• 1 January 1976
    • journal article
    • research article
    • Vol. 117  (2) , 635-638
Abstract
Neonatal infection with mouse thymic virus (TA), a murine herpes virus, produced extensive but temporary necrosis of the thymus which was maximal at 10-14 days of age. Studies of precursor and amplifier cells mediating graft-vs.-host (GVH) reactivity of thymocytes, spleen cells (SC) and lymph node cells (LNC) of normal and TA-infected mice were made at 4 and 8 wk of age. Infection with TA resulted in a profound reduction (70-80%) in the direct GVH reactivity of thymocytes at both ages; by comparison, the capacity of thymocytes to produce synergy when combined with normal LNC was normal at 8 wk. Direct GVH reactivity of SC was depressed 90% 4 wk after infection with TA, but returned to near normal at 8 wk. Direct GVH reactivity of LNC from TA-infected mice was normal at 4 and 8 wk of age, but amplifier T [thymus-derived] cell activity in LNC was markedly depressed at 8 wk. TA has highly selective effects upon subpopulations of T cells in thymus and lymph node.

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