HSV-1 enhances GvHR-associated parent anti-F1 alloreactivity in vivo and in vitro.
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-2bm1)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.
Levy
R B
RB
Department of Microbiology and Immunology, University of Miami, School of Medicine, Florida 33101.
Jones
M
M
Cray
C
C
D000818:Animals; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D006087:Graft vs Host Reaction / Q000276:immunology*; D006561:Herpes Simplex / Q000276:immunology*; D051379:Mice; D008809:Mice, Inbred C3H; D010641:Phenotype; D013154:Spleen / Q000637:transplantation; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
D000945:Antigens, Differentiation, T-Lymphocyte