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Thymus involution induced by mouse hepatitis virus A59 in BALB/c mice
C Godfraind1, K V Holmes, J P Coutelier
1Laboratory of Pathology, St.-Luc Hospital, Catholic University of Louvain, Brussels, Belgium.
Journal of Virology
|October 1, 1995
Summary
Mouse hepatitis virus A59 (MHV-A59) infection causes temporary thymus atrophy in mice by depleting immature T cells. This immune response is linked to thymus epithelial cell infection, not direct T cell lysis.
Area of Science:
- Immunology
- Virology
- Pathology
Background:
- Mouse hepatitis virus A59 (MHV-A59) is a known pathogen.
- The thymus is a critical organ for T cell development.
- Viral infections can impact immune organ function.
Purpose of the Study:
- To investigate the effects of MHV-A59 infection on the mouse thymus.
- To elucidate the mechanism behind MHV-A59-induced thymic atrophy.
Main Methods:
- Infection of adult BALB/c mice with MHV-A59.
- Assessment of thymus size and cellular composition (CD4+ CD8+ lymphocytes).
- Detection of viral components (MHVR, viral genome) using in situ hybridization.
- Evaluation of glucocorticoid independence of thymic atrophy.
Main Results:
- MHV-A59 induced severe but transient thymic atrophy, peaking at 1 week post-infection.
- Immature CD4+ CD8+ lymphocytes were selectively depleted, and lymphocyte apoptosis increased.
- The MHV receptor (MHVR) was found on thymus epithelial cells, not T lymphocytes.
- Viral genome was detected in a small number of epithelial cells, suggesting indirect effects on lymphocytes.
Conclusions:
- MHV-A59-induced thymic atrophy is not due to direct T lymphocyte lysis.
- The atrophy likely results from apoptosis of double-positive T cells.
- This apoptosis may be triggered by infection of thymus epithelial cells or cytokine release.