circulating antibody titers to the virus. This phenomenon may be a consequence of the lymphotropism of MVMi.
Insights
The minute virus of mice (MVM) variant MVMi causes runting syndrome and immune deficiencies in newborn mice, unlike MVMp. MVMi spreads widely, while MVMp replication is only detected by antibody response.
Area of Science:
- Virology
- Immunology
- Pathogenesis
Background:
- The minute virus of mice (MVM) exists in strains with differing cellular tropisms.
- MVMp primarily infects fibroblasts, while MVMi targets lymphocytes.
Purpose of the Study:
- To investigate the pathogenic effects and infection patterns of MVMp and MVMi in laboratory mice.
- To compare the impact of neonatal versus adult infection with these MVM strains.
Main Methods:
- Infection of adult and newborn mice with MVMp and MVMi.
- Assessment of T-cell function.
- Monitoring for runting syndrome and immune deficiencies.
- Viral DNA detection using nucleic acid hybridization.
- Seroconversion assays to detect MVMp replication.
Main Results:
- Neither MVMp nor MVMi affected T-cell function in adult-infected mice.
- Neonatal infection with MVMi induced runting syndrome and mild immune deficiencies.
- MVMi disseminated to multiple organs in neonatally infected mice, with detectable viral DNA.
- MVMp replication was only evidenced by seroconversion in infected animals.
- Neonatally MVMi-infected mice exhibited abnormal growth and low antibody titers.
Conclusions:
- MVMi, but not MVMp, causes significant pathogenesis in neonatally infected mice.
- The lymphotropism of MVMi may contribute to the observed immune deficiencies and low antibody titers.
- MVM strains exhibit distinct pathogenic potentials depending on the host's age and viral tropism.