The present studies were performed to demonstrate whether concurrent HSV-1 infection could enhance the immune alterations and dysfunction associated with P → F1-induced graft-versus-host reactions. Examination of phenotypic and functional parameters revealed that Gv-HR-related immune abnormalities in the (C3H.SW X H-2bm 1)F1 recipient were dependent on the parental donor inoculum. Together with HSV-1 infection, virus was found to exacerbate the phenotypic changes and functional abnormalities induced in this GvHR model. In addition, the presence of concurrent HSV-1 was shown to augment the level of specific in vivo donor anti-host reactivity present in F1 recipient spleen cells. Moreover, in vitro studies demonstrated that HSV-1 also enhanced the levels of parent anti-F1 allospecific cytotoxic activity. In total, these findings support the hypothesis that viral exacerbation of GvHR is mediated by its enhancement of donor anti-host alloreactive responses.
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