Abstract

Abstract Reactivation of cytomegalovirus (CMV) is a frequent complication of bone marrow transplantation (BMT) and results in morbidity and mortality in immunocompromised recipients. In a previous study using murine CMV (mCMV) as a model, we have shown that transfer of memory B cells protects the immunodeficient host from the lethal course of mCMV infection. Here we demonstrate the impact of antibodies on the reactivation of mCMV in a murine model of BMT. We find that previous depletion of B cells (anti-CD20 antibody) during primary mCMV infection results in a profound reactivation of mCMV after syngeneic BMT. Our data show a negative correlation between virus-specific serum IgG titer and reactivation of mCMV after BMT. Therefore, our studies suggest that antibodies play a major role in controlling recurrent mCMV infection after BMT.

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