QIMR Berghofer

Strain-specific antibody therapy prevents cytomegalovirus reactivation after transplantation.


Cytomegalovirus infection is a frequent and life-threatening complication that significantly limits positive transplantation outcomes. We developed preclinical mouse models of cytomegalovirus reactivation after transplantation and found that humoral immunity is essential for preventing viral recrudescence. Preexisting antiviral antibodies decreased after transplant in the presence of graft-versus-host disease and were not replaced, owing to poor reconstitution of donor B cells and elimination of recipient plasma cells. Viral reactivation was prevented by the transfer of immune serum, without a need to identify and target specific antigenic determinants. Notably, serotherapy afforded complete protection, provided that the serum was matched to the infecting viral strain. Thus, we define the mechanisms for cytomegalovirus reactivation after transplantation and identify a readily translatable strategy of exceptional potency, which avoids the constraints of cellular therapies.

Authors Martins, Jose Paulo; Andoniou, Christopher E; Fleming, Peter; Kuns, Rachel D; Schuster, Iona S; Voigt, Valentina; Daly, Sheridan; Varelias, Antiopi; Tey, Siok-Keen; Degli-Esposti, Mariapia A; Hill, Geoffrey R
Journal Science (New York, N.Y.)
Pages 288-293
Volume 363
Date 1/01/2019
Grant ID 1119298
Funding Body National Health and Medical Research Council of Australia (NHMRC)
URL http://www.ncbi.nlm.nih.gov/pubmed/?term=10.1126/science.aat0066
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