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Blood, 1 February 2006, Vol. 107, No. 3, pp. 1230-1232.
Prepublished online as a Blood First Edition Paper on October 20, 2005; DOI 10.1182/blood-2005-03-1039.
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Submitted March 15, 2005
Accepted July 26, 2005
Donor KIR genotype has a major influence on the rate of cytomegalovirus reactivation following T-cell replete stem cell transplantation
Mark Cook*, David Briggs, Charles Craddock, Premini Mahendra, Donald Milligan, Christopher Fegan, Philip Darbyshire, Sarah Lawson, Elizabeth Boxall, and Paul Moss
Department of Haematology, University Hospital Birmingham NHS Foundation Trust, Birmingham, United Kingdom; Department of Histocompatibility & Immunogenetics, National Blood Service Birmingham, Birmingham, United Kingdom; CRUK Institute for Cancer Studies, University of Birmingham, Birmingham, United Kingdom
Department of Histocompatibility & Immunogenetics, National Blood Service Birmingham, Birmingham, United Kingdom
Department of Haematology, University Hospital Birmingham NHS Foundation Trust, Birmingham, United Kingdom; CRUK Institute for Cancer Studies, University of Birmingham, Birmingham, United Kingdom
Department of Haematology, University Hospital Birmingham NHS Foundation Trust, Birmingham, United Kingdom
Department of Haematology, Heart of England NHS Foundation Trust, Birmingham, United Kingdom
Department of Haematology, Birmingham Children's Hospital, Birmingham, United Kingdom
Department of Histocompatibility & Immunogenetics, National Blood Service Birmingham, Birmingham, United Kingdom; West Midlands Public Health Laboratory, Health Protection Agency, Birmingham, United Kingdom
* Corresponding author; email: mark.cook{at}uhb.nhs.uk.
Reactivation of cytomegalovirus (CMV) is a common complication following allogeneic stem cell transplantation. Genetic determinants in the host and donor that may influence the rate of reactivation are currently unknown. Viral replication is controlled by T-cells and NK cells and these share expression of killer immunoglobulin-like receptors (KIRs). We analysed whether activatory KIRs carried by the donor influenced the subsequent rate of CMV reactivation in the patient. In sibling transplants where both donor and recipient were CMV seropositive, donors with more than one activating KIR gene were associated with a 65% reduction in CMV reactivation. Multivariate analysis confirmed a significantly reduced risk of CMV reactivation in sibling transplants where the donor had more than one activating KIR. Reduced-intensity transplant and GvHD  grade 2 were associated with an increased risk of CMV reactivation. This observation indicates that activating KIRs play an important role in the cellular control of CMV reactivation.
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