The primary cause for late failure of all vascularized organ allografts is TVS, a vascular lesion associated with chronic allograft rejection. TVS is characterized by concentric neointimal smooth muscle cell proliferation that results in vessel occlusion and ultimately graft failure. CMV infection is known to accelerate TVS development. The mechanism by which CMV infection accelerates TVS may involve a direct effect of CMV, the recipient's immune response to CMV, or an interaction of CMV and the recipient's alloreactivity to donor tissue. The aim of this project was to determine if TVS developed in CMV-infected solid organ allograft recipients when the host's alloreactivity to the donor organ was eliminated. F344 hearts were transplanted into Lewis or F344→Lewis bone marrow chimeras (BMCs). The transplanted hearts were assessed for the mean time to failure (POD) and the mean percentage of vessel occlusion (NI). F344 hearts demonstrated TVS when transplanted into Lewis recipients. With CMV infection, the time interval to graft failure decreased (POD = 58.8 vs. 90 days) and the degree of TVS increased (NI = 82.9 vs. 69.6%). F344 hearts did not demonstrate rejection or TVS when transplanted into BMC recipients. In contrast to the Lewis recipients, in BMC recipients CMV infection did not influence rejection or development of TVS. These results suggest that CMV acceleration of the development of TVS is dependent on recipient alloreactivity to the donor tissue.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology