Mouse hepatitis virus A59 (MHV-A59) infection of adult BALB/c mice ind
uced a severe, transient atrophy of the thymus. The effect was maximal
at 1 week after infection, and thymuses returned to normal size by 2
weeks after infection. There was no effect of glucocorticoids, since t
hymus atrophy was also found in adrenalectomized, infected mice. In in
fected thymus, immature CD4(+) CD8(+) lymphocytes were selectively dep
leted, and apoptosis of lymphocytes was increased. The MHV receptor gl
ycoprotein MHVR was detected on thymus epithelial cells but not on T l
ymphocytes. In a small number of stromal epithelial cells, but in very
few lymphocytes, the viral genome was detectable by in situ hybridiza
tion. These observations suggested that MHV-A59-induced thymic atrophy
results not from a generalized lytic infection of T lymphocytes but r
ather from apoptosis of immature double-positive T cells that might be
caused by infection of a small proportion of thymus epithelial cells
or from inappropriate secretion of some factor, such as a cytokine.